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First Year Semester One > Introduction To Pharmacology > Flashcards

Introduction To Pharmacology Flashcards

1
Q

What do we regulate in blood plasma?

A

Oxygen
Glucose
Ions
Volume

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2
Q

What do we regulate in interstitial fluid?

A

Glucose
Ions

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3
Q

What do we regulate in intracellular fluid?

A

ATP
Glucose
Ions
Volume

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4
Q

What is total body water?

A

42 L
~ 60%

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5
Q

How much water in blood plasma?

A

3L

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6
Q

How much water in interstitial fluid?

A

13L
- liquid surrounding cells

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7
Q

How much water in transcellular fluid?

A

1L
- CSF, lymph ect

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8
Q

How much water in intracellular fluid?

A

25L

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9
Q

What is the osmolality?

A

290 mOsm

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10
Q

What’s the distribution of ions ECF vs ICF?

A

ECF = more Na+, Cl-, Ca2+
ICF = more K+

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11
Q

What is amphipathic?

A

Have a region of polar and non-polar.
- Phospholipid bilayer

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12
Q

What is the cell membrane’s permeability?

A

Impermeable to large & charged.
Permeable to hydrophobic (O2, CO2, steroid hormones)

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13
Q

What are the two types of active transport?

A

Primary - direct - pumps using a chemical reaction
Secondary - indirect - cotransporters and exchangers - coupled uphill movement of one thing with downhill of another e.g. sodium potassium ATPase.

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14
Q

What is the effect of electrochemical gradients on transport?

A

Drives passive transport.
Depends on concentration gradient.
For charged molecules - also depends on voltage.

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15
Q

What is simple diffusion?

A

It is the movement of an uncharged hydrophobic solute through lipid bilayer.
How fast it moves = describes by flux (Jx)

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16
Q

What does flux (Jx) depend on?

A
  • permeability coefficient of X (Px)
  • concentration gradient
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17
Q

What is the flux equation?

A

Jx = Px(conc gradient)

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18
Q

What is a transmembrane protein?

A
  • an integral membrane protein
  • composed of membrane-spanning alpha helix domains
  • can be single pass or multipass
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19
Q

What defines a protein membranes topology?

A

Location of sequence

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20
Q

What are the types of transmembrane proteins?

A

Pore - non-gated channel
Channel - gated pore
Carrier
Pump - requires energy

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21
Q

What is a transmembrane protein?

A

All have multiple transmembrane segments surrounding a solute permeation pathway.
Allow hydrophilic molecules to pass the membrane.

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22
Q

What is the structure of a transmembrane protein?

A
  • Amphipathic helices - alternating hydrophobic and hydrophilic amino acids - hydrophobic surfaces face the membrane, hydrophilic surfaces create a central pore.
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23
Q

What do pores do?

A

Always open - facilitated diffusion
Have multiple subunits
e.g. aquaporins
Driving force = electrochemical gradient.

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24
Q

What does each channel have?

A

1) a moveable gate
2) a sensor: voltage, ligand, mechanical
3) a selectivity filter
4) an open channel pore

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25
Q

What do carriers do?

A

Never has a continuous path.
Driving force = electrochemical gradient
Slow
Can become saturated
e.g. GLUT

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26
Q

How does carrier diffusion work?

A

1) The carrier is open to the outside
2) X enters and binds to binding site
3) Outer gate closes - X still bound
4) Inner gate opens
5) X enters cell

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27
Q

Why can carrier diffusion become saturated?

A

Flux limited by # of carriers and speed of carrier cycle.
Jmax = conc high enough to occupy all carriers.

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28
Q

What carriers use active transport?

A

Pumps
Cotransporters
Exchangers

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29
Q

How do cotransporters work?

A
  • Requires a solute whose electrochemical gradient provides the energy.
  • Move both in (symporters e.g. Na/glucose)
  • Can become saturated.
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30
Q

What is osmolality?

A

Total conc of all particles free in a solution.
mOsm = milliosmoles per kg of water

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31
Q

What does a channel do?

A

Gated ion channels e.g. potassium channel.
Driving force = electrochemical gradient

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32
Q

How do exchangers work?

A

Solutes move in opposite directions (antiporters e.g. Na/Ca).

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33
Q

What did Henry Dale do?

A

He won a Nobel prize for studying acetylcholine as an agent in the chemical transmission of nerve impulses.

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34
Q

What is a mediator?

A

A chemical, peptide or protein which communicates between cells.

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35
Q

What are the criterias for a mediator?

A
  • released in sufficient amounts to produce a biological action on a specific cell in a time frame.
  • applying a sample will have the same biological effect
  • interference on synthesis, release or action will stop/control response.
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36
Q

What is the general path for mediators?

A

They are extracellular signal molecules –> bind to receptors on target cells –> initiates intracellular signals which alter cell behaviour through effector proteins (cell signalling)

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37
Q

What is signal transduction?

A

Converting extracellular signals to intracellular.

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38
Q

What are the five types of intercellular communication?

A
  • contact-dependant
  • autocrine
  • synaptic
  • paracrine
  • endocrine
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39
Q

What is contact dependant signalling?

A

Shortest type of signalling.
e.g. immune responses and development (delta-notch signalling)

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40
Q

What is paracrine signalling?

A

Extracellular mediators act locally - stored in vesicles or synthesised on demand.
e.g. histamine, nitric oxide (vessel diameter), prostaglandins.

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41
Q

What is autocrine signalling?

A

Similar to paracrine but activates itself.

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42
Q

What is neuronal signalling?

A

Uses synapses - fast - to specific cells.
Mediators - neurotransmitters e.g. ACh (neuromuscular junction &heart), Noradrenaline (on heart)

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43
Q

What is endocrine signalling?

A

Long distance - uses hormones through the blood.
Slow and non-specific.
Hormones can be protein (insulin), aa derives (adrenaline) or steroid (estradiol).

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44
Q

What two ways are mediators synthesised?

A

1) small molecular - regulated by specific enzymes.
2) peptides - regulated by transcription - depends what genes are active and cells can produce multiple types of mediator. Vesicles can store more than one.

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45
Q

What are the two groups of mediators?

A
  • preformed and stored in vesicles until released by exocytosis - rapid - includes noradrenaline and insulin –> conc usually mM which is good so we can have high conc for response.
  • on demand synthesised and released by diffusion or constitutive secretion - slower to act - e.g. nitric oxide and prostaglandins.
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46
Q

How did we know that neurotransmitters are released in vesicles?

A

Studies showed quantal nature which suggested packages.

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47
Q

How does neurotransmitter action stop?

A

Enzymes can stop it e.g. acetylcholinesterase.
The NT can also be taken back into the neuron or supporting cells e.g. glia - this is due to specific transporters in membrane

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48
Q

Who discovered acetylcholine?

A

Otto Loewi

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49
Q

How are noradrenaline and adrenaline made?

A

From tyrosine –> dopamine –> noradrenaline —> adrenaline

Enzymes required for each step.

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50
Q

What regulates both types of mediator release?

A

Calcium

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51
Q

What is a ligand?

A

Any molecule which binds to a receptor - can be antagonist or agonist
Hydrophilic or hydrophobic

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52
Q

What is an endogenous agonist?

A

Mediator in the body which binds to a receptor - produces a response
e.g. ACh, noradrenaline, insulin

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53
Q

What is converging cell signalling?

A

All cells have multiple types of receptors - can integrate information
Receptors can use similar transduction mechanisms = amplify signal

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54
Q

What is diverging cell signalling?

A

Molecules can act on more than one type of cell type.
Allows coordinated responses.

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55
Q

What are receptors?

A

Proteins - recognition sites which can bind to a molecule and modulate activity of the cell

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56
Q

What do the first three receptor classes have in common?

A
  • each has transmembrane spanning segments
  • each has a ligand binding domain
  • ligands here are hydrophilic
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57
Q

What are the four classes of receptors?

A

1) Ligand-gated ion channels (ionotrophic) - could cause electrical signals - takes milliseconds
2) G protein-coupled receptors (metabotropic) - could contact muscles - takes seconds
3) Kinase-linked receptors - can change enzyme activity - takes hours e.g. insulin receptor
4) Nuclear (intracellular) - more channels in cell membrane - takes hours

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58
Q

What are nuclear receptors?

A

Polypeptides with multiple domains
Ligands here are hydrophobic
Act as a transcription factor - binds to DNA and regulated gene expression
e.g. oestrogen receptors

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59
Q

Which chemical mediators use which receptors?

A

Most small mediators = ligand or g protein-coupled
Peptide hormones = g protein-coupled or kinase-linked
Steroid = nuclear

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60
Q

What are ligand-gated ion channels?

A
  • Ion channels
  • involved in fast synaptic transmission
  • agonists = neurotransmitters
  • made of 3-5 subunits
  • had central aqueous pore
  • channel closes when agonist removed

e.g. NAChR

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61
Q

What is nAChR?

A

Nicotinic Acetylcholine Receptor
- excitatory ligand gated ion channel
- on every skeletal muscle
- in NMJ and autonomic NS
- has 5 subunits
- agonist = ACh or nicotine - when bind cause depolarisation as ions flow through

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62
Q

What is GABA?

A

Bind to ligand gated ion channels (GABAa receptors) - causes inhibition as cause hyperpolarisation

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63
Q

What is a G protein-coupled receptor?

A
  • Single transmembrane protein which spans membrane 7 times (7TM)
  • > 800 genes code for these
  • Interacts with an intracellular G protein (heterotrimeric GTP-binding protein) - has 1 alpha, 1 beta, 1 gamma subunit

e,g, MAChR

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64
Q

What do the heterotrimeric g proteins do?

A

1) beta and alpha units are bound to the receptor
2) when ligand binds - g protein changes and causes GTP to bind to alpha instead of GDP
3) G protein leaves receptor
4) a-GTP and beta-gamma dissociate
5) they can bind with their effectors
6) when GTP –> GDP again - trimer reassembles

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65
Q

What are examples of effectors that G proteins may control?

A
  • ion channels
  • enzymes: adenylyl cyclase, phospholipase C
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66
Q

What are secondary messengers?

A

Small diffusible molecules that spread a signal
Amplify a signal

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67
Q

How is adenylyl cyclase modulated?

A

GAs - stimulates - more adenylyl cyclase, more cAMP and more protein kinase A

GAi - inhibits - less adenylyl cyclase, less cAMP, less protein kinase A

cAMP - secondary messenger

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68
Q

How do g proteins increase calcium levels?

A

Gaq (alpha subunit) activates phospholipase C which breaks down PIP2 into IP3 & DAG. IP3 triggers release of calcium from the ER.

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69
Q

What do specific G proteins do?

A

Gs - activates adenylyl cyclase - e.g. adrenergic B1/2
Gi - (a) inhibits adenylyl cyclase or (By) activates potassium channels - e.g. adrenergic a2/muscarinic M2
Gq - activates phospholipase C - increases calcium e.g. adrenergic a1/muscarinic M1/M3

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70
Q

What is a drug?

A

A known chemical substance which, when administered, causes a biological response.

Can interfere with synthesis, storage, release, degradation or receptor-dependent response produced by a mediator.

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71
Q

What is an assay?

A

Lab test where we investigate the function of mediators, measure toxicity and test phamacological activity.

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72
Q

What are the principles of pharmacology?

A
  • drug action must be explicable
  • drug molecules must be bound to cells/tissues to produce an effect
  • drug molecules must exert a chemical influence on 1 or more parts of a cell to produce a pharmacological response
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73
Q

What proteins are usually targeted by drugs?

A
  • enzymes
  • transporters
  • ion channels
  • receptors
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74
Q

What is an antagonist?

A

Drug which inhibits the response of an agonist - competes with agonist and binds instead
DO NOT MAKE A RESPONSE

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75
Q

When are side effects caused?

A

When drugs lack specificity - drugs will bind to its specific receptor anywhere.

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76
Q

What is therapeutic manipulation of contact-dependant signalling?

A

e.g. CAR T immunotherapy uses this signalling to kill cancer cells - engineered by altering genome of T cells

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77
Q

How is paracrine signalling affected by drugs?

A

e.g. mast cells secrete histamine - antihistamines will block histamine receptors

e.g. prostaglandins (a type of eicosanoid) are formed from different enzymes - paracetamol can target these enzymes

e.g. nitric acid relaxes blood vessels - viagra inhibits an enzyme - prolongs NO action

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78
Q

How can drugs target neurotransmission?

A

e.g. can block voltage gated sodium channels - prevent action potential - used as local anaesthetic - lidocaine

e.g. Botulinum toxin - from bacteria - cleaves proteins needed for synapses

e.g. amphetamines increase noradrenaline by displacing it from vesicles

e.g. fluoxetine blocks 5HT reuptake - antidepressant

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79
Q

What are endocrine cells?

A

Hormones are secreted from here into blood.
Have close proximity to capillary beds.
Found in endocrine tissues or glands (NO DUCTS)

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80
Q

What is endocrine signalling?

A

Enables signalling along long distances
Slow
Specific to receptors - not specific organs or tissues

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81
Q

What are the different hormone types?

A

Protein e.g. Insulin
Amino acid e.g. adrenaline
Steroid e.g. estradiol

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82
Q

What is a peptide hormone?

A
  • from amino acids
  • released by exocytosis by secretory granules
  • receptors = cell membrane surface
  • response - s to min
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83
Q

What are amino acid derived hormones?

A
  • derived from tyrosine (requires specific enzymes)
  • released from vesicles via exocytosis (except thyroid hormone)
  • receptors = cell membrane surface (except thyroid hormone)
  • response = s to min (except thyroid)
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84
Q

What is a steroid hormone?

A
  • metabolite of cholesterol (needs enzymes)
  • lipid soluble = diffuses out
  • diffuses into cells and binds to nuclear receptors
  • response = hours to days
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85
Q

What are the 7 endocrine glands?

A
  • Pituitary
  • Thyroid
  • Parathyroid
  • Adrenals
  • Ovaries
  • Testes
  • Pancreas
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86
Q

What are endocrine tissues?

A
  • hypothalamus
  • kidneys
  • GI tract
  • heart
  • liver
  • adipose tissue
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87
Q

What is the anterior part of the hypothalamus?

A

Adenohypophysis
- developed from upward projection of pharynx
- troph cells are stimulated by hormones from hypophyseal portal system from hypothalamic neurons

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88
Q

What is the posterior lobe of pituitary called?

A

Neurohypophysis
- developed from downward projection of brain
- releases hormones from large diameter neurones into bloodstream

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89
Q

What are the main pituitary hormones?

A

Tropic hormones - stimulate effects from other hormones - GH, ACTH, TSH, FSH, LH, Prolactin
Posterior - ADH & Oxytocin

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90
Q

How is the thyroid an endocrine gland?

A

Secretes T3 & T4 (amino acid derived) - these depend on hypothalamic-pituitary hormones and iodine
These transport across cell membranes by facilitated diffusion and bind to nuclear receptors.
This regulated metabolism, development and growth

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91
Q

How is the parathyroid gland endocrine?

A

Parathyroid hormone (peptide) regulates plasma calcium and phosphate and targets bone, intestine and kidneys.

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92
Q

What is the feedback loop for PTH?

A

High plasma calcium is sensed by chief cells - lower PTH, lower kidney reabsorption, less bone resorption and low intestinal absorption.

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93
Q

What does adrenal cortex release?

A

Releases steroid hormones: glucocorticoid (cortisol), mineralcorticoid (aldosterone)
Zona glomerulosa - mineral
Zona fasciculata - gluco

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94
Q

What does the adrenal medulla release?

A

Chromaffin cells release adrenaline
Noradrenaline is also released

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95
Q

What is the hypothalamic-pituitary-adrenocortical axis?

A

Hypothalamus releases CRH - this causes the anterior pituitary to release ACTH - causing adrenal cortex to release cortisol.
Cortisol inhibits CRH and ACTH release

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96
Q

What do the ovaries secrete?

A

Steroid hormones: oestrogen and progesterone
This gland can switch from negative to positive feedback

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97
Q

What do the testes secrete?

A

Leydig cells secrete steroid hormone - testosterone

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98
Q

What is the somatic NS route?

A

Somatic NS

Afferent to CNS (brain and spinal cord)

Efferent to somatic NS (voluntary)

Skeletal muscles

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99
Q

What is the visceral nerve route?

A

Visceral nerves (sensory part of peripheral NS)

Afferent to CNS

Efferent to autonomic NS (involuntray - motor part of peripheral NS)

Smooth muscle, cardiac, glands ect.

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100
Q

What are the parts of the autonomic nervous system?

A

(part of peripheral)

Sympathetic - fight or flight - coordinated full body or organ specific
Parasympathetic - rest and digest - organ specific

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101
Q

What are examples of sympathetic stimulation?

A
  • eye - dilation
  • heart - increase heart rate
  • blood vessels - constricting
  • lungs - bronchiole dilatione
  • liver
  • reproductive systems
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102
Q

What are examples of parasympathetic stimulation?

A
  • heart - decrease heart rate
  • eyes
  • GI tract
  • bladder
  • reproductive organs
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103
Q

How do parasympathetic and sympathetic work together?

A

Innervate the same tissues but have opposite effects - work synergistically.
Except for sweat glands, hair, blood vessel sm and adrenal medulla which are mainly sympathetic

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104
Q

What is the structure of the autonomic nervous system?

A

Preganglionic neuron in CNS
Postganglionic neuron in peripheral ganglion
both symp and parasymp have this organisation

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105
Q

What are preganglionic neurons?

A

Always cholinergic - release ACh
ACh activated nicotinic ACh receptors on postsynaptic cell

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106
Q

What is the sympathetic pathway?

A

Short cholinergic from thoracic and lumbar spinal cord - long adrenergic postganglionic
Target tissue express alpha and beta adrenergic receptors

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107
Q

What is the exception to the sympathetic pathway?

A

Adrenal medulla - chromaffin cells are similar to postganglionic neurones but release adrenaline - target is a and b adrenergic receptors

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108
Q

What is the parasympathetic pathway?

A

Long cholinergic neurons from brainstem and sacral spinal cord
Short cholinergic postganglionic neurones
Target tissues express muscarinic ACh receptors

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109
Q

What is the vagus nerve?

A

Cranial nerve 10
Carries 80% of parasympathetic outflow
Also carries visceral afferents

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110
Q

What mediates autonomic reflexes?

A

The spinal cord - also receives sensory afferent and brainstem input
Brainstem nuclei - mediate autonomic reflexes
Forebrain - cortical control could cause autonomic output e.g. anxiety
Visceral afferents - sensory from organs takes priority over cortical e.g. needing the toilet badly

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111
Q

What does the hypothalamus do?

A

Feeding
Thermoregulation
Circadian rhythms
Water balance
Sex drive
Reproduction

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112
Q

What are the principle transmitters in the ANS and where do they act?

A

Acetylcholine and NA
They act on nAChRs, mAChRs, alpha and beta adrenoceptors

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113
Q

How are cAMP and protein kinase A levels changed?

A

Gas - stimulates
1) stims adenylyl cyclase
2) This increases cAMP
3) This increases PKA

Gai - inhibits
1) inhibits adenylyl cyclase
2) lower cAMP
3) lower PKA

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114
Q

What is Gaq?

A

Part of g protein

It increases phospholipase C - increases IP3 + DAG - this increases calcium levels

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115
Q

What are the different g proteins?

A

Gs, Gi, Gq
They are g proteins
Gs - alpha - activated adenylyl cyclase
Gi - alpha - inhibits adenylyl cyclase
- betadelta - activates k+
Gq - activates PLC - increase calcium

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116
Q

What are cholinergic receptors?

A
  • Nicotinic - agonists = nicotine, antagonist = curare
  • Muscarinic - agonists = muscarine, antagonist = atropine

Both have ACh as agonist

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117
Q

What are the mAChR subtypes?

A

M1, M3, M5
- These have Gq -> increased PLC - Increased calcium

M2, M4
- These have Gi - inhibits adenylyl cyclase

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118
Q

Where are the different mAChRs found?

A

M1 = autonomic ganglia, glands, cerebral cortex - allows for gastric secretion and CNS excitation

M2 = atria, CNS - cardiac and neural inhibition

M3 = exocrine glands, smooth muscle, blood vessels - gastric and salivary secretion, GI SM contraction, vasodilation, eye accomodation

M4 = CNS - enhanced locomotion

M5 = substantia nigra, salivary glands - not known

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119
Q

How does our heart rate decrease?

A

Parasympathetic stimulation activated M2 receptors in atria - betadelta subunit will open k+ channels - moves out - more negative
- decreases HR
- slow AV conduction
- decrease atria force

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120
Q

What do M1 and M3 do?

A

Gq coupled -
contract smooth muscle (bronchoconstriction, GI motility, bladder voiding)
Stimulate secretion from glands (mucus, lacrimal glands, salivary, sweat)

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121
Q

What effect would muscarine have?

A

low BP, high saliva, high tear flow, high sweat, nausea

overdose: death from cardiac and resp failure

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122
Q

What effect would atropine have?

A

Inhibit secretion of saliva, tears, sweat ect.
Relax smooth muscle
Dilate pupils
Increase heart rate

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123
Q

What’s the name for drugs that indirectly enhance cholinergic transmission?

A

Cholinomimetic
Inhibit acetylcholinesterase

Anticholinesterase drugs:
1) long acting (irreversible)
2) nerve gas (organophosphates, pesticide)

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124
Q

What are noradrenaline and adrenaline receptors?

A

On tissues responding to postganglionic sympathetic neurons
Beta - All Gas - all increase cAMP

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125
Q

What adrenaline receptor effects the heart?

A

NA (sympathetic neurones), A (chromaffin cells) bind to B1 receptors on ventricles and nodes
1) binds
2) stims adenylyl cyclase - more cAMP and PKA
3) This phophorylates calcium channels
4) calcium enter - contraction

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126
Q

What causes SM relaxation in bronchioles?

A

B2 activation - Gas activation - stims adenylyl cyclase - more cAMP, more PKA - phosphorylates SM

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127
Q

What are clinical uses of adrenoceptor agonists?

A

Adrenaline - cardiac arrest & anaphylaxis

B2 selective - bronchodilator (salbutamol)

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128
Q

What are clinical uses of adrenoreceptor antagonists?

A

Can treat hypertension, heart failure, anxiety
But can cause bronchocontriction and cardiac depression

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129
Q

What germ layers do epithelia develop from?

A

Endoderm (GI lining)
Mesoderm (CV lining)
Ectoderm (Epidermis)
- in every organ

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130
Q

What are the functions of epithelia?

A
  • protection - skin
  • absorption - SI
  • barrier - BBB
  • diffusion - lung
  • secretion - gland
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131
Q

What are the common properties of epithelia?

A
  • can import or expel substances
  • have tight junctions
  • have apical (faces external environment) and basolateral domains with differing membrane properties (polarised)
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132
Q

Are epithelia cellular?

A

Entirely!
- avascular (no blood vessels)
- lack extracellular fibres
- little extracellular space

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133
Q

Are epithelia polar?

A

Yes!
There are differences between the apical and basal membranes (both specialised in different ways)

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134
Q

What is the basement membrane?

A

Separates cells from underlying connective tissue (collagen IV).

ECM proteins secreted by epithelial cells: collagens, laminins, proteoglycans

Structural support - basal lamina, reticular lamina (anchors BM to connective tissue below)

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135
Q

What are tight junctions?

A

Impede paracellular (between cells) movement

Protein strands (claudins) determine tightness - 24 claudin genes

Have high barrier function e.g. renal thick ascending limb

Are leaky e.g. proximal tubule

Variation in the permeability

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136
Q

What are adhering junctions?

A

Form belt around cell - under tight junctions - linked actin and cadherins

Disruption can cause spread of cancer (metastasis)

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137
Q

What regulates epithelia?

A
  • underlying mesenchymal cells form epithelium as cadherins change expression
  • this is epithelial-mesenchymal transition (EMT)
  • used for embryonic development and cancer metastasis
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138
Q

What are gap junctions?

A

Lateral communication between cells - allows small molecule diffusion between cytoplasms - cells electrically coupled

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139
Q

What are the junctional complexes of epithelia?

A
  • Tight junctions
  • Adhering junctions
  • Gap junctions
  • Desmosomes
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140
Q

What are desmosomes?

A

Strong adhesion - has extracellular domains (cadherin).

Anchor proteins (plaques) link cadherin domains to intermediate filaments

There are some myosin filament interactions - contract

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141
Q

What links epithelia to basement membrane?

A

Actin-linked cell matrix junction
Hemidesmosome

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142
Q

How are epithelial cells replaced?

A

From stem cells - tissue homeostasis
Intestines - 5 days
Lungs - 6 months

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143
Q

What are the four types of epithelia?

A

Simple - single layer
Stratified - many layers (skin)
Pseudostratified - upper resp
Transitional - urothelium

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144
Q

What are the simple epithelia?

A

Simple squamous - thin, allow rapid passage
Simple cuboidal - secretion/absorption of molecules by active transport - some have cilium

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145
Q

What is simple columnar and pseudostratified?

A

Simple columnar: may have cilia/microvilli, majority of GI tract, in fallopian tubes, in some respiratory

Pseudostratified: single layer but looks like more, can be ciliated - these have goblet cells

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146
Q

What are the stratified epithelia?

A

Stratified squamous: most common stratified, in areas of abrasion

Stratified cuboidal: less common, glands

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147
Q

What epithelia can change shape?

A

Stratified columnar: rare - in pharynx, anus, male urethra, embryo

Transitional: round cells when relaxed

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148
Q

What secretes mucus, sebum and protein?

A

Mucus: mucus glands

Protein: serous glands e.g. salivary

Sebum: sebaceous glands e.g. oils on face

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149
Q

What are skeletal muscles responsible for?

A
  • voluntary movement of bones
  • control of inspiration by diaphragm
  • skeletal-muscle-pump - returns venous blood
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150
Q

What is the skeletal muscle structure?

A

Striated
Myofilaments - myofibril - muscle fibre - fascicle

T tubules and sarcoplasmic reticulum form triad

H and I change shape
A doesn’t

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151
Q

What causes skeletal muscle contraction?

A

ACh at neuromuscular junction - action potential in membrane of muscle

Wave of depolarisation through t-tubule to interior of cell - runs near 2 areas of SR - triad

Reaches sarcoplasmic reticulum

Increase of intracellular calcium

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152
Q

What are the steps in cross-bridge formation and sarcomere contraction?

A

1) ATP binds to myosin head - dissociation of actin-myosin complex
2) ATP is hydrolysed - returns to resting state
3) crossbridge forms - myosin head binds to actin
4) Pi released
5) change in myosin - power stroke - filaments slide
6) ADP released

5 times a second

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153
Q

How many myosin heads in a thick filament?

A

~ 300 heads
each head cycles 5x a second

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154
Q

What are the 3 types of muscle fibers?

A

Type 1 (slow oxidative) - non fatigue, red, low glycogen, high mitochondria e.g. soleus
Type IIa (fast oxidative) - non fatigue, red, some glycogen, higher mitochondria e.g. gastrocnemius
Type IIb (fast glycolytic) - fatigable, white, high glycogen, anaerobic, few mitochondria e.g. biceps

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155
Q

What are slow and fast fibres?

A

Slow - half the diameter and take longer to contract
Fast - take 10 msec or less

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156
Q

What is muscle twitch?

A

Involuntary contraction - in three phases: latent - contraction - relaxation

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157
Q

What is isometric and isotonic contraction?

A

Isometric - muscle at fixed length - tension generated e.g. plank
Isotonic - muscle stimulation causes a change in length e.g. bicep curl

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158
Q

What is botulinum toxin?

A

Linked to food poisoning - muscle weakness, paralysis - endoproteinase which cleaves exocytosis of ACh

can be used for cross-eyedness (strabismum), uncontrolled eye movements (blepharospasm), and botox

ADD TOXINS FOR ALL CHANNELS

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159
Q

What is the integumentary system?

A
  • skin
  • largest organ - 12-15% of body weight
  • layers by 4 months in utero, 3rd trimester skin hardens (pigment absorbs light, blood and fat scatters light)
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160
Q

What are the layers of the skin?

A

Epidermis (epithelia)
Dermis
Hypodermis (adipose tissue)

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161
Q

What is the dermis?

A

2mm in soles/ 0.2 mm in eyelid
Fibroblasts produce ECM proteins: collagen, laminin/fibronectin

2 zones:
- papillary - thin loose connective tissue, motibility of leukocytes, mast cells and macrophages
- reticular - thick dense irregular - adipocyte clusters

Has all accessory organs: hair, nail, sweat glands

Rich layer of blood, nerve endings and lymphatic vessels

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162
Q

What is the dermal-epidermal boundary?

A

Wavy boundary - dermal papillae (raised areas e.g. fingerprint), epidermal ridges

The papillae facilitate nerve fibres reaching close to the surface

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163
Q

What is the epithelia in the epidermis of the skin?

A

keratinised stratified squamous epithelium

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164
Q

What are the layers of the epidermis?

A

Stratum corneum
lucidum - stress protect
granulosum
spinosum
basale

Thin doesn’t have lucidum - thick does

No blood vessels
Self-regeneration

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165
Q

What is the stratum basale?

A

Has keratinocytes - in touch with basement membrane (stem cells)
Melanocytes give skin colour
Merkel/tactile cells connected to sensory nerves

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166
Q

What are melanocytes?

A

Release melanin - UV absorb, antioxidant

pheomelanin - red/yellow
eumelanin - brown/black

Pigment of skin = melanin + carotine (in fat + corneum) + blood

Form melanosomes which are phagocytosed by keratinocytes

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167
Q

What is the stratum spinosum?

A

Several keratinocyte layers - usually thickest (unless thick skin - corneum)

Produce keratin filaments - keratinocytes are linked by desmosomes so water retention

Dendritic cells present

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168
Q

What is the stratum granulosum?

A

3-5 layers of flat keratinocytes
Have dark staining granules

Cells undergo apoptosis

Produce glycolipid-filled vesicles which produce barrier between stratum spinosum

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169
Q

What is the stratum corneum?

A

Most superficial
15-30 layers of flattened corneocytes (dead keratinocytes)

  • stratum disjunctum: have corneodesmosomes which regulate desquamation
  • stratum compactum

have a cornified envelope full of keratins - enclosed within proteins and surrounded by lipid envelope

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170
Q

What are nails?

A

Derivative of stratum corneum
Packed with keratin
New cells added in nail matrix

Iron deficiency = fat/concave
Hypoxemia = clubbed

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171
Q

What is hair?

A

Filament of keratinised cells from follicle.
Hair bulb - in dermal papilla - hair matrix above

Lanugo (soft hair) - vellus - terminal

medulla - loose cells
cortex - keratinised cuboidal cells
cuticle - surface scaly cells

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172
Q

What are the 5 skin glands?

A

Eccrine/merocrine sweat glands - watery perspiration, controlled by SNS, temp regulation

Apocrine sweat glands - cells pinch off and released into scent follicles - respond to stress and sex - armpits and gentials

Holocrine sebaceous glands - cell disintegrates - oily skin and hair

Ceruminous glands - e.g. earwax

Mammary glands

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173
Q

How is skin a barrier?

A

Physical - keratin scaffold
Biochemical - mild acidic, sebaceous glands (FAs inhibit bacteria, C6H)
Immunological - dermal and epidermal langerhans cells

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174
Q

What are epidermal langerhans cells?

A

Immunological barrier - process antigens

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175
Q

How does vitamin D synthesis work?

A

Fat soluble - increases intestine absorption of Calcium

Previtamin D3 in the keratinocytes is photolysed by UV acts via a nuclear receptor prohormone - first step

Photochemical reaction

176
Q

How does skin help with thermoregulation?

A

Anterior hypothalamus senses body temp

Receptors
Insulation
Sweating
Vasodilation/constriction

There are arteriovenous anastomoses - have sympathetic innervation - low temp - increase innervation ect.

177
Q

What is cardiac muscle?

A

Striated - branched with intercalated disks
There are electrical coupling between myocytes by gap junctions

178
Q

What is smooth muscle?

A

Involved in mechanical control of organ systems
Non-striated - multiple actin fibres join at dense bodies
Can be multiunit or unitary

179
Q

How is calcium increased in skeletal muscles?

A

Depolarisation activates L-type calcium channels in T-tubule membrane - influx of calcium

There’s a mechanical tethering between the L-type channels in t-tubules and Ca channels (Ryanodine receptors) in sarcoplasmic reticulum - they open

180
Q

Does cardiac muscle have t-tubules?

A

Yes! but only one branch of t-tubule is near SR (no triad)- dyad at the Z line

No mechanical interaction between t-tubule receptors and ryanodine receptors

The calcium instead triggers the receptors on the SR

Calcium induced calcium release

181
Q

How is calcium removed from muscle cells?

A

1) across the membrane by plasma membrane calcium ATPase (PMCA) or Na/Ca exchanger

2) back into SR via calcium ATPase

182
Q

How do we increase calcium in smooth muscle?

A

No t-tubules, no triads or dyad - instead have shallow invaginations - caveolae

Have two parts of SR - peripheral (next to caveolae) and central

L-type ca channels still activate from action potential

Activation of ryanodine receptors - calcium induced calcium

Activation of Gq-coupled - IP3 production - IP3 receptors in SR (calcium channels)

183
Q

What role does calcium have in cross-bridge formation?

A

Calcium binds to TnC - causes TnT to pull tropomysosin and TnI out of the way

Myosin can now bind

When calcium dissociates - everything goes back to normal

184
Q

How does smooth muscle contract?

A

No troponin!!

There’s calponin and caldesmon instead.

Calmodulin is stimulated by calcium
Myosin light chain is phosphorylated by myosin light chain kinase
- allows formation of crossbridge

To stop - de-phosphorylate with MLCP

185
Q

What is a motor unit?

A

Motor neuron and muscle fibres

186
Q

What is the function of the circulatory system?

A

Primary - distribute gases

Secondary:
- fast chemical signalling
- dissipation of heat
- mediated inflammatory and host defences

187
Q

What are the two types of circulation?

A

Left - systemic
- Parallel pathway from left to right
- Usually through single capillary bed - two in kidney ect.

Right - pulmonary
- single pathway from right to left

188
Q

What does branching do for blood vessels?

A

Radius decreases with branching
Combined cross-sectional area in daughter cells>parent cells

CSA increase highest in capillaries

189
Q

What are the layers in a blood vessel?

A

Endothelial cells -> elastic fibres -> collagen fibres -> smooth muscle cells

Adventitia (outside) -> Media -> intima

190
Q

What are the elastic arteries?

A

Large arteries - high compliance and can cope with high pressures

191
Q

What are muscular arteries?

A

Medium sized - there are smooth muscle cells arranged circumferentially - can vasoconstrict and dilate

192
Q

What are arterioles?

A

Connect to capillaries - have precapillary sphincters which monitor blood flow
also have terminal regions - metarterioles
smooth muscle regulated flow - regulated microcirculation

193
Q

What are venules?

A

Are porous - exchange nutrients and waste - excellent reservoirs - have thin smooth muscle

194
Q

What are capillaries?

A

Only endothelial and basement membrane - exchange gases, water, nutrients and waste

Three groups:
- fenestrated
- continuous
- sinusoidal (discontinuous)

195
Q

What is starling’s forces?

A

Fluid transfer in capillaries

Jv = Kf [(Pc-Pi) - (Pi c - Pi i)

+ = filtration, - = absorption
Jv = fluid movement
Kf = hydraulic conductance
Pc/i = Capillary/intestinal hydrostatic
Pi = oncotic

Pc declines down the capillary

196
Q

What is the lymphatic system?

A

Drains excess interstitial fluid
Maintains blood volume
Transports dietary lipids
Immunology

197
Q

How are valves attached to the heart?

A

AV (mitral + tricuspid) connected by chordae tendinae and papillary muscles

198
Q

What is in the heart wall?

A

Epicardium, myocardium (have cells connected by intercalated disks) and endocardium - all electrically active

  • have conducting (spread AP) and contractile (contract due to AP) cells
199
Q

What is the myocardial cell structure?

A

Has gap junctions - allows current to flow
Desmosomes anchor fibres together
Undergoes excitation-contraction coupling

200
Q

What is the cardiac cycle?

A

Depolarisation starts at SAN - spreads to AVN by gap junctions or conducting pathways.
There’s an AV ring - prevents spread to ventricle then carried to ventricle muscle

201
Q

What is the cardiac cycle sequence?

A

1) Atrial systole - atrial depolarisation (contracts) - v fill
2) Isovolumetric ventricular contraction (mitral & tricuspid close)
3) Rapid ventricular ejection - semi lunar valves open
4) Reduced ventricular ejection - ventricle repolarisation
5) Isovolumetric ventricular relaxation - SLV close
6) Ventricular filling

LOOK AT GRAPH

202
Q

What ions are involved in the cardiac cycle?

A

Na+ = depolarise
Ca+ = contracts myocytes
K+ = repolarises
Pacemaker current

203
Q

What is an ECG?

A

Electrodes detect currents from different angles of the heart

204
Q

What’s on an electrocardiograph?

A

P wave = atria depolarisation
QRS = ventricular depolarisation
T wave = ventricular repolarisation

205
Q

What is the BP like in arteries?

A

Arteries - high pressure, have low compliance, volume = stressed volume

206
Q

What is the blood pressure in arterioles?

A

Has tonically active smooth muscle

Have highest resistance to blood which is effected by:
- sympathetic nerves (increases resistance) - alpha receptors = contract skin ect., beta = relax skeletal muscle and heart arterioles - need a balance
- catecholamines e.g. adrenaline
- vasoactive substances e.g. NO

207
Q

What is the blood pressure in capillaries?

A

Low pressure - controlled by diameter of arterioles

208
Q

What is the blood pressure in venules/veins?

A

Low pressure
Has less elastic than arteries
Has largest percentage of blood in CV - unstressed volume
Large capacitance
Has symp nerve fibres in smooth muscle + alpha adrenergic receptors - reduced capacitance - decreased unstressed volume

209
Q

What is the velocity of blood in vessels?

A

V = Q/A
Q - flow (mL/s)
A - cross sectional area (cm)

Small vessels have higher velocity

210
Q

What is the blood flow equation?

A

Q (mL/s) = pressure difference (mmHg)/resistance

211
Q

What is resistance to blood flow?

A

R = 8nl/pi x r^4

n = viscocity
l = length of blood vessel

Directly proportional to length and viscosity

Inversely proportional to fourth power of radius

Series resistance = within an organ: artery-arteriole-capillary ect. Arterioles have largest decrease

Parallel resistance - branches - no loss of pressure

212
Q

What pressures are in systemic circulation?

A

Arterial (Pa) - oscillations reflect diastolic and systolic pressure

Venous (Pv) - by veins and venules (less than 10mmHg)

Pulmonary circulation has lower pressure

Greatest pressure drop in arterioles

213
Q

What is pulse pressure and mean arterial pressure?

A

PP = systolic - diastolic pressure
MAP = diastolic + 1/3 pp

214
Q

How do we regulate BP?

A

Baroreceptors - in carotid and aortic sinuses

Solitary sinus receives signal and directs SNS and PNS changes via medullar CV centres

PNS –> vagus nerve –> SAN

SNS –> SAN –> arteriole vasoconstrict –> vein vasoconstrict –> cardiac muscle contracts more

There’s also chemoreceptors - increase BP if low O2 (low pH)

215
Q

What is a long term control of BP?

A

RAAS: low perfusion in kidney - renin released - converts angiotensinogen to angiotensin I to II.

Angiotensin II increases aldosterone - increases Na and releases ADH - more water - also vasoconstricts arterioles

216
Q

What does chronic hypertension do?

A

Desensitise baroreceptors - reduces stretch sensitivity - reduced sympathetic inhibition - hypertention not corrected

people here don’t usually experience a dip in BP at night - higher risk of heart attack ect.

Can be treated by lifestyle changes, ACE inhibitors, Ca channel blockers, diuretics, beta blockers

217
Q

What is in blood?

A

Cellular components in plasma
- erythrocytes
- leukocytes
- platelets

218
Q

What is in plasma?

A

Albumin
Fibrinogen - precursor of fibrin
Immunoglobulins
Proteins in coagulation cascade

219
Q

What are erythrocytes?

A

Most abundant
non-nucleated biconcave disks
3 main functions: co2/o2 carriage, buffering

220
Q

What are the white blood cells?

A

Granulocytes:
neutrophils (phagocyte)
eosinophils (combat viruses and parasites)
basophils (release histamines ect.)

Non-granular:
lymphocytes (mature into B and T)
monocytes (macrophages and dendritic)

221
Q

What are platelets?

A

Bud off megakaryocytes in bone marrow - thrombopoesis in response to thrombopoetin and IL-3

1) Platelets bind to TPO
2) megakaryocytes not generated
3) If no platelets bind to TPO (as little platelets) - TPO stimulates megakaryocytes and platelets

150000 - 450000 in blood

222
Q

What is haemostasis?

A

Prevention of a haemorrhage

1) vasoconstriction (serotonin, thrombin ect.)
2) Increased tissue pressure
3) platelet plug (primary haemostasis)
4) clot formation (secondary haemostasis)

223
Q

What is the structure of a platelet?

A

No nucleus - have mitochondria, lysosomes, peroxisomes, alpha granules (VWF, fibrinogen, clotting factor, platelet derived growth factor), dense factors (ATP, Ca)

Have lots of receptors

Tubulin helps maintain shape

Cytoskeleton has actin and myosin

224
Q

What are the three parts of a platelet plug formation?

A

1) platelet adhesion
2) platelet activation
3) platelet aggregation

225
Q

What is platelet adhesion?

A

Exposed endothelium exposes collagen - VWF binds to collagen and platelet receptors

Endothelial cells also release VWF

Binding cause IC cascade - activate

226
Q

What is platelet activation?

A

Cascade causes:
- secretion/exocytosis of dense and alpha granules (VWF and ADP - both activate it further)

PDGF - wound healing
Thromboxane - vasoconstrict and inflammation
Cytoskeleton changes
Expression of fibrinogen receptors

227
Q

What is platelet aggregation?

A

Fibrinogen binds to platelet receptors - forms bridges between platelets - this plugs the break in endothelium

Eventually actin and myosin contract - stronger plug

228
Q

What is a blood clot?

A

More permanent fibrin mesh
Mass of erythrocytes, leukocytes, serum and the mesh already there
Thrombus = intravascular clot

229
Q

What is the intrinsic and extrinsic pathways in clotting?

A

Intrinsic (slow) - factors in blood contact with negatively charged membrane of platelet - causes cascade of protease reactions - ends in factor Xa

Extrinsic - endothelium injury causes tissue factor (receptor) to become activated when in contact with factor VII - results in factor Xa

xa from both enter common pathway - generates thrombin - produces fibrin

230
Q

What prevents haemostasis?

A

Normal endothelial cells - through paracrine and anticoagulant factors

Paracrine factors - e.g. prostacyclin promotes vasodilation - inhibits platelet steps

Many anticoagulant factors - some stop thrombin

Promotion of pro-thrombotic state via vascular damage and hypoxia

Turbulent flow causes endothelial injury - caused by stenosis, large radius and high velocity

231
Q

What are virchow triad’s risk factors?

A

Thrombosis:

Abnormal blood flow
Endothelial injury
Hypercoagulability

232
Q

How much Na+ and water is excreted through our urine?

A

water - 1.5L per day in urine (1.1 by respiration, stools and sweat)

Na+ - 140 mmoles per day in urine (10mmoles in stool and sweat)

233
Q

What is the anatomy of the kidney?

A

from T12 to L3 - around 10cm long and 5.5cm wide

Capsule
Cortex
Medullary ray
Pelvis
Ureter

233
Q

What are the two types of the nephron?

A

Superficial nephron (85%) in the cortex
Juxtamedullary nephron - 15%

234
Q

What are some congenital abnormalities in the kidney?

A

Ectopic kidney
Horseshoe kidney - fused
Renal agenesis - lack/failure to develop

235
Q

What is renal failure?

A

Fall in GFR (usually 125ml/minute) - increase in serum urea and creatinine

Can be:
- acute (reversible)
- chronic (irreversible)

236
Q

What are the differences between acute and chronic renal failure?

A

Chronic has longer history
Haemoglobin level lower in chronic
Renal size lower in chronic
Chronic has peripheral neuropathy

237
Q

What is renal failure progression?

A

Thickening glomerular membrane –> damaged glomeuli –> scarring –> reduced renal size

238
Q

What is uraemia?

A

Describes the symptoms of renal failure
- hypertension
- nausea
- anaemia
- bone diseases
- neuropathy
ect.

239
Q

What happens at each stage of renal failure?

A

As the stages progress - GFR decreases
Uraemic syndrome becomes more severe
Serum biochemistry gets severe
Begins with anaemia and bone disease – dialysis

240
Q

What causes renal failure?

A

30% - glomerulonephritus
25% - diabetes
10% - hypertension

241
Q

What does the lymphatic system do?

A

Drain excess interstitial fluid and return to blood via subclavian vein to maintain blood volume

242
Q

What features of a cardiac cell enable the heart to beat?

A

Gap junctions
Intercalated disks
Sarcolemma T tubules
Desmosomes

243
Q

What is the first step in producing urine?

A

Glomerulus (200 micrometers) - ultrafiltration - 180 litres daily

GFR = 125 ml/min

Filtration - allows H2O and other molecules

Ultrafiltrate - protein free plasma

244
Q

What is the second step of producing urine?

A

Filtrate modification
There is reabsorption in PCT and secretion from the blood in the tubules

245
Q

What are the types of tubular transport?

A

Transcellular reabsorption
Transcellular secretion
Paracellular secretion and reabsorption

246
Q

How are genes related to nephron transport?

A

Produce transport proteins

247
Q

What happens at the proximal tubule?

A

Bulk reabsorption (70%)

  • 70% water and sodium
  • 100% glucose and amino acids
    90% bicarb

Sodium pumped out basally by Na/K pump - Na and glucose/phosphate(NaPiIIa)/aa then cotransport into the cell apically - water then diffuses paracellularly

248
Q

What is the NaPiIIa knockout mouse?

A
  • caused less Pi reabsorption
  • more lost in urine
  • issues in renal mineralisation
  • more stones
  • increased calcification
249
Q

What is NHE3 in proximal tubule?

A

Bicarb reabsorption - NHE3 removes H+ (which reacts with bicarb apically - makes h2O and CO2 which can move in an dissociates back to bicarb and H+) and allows Na to move in - Na then leaves and takes bicarb into blood

Knockout mice:
- lower pH as bicarb falls
- inhibits H+ secretion, Na/HCO3- transport

250
Q

What is secreted by PCT?

A

Foreign compounds e.g. penicillin
Removal of plasma proteins bound substances

251
Q

What happens in the loop of henle?

A

Concentration of urine
Reabsorption of Na, Cl and water
Reabsorption of Ca and Mg
Site of action of loop diuretics

252
Q

What are the limbs in the loop of henle?

A

Thin descending - H2O moves out
Thick/thin ascending - Na/Cl moves out

253
Q

Which channels move Sodium and Chlorine out of the thick ascending limb of the LOH?

A

NKCC2 moves sodium, 2 chlorine and a potassium into the cell

Sodium potassium pump - pumps sodium out

CLCK - move Cl out basolaterally

ROMK - move k+ out apically

Calcium and magnesium move paracellularly

254
Q

What is bartter’s syndrome?

A

Recessive - 1 in 1 million

Causes mutations in NKCC2, CLCK and ROMK - loop of henle - Cl accumulates, type 1 = NKCC2 mutations

Causes hypotension
Salt wasting
Hypokalaemia
Alkalosis
Hypercalciuria - high calcium in urine
Polyuria

255
Q

What are loop diuretics?

A

Furosemide
Bumetanide

Effects NKCC2

  • treats high blood pressure
  • has bartter’s like symptoms
256
Q

What is the early DT?

A

Early distal tubule
- reabsorption of Na and Cl
- reabsorption of Mg
- sensitive to thiazide diuretics

257
Q

What channels are involved in the early distal tubule?

A

NCC - cotransports Na/Cl into cell
Na/K pump - pumps sodium out basolaterally
CLCK - pumps calcium out basolaterally
Mg and Ca enter through channels

Thiazide stops NCC - treats high BP - has Gitelman’s symptoms

258
Q

What is Gitelman’s syndrome?

A

Recessive - 1 in 40,000 - 1 in 1000 in Asian populations, 1% of Caucasian are carriers

Affects NCC in distal tubule

  • salt wasting
  • hypotension
  • hypokalaemia
  • metabolic alkalosis
  • hypocalciuria - low calcium in urine
259
Q

How can we see the impact of mutations on Na+ transport?

A

Xenopus oocyte expression studies

  • inject RNA
  • protein made
  • evaluate if the channel is made
260
Q

What does it mean if you carry a mutation for ROMK, NCC or NKCC2?

A

Protection from hypertension

261
Q

What are some NMJ inhibitors?

A
  • K+ - dendrotoxin
  • ACh release - botulinum toxin, tetanus toxin
  • Ca2+ - w-conotoxin
  • Neuronal Na+ - tetrodotoxin, saxitoxin
  • Acetylcholinesterase - physostigmine, DFP
  • Muscle Na+ - tetrodotoxin, saxitoxin
  • AChR channel - a-bungarotoxin, d-tubocurarine
262
Q

What do the late distal T, collecting T and the cortical collecting duct do?

A

Concentration of urine
Reabsorb Na and H2O
Secrete K and H

263
Q

What cells are in the late DT and cortical collecting duct?

A

Principal: reabsorb Na and H2O
secrete K and H+

Intercalated:
- alpha - H+ secretion, bicarb reabsorption
- beta - H+ and Cl- reabsorption, bicarb secretion

264
Q

What channels does the principal cells have?

A

ENAC - allows Na to enter cell apically
ROMK - allows K+ to leave apically
Aquaporin 2 - allows water in apically

Sodium/potassium channel - allows sodium to leave basolaterally
Kir2.3 - allows K+ to leave basolaterally
Aquaporin3/4 - allow water to leave basolaterally

265
Q

What does amiloride do?

A

Stops ENaC in a principal cell - no Na+ can be reabsorbed

Used for Liddle’s syndrome - reduces blood pressure

266
Q

What is liddle’s syndrome?

A

Autosomal dominant - ENaC isn’t removed - more Na
Na+ retention - fluid retention
Hypertension
Hypokalaemia
Metabolic alkalosis
Low renin and aldosterone

267
Q

What is ENaC like in Liddle’s syndrome?

A

COOH tail in beta or gamma subunit is mutated

Proline is deleted - there is a reduced removal of ENaC

Therefore more ENaC - more Na leaves - more water reabsorbed - causes hypertension (MAP = CO x HR)

Also means more K+ secretion - hypokalaemia

268
Q

What channels are in alpha intercalated cells in late DT and CCD?

A

Proton pump apically - pumps H+ out
AE1 exchanges a bicarb out basally, brings in Cl-
Cl- exits basally

269
Q

What channels are in beta intercalated cells in late DT and CCD?

A

AE1 - bicarb out apically, Cl- into cell
Proton pump - pumps H+ out basally
Cl- leaves basally

270
Q

What is the medullary collecting duct?

A

Low Na+ permeability
High urea and H2O permeability in presence of ADH

271
Q

What happens when someone has acute renal failure?

A

Fall in GFR
Impaired fluid and electrolyte homeostasis
Accumulation of nitrogenous waste
Needs dialysis

272
Q

What are the symptoms of acute renal failure?

A

Hypervolaemia
Hyperkalaemia
Acidosis
High urea and creatinine

273
Q

What is the fall in GFR called?

A

Oliguria - due to hypotension - pre-renal cause

Treated by IV saline, add HCO3-

274
Q

Where does most Na reabsorption happen?

A

PCT - 70%
Loop - 20%
DT and CD - 9% - by aldosterone

275
Q

Where does most H2O reabsorption happen?

A

PT - 70%
Loop - 5%
DT and CD - 24% - by ADH

276
Q

Where does most K+ get reabsorbed?

A

PT - 80%
Loop - 20%
DT and CD - only in aldosterone

277
Q

How is the SA node innervated?

A

By vagus nerve (parasymp) - depresses heart rate - this is called negative chronotropic action and is mediated by M2 acetylcholine receptors

Symp - catecholamines increase HR by activating B1 adrenoreceptors - increases cAMP - PKA activation - activates L-type Ca channels and Ca channels on ER

278
Q

What did Otto Loewi see with the frog heart?

A

He collected the fluid bathing heart and applied it on a different heart - it slowed - this meant that it was a chemical, not electrical, released from vagus nerve

279
Q

What is the Langendorff preparation?

A

1) Anesthetise the animal
2) Cut open chest and remove heart
3) Place heart in dish of warm Ringer’s solution - press on heart slightly to remove any blood
4) Tie aorta to cannula and perfuse with warmed, aerated Ringer’s solution - this perfuses the coronary arteries
5) Place in water jacket to keep heart warm
6) attach hook to apex of ventricles and connect to force transducer - allows us to convert physical movement to electrical signal

280
Q

Where is ADH produced?

A

Supra-optic and paraventricular nuclei

281
Q

What are the hypothalamic osmoreceptors?

A

Supra-optic and paraventricular nuclei detect a change of 3 mosmol/Kg of H2O (normal range is 280-300)

Causes release of ADH and thirst - at normal osmolality there is still ADH in the plasma

282
Q

What affects the release of ADH?

A

Increase: water deficiency, stress, drugs (nicotine and ecstasy)

Decrease: excessive fluid, drugs (alcohol)

283
Q

What does ADH do in principle cells?

A

ADH binds to a V2 receptor which causes insertion of AQP2 channels by activating PKA to stimulate vesicles

  • dilutes plasma
  • increases H2O reabsorption
  • fall in body osmolality
  • fast (~ 15 minutes)
284
Q

What is diabetes insipidus?

A

Lots of dilute urine
- we can use a desmopressin nasal spray to stop ADH release
- we can defect the V2/AQP2 channels

285
Q

What does aldosterone do?

A

Released from adrenal cortex - zona glomerulosa (mineralcorti)

Regulates (increases) Na, K and body fluid volume

Released in response to high K, low Na or low volume

Acts on late distal/cortical and medullary collecting duct

286
Q

How does aldosterone act on principle cells?

A

1) binds to cytosolic mineralcorticoid receptor
2) transport to nucleus
3) increases expression of transport proteins
4) There will be Na reabsorption and K/H+ secretion

Can take a few hours

Na comes in via Na/H exchanger - goes to blood by Na/K pump - K leaves apically

287
Q

What does aldosterone do to alpha intercalated cells?

A

1) binds to cytosolic mineralocorticoid receptor
2) transports to nucleus
3) increases transcription of protein transport channels
4) H+ is secreted

288
Q

What is pseudohypoaldosteronism?

A

There is Na loss but high aldosterone - loss response
There are mutations in mineralocorticoid receptor mutations

289
Q

What does renin-angiotensin regulate?

A

Body fluid volume, plasma Na and K+

290
Q

What is RAAS?

A

Renin released from the juxtaglomerular apparatus

Renin causes angiotensinogen to be converted to angiotensin 1

ACE1 (from lungs) causes angiotensin I to convert to angiotensin II

291
Q

What does angiotensin II do?

A

Causes zona glomerulosa to release aldosterone

Vasoconstricts arterioles - increase BP

ACE inhibitor - BP treatment

292
Q

What are the two types of respiration?

A

Internal - within the cell
External - ventilation, gas exchange

293
Q

What are the different parts of the respiratory system?

A

External convection
Pulmonary diffusion
Internal convection
Tissue diffusion

294
Q

What are the branches of the lungs?

A

Trachea –> bronchi –> bronchioles (terminal and respiratory) –> alveoli (from terminal bronchiole)

Conducting zone - air travel
Respiratory zone - air diffusion

295
Q

What is the conducting zone?

A

Nose, nasopharynx, oropharynx, pharynx, larynx, trachea, bronchial tree

  • filters, warms and humidifies air
296
Q

What is the structure of the bronchial wall?

A

Cartilage
Smooth muscle
Elastic tissue
Mucous glands

297
Q

What is respiratory epithelium?

A

Ciliated epithelia
Goblet cells
Sensory nerve endings

298
Q

What is the structure of bronchioles?

A

Lack of cartilage
Has respiratory epithelium
Has more smooth muscle than bronchi proportionally

299
Q

What is the air blood barrier?

A

Created by flattened cytoplasm of type I pneumocyte and capillary wall

300
Q

What is quiet inspiration?

A

Involves primary muscles: diaphragm and external intercostals

  • follows Boyle’s law: pressure volume relationship
301
Q

What is forced inspiration?

A

Uses primary muscles (diaphragm and external intercostals) and accessory (sternocleidomastoid, scalenes, back and neck) muscles

302
Q

What is quiet expiration?

A

Passive - due to elastic recoil

303
Q

What is forced expiration?

A

Uses accessory muscles, internal intercostals, abdominal muscles and neck and back muscles

304
Q

What is the pleura?

A

Pleural cavity - prevents lungs from sticking to wall or collapsing - allows free expansion

Parietal is the outside
Visceral is the inside

305
Q

What is pneumothorax?

A

Collapsed lung

306
Q

What is compliance?

A

= distensibility

c = change in volume/change in pressure

low compliance = more work to inspire e.g. pulmonary fibrosis

high compliance = more work expiring (less elastic recoil) e.g. emphysema

307
Q

What are the components of elastic recoil?

A

Anatomical - elastic nature and extracellular matrix

Surface tension = due to differences in forces, there’s a balance between pressure and surface tension

308
Q

What is Laplace’s law?

A

Pressure = 2(tension)/radius

309
Q

What is surfactant?

A

Produced by type II pneumocytes - prevents alveoli collapsing and reduces surface tension

310
Q

What is dead space?

A

Anatomical - volume of conducting airways

Physiological - volume of lungs not participating in gas exchange - conducting zone + non-functional respiratory zone

311
Q

What are some spirography values?

A

IRV - inspiratory reserve volume (maximum inspiration - tidal volume)
FRC - functional residual capacity

During exercise - changes

Can’t measure RV

312
Q

What is Poiseuille’s law?

A

Impact of resistance to flow

R = (8/pi) x (viscocityXlength/radius ^4)

R = 1/r^4

313
Q

What is the normal airway resistance?

A

1.5 cm H2O.s.litres

314
Q

What factors affect airway resistance?

A

Anything affecting airway diameter

  • increase mucus secretion
  • oedema
  • airway collapse
315
Q

What controls bronchial smooth muscle?

A

Parasymp - ACh from vagus acts on MAChR - constricts

Symp - noradrenaline causes dilation

Adrenaline in blood - dilation
Histamine - constriction

316
Q

How can we calculate residual volume?

A

Breathing with a balloon with helium - gets diluted (measure conc before and after)

317
Q

Is airflow proportional to pressure gradient?

A

yes! directly

It is indirectly proportional to resistance

318
Q

Where is most of the resistance in the airways?

A

Pharynx/larynx - 40%

Airways>diameter 2mm - 40%

Airways<diameter 2mm -20%

319
Q

What is the composition of air at 760mmHg?

A

Dry (atmospheric) - mostly nitrogen (78%), then oxygen (21%)

Wet (trachea) - similar but has H2O

Henry’s law: [gas] = solubility coefficient x pp

320
Q

What is Dalton’s law?

A

The total pressure of a mixture of gases is the sum of their individual partial pressures

321
Q

How can we work out the conc of a gas dissolved in a solution?

A

Using Henry’s law:

[Gas]dis = s (solubility coefficient) x Partial pressure of gas

322
Q

How is oxygen transported?

A

O2 is has a low solubility in saline - 0.003 ml/100ml blood

This is too little so haemoglobin is needed

323
Q

What is haemoglobin’s structure?

A

Tetrameric - 2 alpha and 2 beta

Has a haem group and a globin chain

Can be tensed (low O2 affinity) or relaxed (high O2 affinity)

324
Q

What is the structure of the haem unit?

A

Porphyrin ring with an iron atom

For O2 to bind, iron must be in state Fe2+

Methaemoglobin reductase converts Fe3+ to Fe2+

Haemoglobin can be relaxed or tensed

325
Q

What is the oxygen-haemoglobin dissociation curve?

A

X axis = pp of O2
Y axis = haemoglobin saturation

Increases then plateaus

At high temp = carries less, low temp = carry more

At high pH = carries more, low pH = carries less - BOHR EFFECT

At high 2,3 diphosphoglycerate conc = carries less, at low conc = carries more

326
Q

What causes a right shift in the oxygen-haemoglobin curve?

A
  • increased temp
  • increased CO2 production
  • decreased pH
327
Q

What is fetal haemoglobin?

A

Beta chains are replaced by y chains - left shift in curve - higher O2 affinity

328
Q

How is CO2 transported in the blood?

A

CO2 + H2O <-> H2CO3 <-> HCO3- + H+

The blood can carry CO2 in many ways e.g. carbonic acid, bicarb, dissolved CO2 - grouped as total CO2

329
Q

What is carbon transport?

A

CO2 is in plasma - can remain or enter RBC - 10% remains

Remain - can dissolve, bind to plasma protein, some form bicarb (slow with no carbonic anhydrase)

Entering the RBC - can cross by AQP1 or Rh protein or diffuse through bilayer

Some dissolves in RBC fluid, some bind to haemoglobin (Hb-NH-COO-) doesn’t bind to iron, rest is converted to bicarb by carbonic anhydrase - bicarb can leave by bicarb/Cl exchanger

When at lungs - this is reversed

330
Q

Why do we have a GI system?

A

Breaks down food into nutrients so we can use them for energy and growth& repair

Eliminates waste and undigested food

Helps regulate blood sugar, immune system, promote good mental health

331
Q

What is the GI tract?

A

A muscular tube - intestines are suspended in the cavity by mesenteries

Hollow organs are separated by sphincters

Accessory organs secrete into the lumen

Functions include: Motility propels food, digestion, absorption

332
Q

What is the structure of the GI wall?

A

Mucosal layer: epithelia (villi), lamina propria (capillaries, enteric neurones, immune cells), thin muscularis mucosae

Submucosal layer: connective tissue, glands, larger blood vessels

Circular and longitudinal smooth muscle

Serosa (squamous epithelia)

333
Q

What is the mouth?

A

For mastication

Has exocrine glands: lipase and amylase, saliva lubricates bolus, antimicrobial, buffers and dissolves food

Sensory information is relayed to brainstem

334
Q

What is the oesophagus?

A

Has stratified squamous epithelia

Swallowing causes upper oesophageal sphincter to close - initiates peristaltic wave

Continued distention = second peristaltic wave

Vagovagal reflex controls lower oesophageal sphincter - PNS vagus does this

335
Q

How is the GI tract regulated?

A

By three divisions of ANS:
- extrinsic = PS + S
- intrinsic = ENS (primary)

ENS has two main plexuses - ganglia in submucosal and myenteric plexuses, submucosal is between mucosa and circular muscle, myenteric is between circular and longitudinal

Lots of neurones - >100 million

336
Q

How is the parasympathetic NS involved in the GI tract?

A

Ganglia in plexuses coordinate information to SM, endocrine and secretory cells

Postganglionic neurones are either cholinergic (ACh) or peptidergic (peptides e.g. substance P)

337
Q

How is the sympathetic NS involved in the GI tract?

A

Postganglionic nerve fibres release noradrenaline - mixed efferent and afferent - relayed between GI tract and CNS

338
Q

What are the three phases to motility in the stomach?

A

1) receptive relaxation in thin-walled orad (fundus and some body) stomach

2) 3 layers of caudad region (body and atrium) contract to mix food with gastric juices from mucosal glans (ANS control) - makes chyme - HCl, Pepsinogen –> pepsin, intrinsic factor, mucus

3) gastric emptying through pyloric sphincter into duodenum - fat and H+ slow this

339
Q

What causes motility (GI)?

A

Subthreshold slow waves produce weak contraction (tonic)

Action potentials on top (phasic contractions)

Low pressure organs separated by sphincters (6 + sphincter of oddi)

Regulate antegrade (forward) and retrograde (backward) movement

340
Q

What is the most contractile tissue?

A

Unitary smooth muscle - cells electrically coupled by gap junctions

341
Q

What are the types of GI contractions?

A

Tonic - constant level of contraction
Phasic - periodic contraction then relaxation

Contraction is preceded by electrical activity - cells of cajal

342
Q

What is the small intestine?

A

Digestion and absorption of nutrients - chyme is mixed with digestive enzymes and pancreatic secretions

There are many hydrolytic enzymes in brush border

Duodenum –> jejunum –> ileum

SA increases - plicae - villi - microvilli

343
Q

What is the pancreas?

A

Secretes pancreatic juice (1L daily) into duodenum

  • rich in bicarb (by centroacinar and ductal cells) to neutralise H+
  • enzymes secreted by acinar cells

PNS secretes, SNS inhibits

In cephalic phase - gastic and intestinal

344
Q

What are the GI accessory organs?

A

Pancreas, liver and gallbladder

345
Q

What does the liver and gall bladder do?

A

Hepatocytes secrete bile - gall bladder stores and ejects - CCK is released from SI when chyme enters which relaxes sphincter of oddi

346
Q

What is in bile?

A

Water
Amphipathic bile salts (aids fat digestion)
Bilirubin
Cholesterol
Phospholipid
Electrolytes - Na, K, HCO

  • 95% bile salts recirculate to liver by enterohepatic circulation
347
Q

What are the contractions in the SI?

A

Peristaltic contractions propel chyme

Segmentation contractions split and expose chyme to secretions - enterochromaffin cells release serotonin - peristaltic reflex

Material not absorbed passes through ileocaecal sphincter into caecum of LI

348
Q

What regulates the GI system?

A

GI peptides:
- hormones e.g. GIP
- paracrines e.g. somatostatin
- neurocrines - from neurone after action potential

349
Q

What are the functions of the large intestine?

A

1) absorbs water and electrolytes (aldosterone increases Na absorption)

2) makes and absorbs vitamins K + B

3) forms and propels faeces

350
Q

What is the LI structure?

A

Surface columnar epithelium - interspersed with crypts

Has taenia coli - 3 longitudinal muscles and haustra

Caecum and proximal colon mix contents

351
Q

What are the two types of lung disease?

A

Obstructive - reduced flow through airways
Restrictive - reduced lung expansion

Both reduce ventilation

352
Q

What is the flow-volume relationship?

A

Highest flow at low volume then gradual decreases

Negative flow = flow out

353
Q

What is obstructive lung disease?

A

Narrowing airways

Could be due to:
- excess secretions
- bronchoconstriction (asthma)
- inflammation

Increased resistance

FEV1<80% FVC

FVC is usually normal - FEV1 affected

There is a sharp fall in flow-volume - graph isn’t a straight line (normal) - looks like a banana

354
Q

What are some obstructive diseases?

A

Chronic bronchitis - persistant cough and mucus
Asthma - inflammatory
COPD
Emphysema - loss of elastin

355
Q

What is asthma?

A

Hyper-active airways

Trigger could be:
- atopic (extrinsic) = allergies
- non-atopic (intrinsic) = cold air, stress, exercise, drugs, irritants, resp infections

Causes bronchoconstriction

Short acting treatment = salbutamol (B2 adrenoreceptor agonist)

Long acting treatment = inhaled glucocorticoid steroids or long acting B2 agonists

356
Q

What is restrictive lung disease?

A

Reduced chest expansion - chest wall abnormalities, muscle contraction deficiencies

Loss of compliance - ageing, increased collagen, environment

Vital capacity is reduced - FEV1 is the same

Flow-volume graph tends to be normal

357
Q

What is asbestosis?

A

Slow build up of fibrous tissue leading to loss of compliance

358
Q

What are the two medullary centres?

A

Dorsal respiratory group - controls inspiration by sending signals to inspiratory muscles - spontaneously active

Ventral respiratory group - controls inspiration and expiration - inactive during quiet respiration - helps when forceful

359
Q

What two centres are in the pons?

A

Pneumotaxic centre - increases breathing rate by shortening inspiration - inhibitory effect on inspiratory centre

Apneustic centre - increases depth and reduces breathing rate by prolonging inspiration - stims inspiratory centre

360
Q

Can stretch receptors feedback for breathing?

A

Yes!

Hering-Breuer reflex - stretch receptors in lungs send signals to medulla and limit inspiration and prevent over-inflation

Phrenic nerve –> diaphragm –> lung stretch receptor –> vagus nerve –> inspiratory centre inhibited

361
Q

Can chemoreceptors feedback for breathing?

A

Yes!

Central: monitor CSF CO2 and pH - if rise in CO2 - increase ventilation

Peripheral: in carotid body and aortic arch - respond to increased CO2, decreased pH, decreased O2 - increases ventilation

362
Q

What is the pre-botzinger complex?

A

Provides breathing rhythm - pattern generator

363
Q

What is the secretion in the Gi tract?

A

Controlled by hormonal, paracrine and neurocrine control.

> 9L of fluid daily - most absorbed in SI - rest lost in LI or in faeces

Salt and water balance regulates ECF volume and BP

364
Q

What is the secretion in the stomach?

A

Distal: gastrin, somatostatin, pepsinogens

Proximal: HCl, pepsinogens, intrinsic factor, mucins, bicarb

365
Q

What is the stomach’s main three functions?

A

Secretion

Motor

Humoral (gastrin, somatostatin)

366
Q

What are the stomach’s secretory cells?

A

Mucosal layer
Secrete >2L daily

Body: oxyntic glands
- epithelial cells (bicarb)
- mucous neck cells (mucus)
- Parietal cells (HCl, intrinsic factor)
- enterochromaffin-like cells (histamine)

Antrum: pyloric glands (same as pyloric but no parietal cells)
- G cells (gastrin hormone)
- Chief cells (pepsinogen)
- enterochromaffin cells (serotonin, VIP, substance P)
- D cells (Somatostatin)

367
Q

What do the stomach’s secretions do?

A

Protective:
- Bicarb - neutralises acid and combines with mucus to form a protective barrier
- Mucus - protects epithelia

Hydrolytic:
- HCl - activated pepsinogen and denatures proteins
- Pepsinogen - precursor of pepsin - digests protein

Endocrine:
- Gastrin - increases HCl secretion and pepsinnogen release-
Intrinsic factor - B12 absorption

Histamine - increases parietal cell HCl secretion

Serotonin/VIP - motility and secretion, VIP decreases HCl

Substance P - SM contract

Somatostatin - inhibit gastrin release

368
Q

What is the parietal cell structure?

A

While resting: cytoplasmic pool of tubulovesicular membrane - contains acid secreting H,K-ATPase

Stimulated: induces cytoskeletal changes - tubulovesicular and canalicular membranes fuse - increases SA by 50/100x, microvilli are present, insertion of H,K-ATPase pump, K+ + Cl- channels

369
Q

How is gastric acid secreted by parietal cells?

A

H2CO3 in the cell - H+ is secreted apically through H+/K+ ATPase

Cl- follows out

HCO3- absorbed into blood via Cl–bicarb exchanger

There are Na/K+ exchangers basally

Theres K+ channels allowing K+ to exit the cell apically

370
Q

What regulated HCl secretion?

A

Stimulation: ACh (Vagus), histamine (ECL) and gastrin (G cells)

Inhibition: low pH, somatostatin, prostaglandins

371
Q

What is fluid and electrolyte absorption like along the intestine?

A

SI and LI have crypts of leiberkuhn - secrete fluid and electrolytes

Si absorb fluid and Na/K/Cl/bicarb by villi, Li by surface epithelia

Crypt epithelial cells - secrete fluid + electrolytes - protective

LI - has a net absorption of water/ Na/ Cl, secretes bicarb and K

SI - have plicae (folds of kerckring), villi and microvilli - increase SA by 600x

Duodenum and jejunum is the primary site for Na/Cl/K/bicarb absorption

372
Q

How does secretion in the intestine happen?

A

In epithelial cell of crypts of leiberkuhn

Na/K/Cl cotransporter brings ions into the cell from the blood

Cl diffuses into the lumen through Cl channels - open when cAMP increases due to GPCR - open by ACh/VIP ect.

Na follows paracellularly (passive)

Water follows

373
Q

How does absorption happen in the jejunum?

A

All Na absorption - Na/K ATPase

Low intracellular Na (by sodium potassium exchanger) drives entry via Na channels/ Na-H exchangers/ Na-glucose/aa cotransport - secondary active transport

The Na/H exchangers are stimulated by bicarb

Net absorption of NaHCO3

374
Q

How does absorption happen in the ileum?

A

Same as jejunum but also involves Cl

Has a bicarb/Cl exchanger which brings Cl into the cell

There is a Cl transporter - Cl absorbed

Net NaCl into cell

375
Q

What happens in pancreatic secretion?

A

Acinar cells secrete CCK

Bicarb secreted into pancreatic juice by Cl/bicarb exchanger

H is transported into blood by NaH exchanger

Net secretion of bicarb and H absorption

Ductal cells - recs for CCK, ACh and secretin to upregulate production

376
Q

What is absorption in the large intestine?

A

Aldosterone causes Na to enter colon cell apically

Na leaves into blood by Na/K ATPase

This brings in potassium - leaves apically

377
Q

What products do the jejunum and ileum absorb?

A

Carbohydrases: alpha/beta amylase, maltase, sucrase, trehelase, lactase —- into villus blood

Protease: pepsin, trypsin, chymotrypsin, elastase, carboxypeptidases —- into villus blood

Lipases and bile salts —- into lacteals in villus

378
Q

How does the SI absorb carbohydrates?

A

Epithelial cells

SGLT1 - brings Na and Glucose/galactose in

GLUT5 - brings fructose in

GLUT2 - takes all sugars to blood

Na/K pump basally

379
Q

How does the SI absorb protein?

A

Na brings in amino acids

H brings in di/tripeptides - peptidases break them down in the cell

A channel takes AAs into blood

Theres a NA/H exchanger apically

Na/K pump basally

380
Q

How are lipids absorbed?

A

Pancreatic lipase and other lipids hydrolyse by bile salts in duodenum and jejunum

Products: cholestrol, lysophospholipids, monoglycerides, micelles (have amphipathic bile salts)

In mucous gel layer epithelia - FAs become protonated and cross the enterocyte by diffusion, carrier mediated transport, incorporated into membrane

Products are resterfied in SER - packaged into chylomicrons - absorbed into lacteals

381
Q

What are the islets of langerhan?

A

In kidneys

Beta cells (65%) - insulin, pro insulin, C peptide, amylin
Alpha cells (20%) - glucagon
Delta cells (10%) - somatostatin

There are also:
F cells - pancreatic polypeptide
e cells - ghrelin protein
enterochrommafin cells - not in islets

Richly perfused with blood

382
Q

What is the communication to the islets?

A

Small arteries enter islet - distribute by fenestrated capillaries

Vascular arrangement

383
Q

How do the islets cells communicate to eachother?

A

Gap junctions between beta and alpha cells

Delta cells send dendrite-like processes to beta cells

384
Q

What are the islets innervated by?

A

Adrenergic, cholinergic and peptidergic neurones

385
Q

How is insulin secretion regulated?

A

High blood glucose stimulates

Symp stimulation: Beta-adrenergic increases secretion, alpha decreases

Parasymp stimulation: vagus ACh increases release

GIP (SI K cells), Amylin (beta cells) and somatostatin

Drugs e.g. sulphonylureas act on KATP increasing insulin secretion

385
Q

How is insulin secreted?

A

GLUT2 lets glucose in - makes ATP from glycolysis

ATP closes k+ channels - depolarisation

Ca channels open causing exocytosis

CCK acetylcholine - Gq coupled

Somatostatin decreases, Glucagon and beta adrenergic agonists increases

386
Q

How does insulin act to a receptor?

A

Heterotetramer - alpha/beta subunits + IC tyrosine kinase

Receptor activation activates or inhibits - PKC, phosphatases, phospholipases, G proteins

Causes cell growth, division, gene expression

High insulin levels –> receptor downregulation

387
Q

What is insulin’s action?

A

Binds to receptor –> signal transduction cascade –> causes exocytosis of a vesicle with GLUT4 —> allows glucose to enter

Target all cells - especially muscle and liver to make glycogen - increases fat cell glucose intake when glycogen levels replenish

388
Q

How is the liver acted on by insulin?

A

Promotes glycogenesis

Inhibits glycogenolysis

Inhibits gluconeogenesis

389
Q

How does insulin effect muscle?

A

1) Promotes glucose uptake (GLUT4)

2) Promotes glycogen synthesis

3) Promotes glycolysis and carbohydrate oxidation

4) Promotes proteinsynthesis and inhibits protein breakdown

390
Q

How does insulin effect adipocytes?

A

Increases GLUT4 expression, converts glucose to FAs (stores as triglycerides), increases lipoprotein lipase - makes triglycerides from FAs, inhibits oxidation of fat

Overall decreases levels of FAs and keto acids

391
Q

How does insulin cause satiety?

A

Promotes K+ uptake through Na/K ATPase

This effects hypothalamic satiety centre

392
Q

What is type I diabetes?

A

This is where there is islet destruction - autoimmune

There is hyperglycaemia and increased blood fatty acids and keto acids

Hyperkalaemia
Hypotension
Polyuria

Symptoms: hunger, increased thirst, weight loss, fatigue, fruity breath, blurred vision

Treatment: insulin replacement therapy

393
Q

What is type II diabetes?

A

Insulin resistance

Symptoms: increased thirst, hunger, urination, weight loss, headaches, tired, blurred vision

Treatments: sulphonyurea drugs e.g. tolbutamide (stimulate insulin secretion), biguanide drugs e.g. metformin (upregulate receptors on targets), weight control

394
Q

What are the functions of the female reproductive system?

A
  • Produces haploid gametes
  • Facilitate fertilisation with spermatozoan
  • Site for implantation of the embryo
  • Provide physical and nutritional needs to nurture baby (mammary glands)
395
Q

What are the ovaries?

A

Female gonads - mature ova

Medulla - blood vessels and lymph
Cortex - outer epithelia layer containing oocytes (in a follicle - folliculogenesis)

Follicular cells secrete steroid hormones:
- granulosa - 17b oestrogen
- theca - progesterone

Primary follicle - graafian follicle - corpus luteum

396
Q

What are the fallopian tubes?

A

Transport egg to uterus - 10cm

Has Isthmus -> ampulla -> infundibulum with fimbriae.

Smooth muscle (circular & longitudinal) in walls - peristalsis

Has highly folded mucosa - ciliated and secretory cells

397
Q

What are the walls of the uterus?

A

Perimetrium (outer)
Myometrium
Endometrium

398
Q

What is the endometrium?

A

Uterus inner layer

Simple columnar with leukocytes and macrophages

Lamina propria - lots of connective tissue

Compound tubular glands

Has spiral arteries

399
Q

What is the cervix?

A

Connects uterus to vagina

Has external and internal os

Cervical glands secrete mucus - prevents microbes

400
Q

What is the vagina?

A

Birth canal 8-10cm

Thin wall of:
- adventitia
- muscularis
- mucosa

Has stratified squamous epithelium (with glycogen) which ferments to lactic acid to prevent bacteria

Also has dendritic cells

401
Q

What are the two female cycles?

A

Ovarian (follicular and luteal) and endometrial (menstrual) (menses, proliferative and secretory)

402
Q

What drives the endometrial cycle?

A

The hypothalamic-pituitary-gonadal axis - hypothalamic neurones release gonadotropin-releasing hormones (GnRH)

This travels to the anterior pituitary by the hypophyseal portal system

GPCRs on pituitary (gonadotrophs) release gonadotropins:
- FSH
- LH

403
Q

What do LH and FSH do?

A

Stim ovarian follicular cells to secrete steroid hormones: progesterone (theca cells) and 17b-oestrodoil (granulosa - these also release inhibin (decreases FSH) and activin (increases FSH))

This produces mature gametes

LH - triggers ovulation
FSH - grows and matures follicles

404
Q

What regulates the ovarian cycle?

A

HPGA is controlled by +ve and -ve feedback

Follicular phase: 17b-oestrodiol - -ve feedback

Luteal phase: progesterone - -ve feedback

Ovulation (midcycle): follicular cell proliferation, oestrodoil rapidly decreases - +ve feedback - more FSH/LH - triggers ovulation of oocyte

405
Q

What happens at phases of ovarian cycle?

A

Follicular - FSH/LH - increases follicles so there is a surge of oestrogen as they are making more (proliferative phase)

The oestrogen reaches a point where it causes positive feedback - LH and FSH - ovulation happens

Luteal - corpus luteum secretes progesterone - this stimulates endometrial glands - they will secrete (secretory phase)

At day 22 - corpus luteum will degenerate - endometrium is lost - as oestrogen and progesterone is falling

406
Q

What causes changes in endometrium?

A

17B-oestrodiol and progesterone cause the changes

407
Q

What happens to the mucus levels in the follicular and secretory phases?

A

Follicular: mucus copious, watery and elastic, forms channels to propel sperm

Secretory: mucus is thick

408
Q

What is the proliferative phase?

A

In endometrial cycle

17B-oestrodiol increases loads

Causes growth of:
- endometrum
- glands
- stroma
- spiral arteries elongate

409
Q

What is the secretory phase?

A

After ovulation - dominated by progesterone

Proliferation slows - thickness decreases

Glands have glycogen and mucus

Spiral arteries elongate and coil

Ends in menses

410
Q

What are some hormonal contraceptives

A
  • oestrogen and progesterone - decreases LH/FSH so no ovulation or folliculogenesis
  • progesterone only
  • monophasic (fixed dose)
  • multiphasic (varying dose)
411
Q

How is Progestin a contraceptive?

A

Only progesterone

Thick cervical mucus - no sperm penetration

Less uterus and fallopian tube motility

Less endometrial glycogen

412
Q

How does the morning after pill work?

A

High oestrogen and progesterone dose
- interferes with implantation
- inhibit ovulation
- thickens mucus so sperm can’t reach

413
Q

How do contraceptives work?

A

Some feedback on hypothalamus - less GnRH - low FSH and LH - no ovulation or folliculogenesis

414
Q

What is fertilisation?

A

Gametes are transported to the ampulla of the oviduct

The oocyte is surrounded by granulosa cells

Sperm(150-600 million): capacitation, SM contraction and cervical mucus helps the sperm

The sperm penetrates via an acrosomal reaction

This activates the oocyte - increases calcium - causes 2nd meiotic division and prevents another sperm in (polyploidy)

The haploid pronuclei fuse = diploid zygote

Happens early in fallopian tube

415
Q

What happens after fertilisation?

A

Move along oviduct for three days - nourished by oviduct secretions - isthmus contractions slow it down to allow endometrium to prepare

Will divide until 8 - then becomes morula then blastocyst - then implanted (6 days)

416
Q

What is the blastocyst?

A

Before implantation - fluid filled cavity.

Lined by trophoectoderm layer - this makes the yolk sac, fetal placenta and amnion

417
Q

What is implantation?

A

At 6-10 days after ovulation

Blastocyst promotes stromal cells from endometrium to transform into decidual cells (predecidualisation)

Endometrial reception to blastocyst - low oestrodiol:progesterone (secretory phase)

There is several parts of the invasion

418
Q

What are the trophoblastic cells?

A

In blastocyst:
- inner cytotrophoblast: single mitotic layer which differentiates into syncytiotrophoblast
- outer syncytiotrophoblast: produces hormones e.g. HCG

419
Q

How does the blastocyst invade the endometrium?

A

1) Hatching: zona pellucida (outer layer) degenerates due to lytic factors - releasing inner cells

2) Apposition: the trophoblastic and endometrial epithelium meet

3) Adhesion: intracellular and extracellular integrins bind to receptors on the deciduous endometrium

4) Invasion: syncytiotrophoblast cells penetrates endometrium

420
Q

What is the outer layer of the blastocyst called?

A

Zona pellucida

421
Q

How does the placenta develop?

A

Allows materials to pass from maternal system to foetus

Have 120 spiral arteries from the mother - empty into intervillous places - washes over foetal projections and decreases the force from the mothers blood

Syncytiotrophoblast lacunae - merge and fill with maternal blood

Syncytiotrophoblast and cytotrophoblast form villi and microvilli

422
Q

How is foetal and maternal blood separated in the placenta?

A
  • foetal capillary epithelium
  • mesenchyme
  • cytotrophoblasts
  • syncytiotrophoblasts
423
Q

What is transported between maternal and foetal blood?

A

From maternal:
- glucose (fac diff)
- amino acids (2nd active transport)
- vitamins (active transport)
- antibodies/hormones (endocytosis)

From foetal:
- waste urea and creatinine

424
Q

What are the hormonal changes in trimester 1?

A

Trophoblast: HCG (rescues the corpus luteum) - up to week 9

Corpus luteum: progesterone and oestrogen to support endometrium

425
Q

What happens in trimester 2/3?

A

Placenta: steroid hormones.

This includes human placental lactogens (hCS) which:
- coordinate fuel economy
- develop mammary glands

Progesterone from cholesterol

Oestrogen from foetal-placental

426
Q

What is stage 0 of parturition?

A

Stage 0 (quiescence): before birth, uterus is relaxed and insensitive to uterotonic hormones, progesterone suppresses myometrial contractions, braxton-hicks

427
Q

What is stage 1 of parturition?

A

Stage 1 (activation): cortisol increases by H-P-adrenal axis - this increases oestrogen - contracts and stimulates prostaglandin release (promotes formation of gap junctions and softens and thins cervix)

Contraction- associated proteins are expressed e.g. uterotonic recs of oxytocin

Enzymes to hydrolyse collagen are expressed

428
Q

What is stage 2 of parturition?

A

Stimulation of birth:
PG increase: myometrial contraction, cervical dilation

Increased myometrial connectivity and responsiveness

positive feedback loops: ferguson reflex and uterine contraction increasing PG + oxytocin

Labour: dilation –> expulsion –> placental

429
Q

What is parturition stage 3?

A

Recovery from birth

Haemostasis - vasoconstriction of spiral arteries

Decrease in oestrogen - myometrium will regress

The endometrial lining will reestablish after 3-5 months

430
Q

What is lactation?

A

From secretory unit of breast = alveoli (contractile cells and adipose tissue)

During pregnancy: oest and prog stim breast growth, oest will stimulate anterior pituitary to release prolactin but prog and oest prevent it acting on breast

Postpartum: oest increases cell proliferation, prolactin initiates milk, oxytocin increases contraction and release of milk, prolactin and cortisol maintain milk

431
Q

What does prolactin do?

A

For milk production

Inhibiting dopamine releases prolactin from anterior pituitary

Oxytocin is released from posterior pituitary

Downregulates GnRH to inhibit ovarian cycle

432
Q

What is the spirometer graph?

A

Look on the lab on lt

433
Q

Where do we place the lead II ecg electrodes?

A

+ve - left ankle
-ve - right wrist
earth - left wrist

If the electrical vector moves towards +ve vector - positive defection

434
Q

What are the AV valves?

A

Mitral - left
Tricuspid - right

First Year Semester One (4 decks)

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