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SUGER Flashcards

1
Q

which parts of the nephron aer in the cortex and which parts are in the medulla

A
  • Cortex
    • bowman’s capsule
    • proximal tubule
    • distal tubule
  • Medulla
    • loop of henle
    • collecting duct
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2
Q

How much blood goes to the kidneys?

A
  • ~0.5L per minute per kidney
    • that’s 10% of cardiac output to each kidney
  • this is not just to meet the metabolic requirements but to filter waste too
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3
Q

urine production

A

1ml/min

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4
Q

renal blood supply

A
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5
Q

what is the peritubular capillary

A
  • it comes from the efferent arteriole (leaving the glomerulus)
  • it travels adjascent to the tubule so that it can secrete and reabsorb things
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6
Q

name each number and letter

A
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7
Q

factors that determine whether something can cross the filtration barrier

A
  • pressure
  • size of the molecule
  • charge of the molecule (-ve charge in glomerular basement membrane repels negatively charged anions)
  • rate of blood flow
  • binding to plasma proteins
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8
Q

Podicytes

A
  • line the glomerular capillaries
  • foot projections intertwine and wrap to cover the glomerular capillaries
  • the slits between the podocytes is called a slit diaphragm
  • the proteins between the podicytes that form the slit diaphragm are called nephrin and podicin
  • it is through these slits that the blood is filtered
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9
Q

effects of constricting and dilating afferent and efferent arterioles on glomerular filtration rate

A
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10
Q

what is the juxtoglomerular apperatus?

A
  • the distal tubule comes very close to the glomerulus of the same nephron
  • this area is called the juxtoglomerular apparatus
  • it includes
    • macula densa (of distal tubule wall closest to glomerulus)
    • mesangium (an extraglomerular cell)
    • granular cells
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11
Q

what to processes maintain GFR in health?

A
  1. tubuloglomerular feedback
  2. autoregulation
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12
Q

autoregulation

A
  • the kidney can maintain its GFR to an almost constant level independantly of the systemic mean arterial pressure
    • as long as pressure is within the range 90-200
  • even denervated kidneys and isolated perfused kidneys can do this
  • this is because of the intrinsic properties of vascular smooth muscle
    • see CVS
  • Pressure within afferent arteriole rises and stretches vessel wall
  • ​This triggers contraction of smooth muscle of AA
  • AA constricts
  • the reverse happens when systemic pressure falls
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13
Q

Tubuloglomerular feedback

A
  • GFR of individual nephrons are regulated by the rate at which fluid reches the distal tubule
  • cells of the macula densa detect NaCl arrival
  • macula densa cells release prostaglandins in response to reduced NaCl delivery
    • blood pressure too low
  • this acts on granular cells, triggering renin release
  • this activates the renin-angiotensin system
    • this will increase blood pressure
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14
Q

factors that affect GFR

A
  • hydrostatic pressure
  • oncotic pressure
  • surface area
  • permeability
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15
Q

How do we measure GFR

A
  • use a marker that is freely filtered
    • i.e. that has the same conc in blood and tubular fluid
  • it should not be secreted or absorbed in tubules
  • it should not be metabolised
  • measure the amount exreted per minute (not concentration)
  • amount of marker in fluid =
    • conc in fluid x volume on fluid
    • the equation in the picture holds because the marker is the same conc in blood as in urine
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16
Q

Significance of GFR

A
  • good measurement of kidney function - how much fluid can the kidney handle
  • diseases cause you to lose nephrons so GFR will fall
  • but it only describes one aspect of kidney function
  • even with a normal GFR there could be other renal problems
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17
Q

what’s a normal GFR

A

125ml/min

180 litres in 24 hrs

total plasma volume is 3 litres so entire volime is filtred 60x per day

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18
Q

clinically how do we estimate GFR

A
  • we use creatinine
  • this is a muscle metabolite which is in constant production
  • serine creatinine level varies with muscle mass
  • it is freely filtered by the clomerulus
  • there is additional secretion by the tubules
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19
Q

Filtation fraction

A
  • FF = GFR/renal plasma flow
  • GFR is 125ml/min
  • Renal blood flow is 1000ml/min
  • Renal plasma flow is 600ml/min
    • 40% of RBF is cells - the rest is plasma
  • Urine flow is 1ml/min
    • So most of the filtrate is reabsorbed
  • the filtration fraction is:
    • 125/600 = ~0.2 or 20%
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20
Q

what are the reasons that something might not be freely filtered

A
  • it may be bound to a protein
  • it may be too large
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21
Q

what is renal clearance

A
  • the amount of plasma from which a substance is completely removed by the kidney per minute
  • clearance = (urine conc x urine volume) / plasma volume
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22
Q

pH =

A

pH = negative log of [H+]

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23
Q

acidaemia

A

low blood pH

acidosis is a word used to describe disorders that cause this

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24
Q

alkalemia

A

high blood pH

alkalosis is a term used to describe disorders that cause this

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25
Q

what is standard bicarbonate

A
  • absolute bicarbonate is affected by respiratory and metabolic components
  • standard bicarbonate is the bicarbonate concentration standardised to PaCO2 5.3kPa and temperature 37
  • so standard bicarbonate represents the metabolic contribution to metabolic change
  • it’s calculated not actually measured
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26
Q

Base excess

A
  • the quantity of acid required to return pH to 7.4 under standard conditions
  • standard base excess is corrected to Hb 50g/L
  • base excess is negative in acidosis
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27
Q

ABG

A
  • arterial blood gas - it’s what we can actually measure
  • it includes:
    • pH
    • pO2
    • pCO2
    • std HCO3-
    • std base excess
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28
Q

what are the two major approaches to interpreting acid-base status

A
  • henderson hasselbach
  • stewart’s theory (strong ion difference)
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29
Q

Henderson hasselback for Blood

A

pH = 6.1 + log([HCO3-]/0.03xpCO2)

blook has a pKa of 6.1

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30
Q

Stewart’s strong ion difference

A
  • The strong ion difference is the difference between the positively and negatively charged ions in plasma
  • So the principle is that pH and [HCO3-] are dependent on 3 factors:
    • pCO2
    • concentration of weak acids
  • SID = [strong cations] – [strong anions]
    • = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + lactate-]
  • It’s designed to help characterise the mechanism of the disorder rather than to simply catagorize it at metabolic or respiratory
  • basically it’s too complicated to actually really use in practice
  • but theorhetically it’s much more accurate than the HH abroach
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31
Q

causes of metabolic acidosis

A
  1. Dilutional
    • rapid ECF volume expansion causes HCO3- to be diluted
    • but H+ is not diluted for some reason
  2. Failure of H+ excretion
    • renal failure
    • type 1 renal tubular acidosis
  3. Excess H+ load
    • lactic acidosis
    • ketoacidosis
  4. HCO3- loss
    • diarrhoea
    • type 2 renal tubular acidosis
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32
Q

compensatory mechanisms for metabolic acidosis

A
  • Hyperventilation to increase CO2 excretion
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33
Q

Causes of Metabolic Aclkalosis

A
  • alkali ingestion
  • GI acid loss (vomiting)
  • renal acid loss
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34
Q

Compensatory mechanism of Metabolic Acidosis

A
  • hypoventilation but this is limited by hypoxic drivs
  • renal bicarbonate excretion
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35
Q

Respiratory Acidosis

A
  • CO2 retention leading to increased carbonic acid dissociation
  • The compensatory mechanism is renal H+ excretion and bicarbonate retention
    • but only if the acidosis is chronic
    • so if there’s low pH and high CO2 with a partially raised HCO3- it means that there’s some degree of renal compensation: chronic
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36
Q

Respiratory Alkalosis

A
  • CO2 depletion due to hyperventilation
  • Causes: Type 1 respiratory failure, anxiety and panic

Compensation: increased renal bicarbonate loss (if chronic)

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37
Q

What are the vasa recta

A
  • capillaries derived from the efferent arteriole that follow the nephron
    *
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38
Q

Renal blood flow, renal plasma flow, GFR and urine flow rate

A
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39
Q

Bicarbonate reabsorbtion: can you draw the diagram

A
  • this happens in the proximal tubule
  • the things that we want to re-absorb are the bicarbonate ions and the Na+ ions
  • the Na+ ions are antiported with H+
  • That H+ is recycled
  • carbonic anhydrase in the luminal space allows us to re-absorb H2O and CO2 (from the H+ and luminal HCO3-)
  • In the tubular cells H2O and CO2 then form H2CO3 which dissociates to form H+ and HCO3-
  • HCO3- can be re-absorbed into the blood and the H+ is recycled for the same process
  • NB CA does H2CO3 –> H2O and CO2 as well as the reverse reaction
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40
Q

an altitude sickness treatment

A
  • key component of altitude sickness is alkalosis due to the need to hyperventilate
    • they blow off all their CO2
  • this can be treated with a CA inhibitor which promotes the excretion of HCO3-
    • one of these is called acetazolamide
      • i don’t think you need to know that
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41
Q

Control of blood pressure flow diagram: can you draw it

A
  • ANP is atrial natriuretic peptide
    • think of natriuretic as like a uretic triggered by high sodium
  • The JGA detects a fall in Na+ delivery to the distal tubule
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42
Q

Affect of aldosterone

A
  • it’s a steroid hormone
  • It affects cells in the collecting duct
    • Principal cells
      • these are the main Na+ reabsorbing cells
      • aldosterone increases PC expression of
        • ENaC (Na+ transporter into cell out of lumen)
        • Na/K ATPase (3Na+ into blood in exchange for 2K+)
      • net effect is reabsorbing Na+ and getting rid of K+
      • K+ diffuses into the tubular lumen down an electrochemical gradient (because so much Na+ has been reabsorbed)
      • if the body needs to reabsorb Na+ due to low blood pressure, it sacrifices K+
      • this could cause hypokalaemia
    • Intercalated cells
      • these reabsorb K+ in exchange for H+
      • but doing too much of this would develop an alkalosis
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43
Q

Hypokalaemic Alkalosis

A
  • As aldosterone levels rise in response to volume contraction (low bp) the secretion of K+ (in exchange for Na+) will increase
  • this can cause hypokalaemia
  • the body may try to compensate by reabsorbing K+ in exchange for H+
  • this can cause alkalosis
  • combined effect is hypokalaemic alkalosis
    • this is what happens in Barrter’s when there is lots of salt wasting
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44
Q

excessive aldosterone production

A
  • Hyperaldosteronism
  • Primary
    • disorder of the adrenal gland increases production
  • Secondary
    • the systems that control aldosterone production are aberrant
    • classic excample is renal artery stenosis
      • JGA recieves decreased Na+ and so thinks there’s very low blood pressure when there isnt’
      • promotes increased aldosterone production unnecessarily
  • both cause hypokalaemic alkalosis as well as high blood pressure
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45
Q

Cortisol and the kidney?

A
  • cortisol could activate the same nuclear receptor as aldosterone
  • it doesn’t because it’s broken down at the surface of the cell by an enzyme called
    • 11-beta hydroxysteroid dehydrogenase
      • don’t think you need to know that
  • in some people this enzyme is deficient
  • this can cause secondary hyperaldosteronism and the associated hypokalaemic alkalosis and hypertension
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46
Q

Type 4 Renal Tubular acidosis

A
  • this is not uncommon in elderly diabetic patients
  • the problem here is a lack of aldosterone
  • there’s a reduced generation of the electrochemical gradient that results in K+ of H+ secretion
  • so you develop a metabolic acidosis
  • the treatment is with diuretics
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47
Q

Nephrogenic diabetes insipidus

A
  • not related to diabetes mellitus
    • diabetes just means weeing a lot
  • there’s a defect in Vasopressin, its receptor or in aquaporin 2 itself
  • leads to the inability to concentrate urine
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48
Q

which hormones are important in pregnancy?

A
  • prostaglandins
  • oxytocin
  • relaxin
  • progesterone
  • human chorionic gonadotrophin
  • oestrogen
  • prolactin
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49
Q
A
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50
Q

hCG

A
  • stimulates the ovary to produce oestrogen/progesterone
  • it’s the pregnancy test hormone
  • it diminishes once the pregnancy is mature enough to take over oestrogen and progesterone production
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51
Q

oestrogen in pregnancy

A
  • produced throughout the pregnancy
  • regulates the levels of progesterone
  • prepares the uterus for the baby
  • prepares the breasts for lactation
  • drops dramatically at birth
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52
Q

progesterone in pregnancy

A
  • prevents miscarriage
  • builds up the endometrium for support of the placenta
  • prevents uterine contractions
  • drops dramatically at birth
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53
Q

prolactin in pregnancy

A
  • produced by the pituitary gland
  • increases cells that produce milk
  • after birth, levels of progesterone and oestrogen drop dramatically
  • this allows prolactin to stimulate production of milk
  • this is also controlled by suckling
  • it also prevents ovulation but unreliably
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54
Q

relaxin in pregnancy

A
  • this is high early in pregnancy
  • it limits uterine activity and softens the cervix in preparation for delivery
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55
Q

oxytocin in pregnancy

A
  • trigggers ‘caring’ reproductive behaviour
  • it’s responsible for uterine contractions during pregnancy and labour
  • it is the cause of the contractions felt during breast feeding
  • used as a drug to induce labour
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56
Q

Prostaglandins in pregnancy

A
  • have a role in inducing labour
  • synthetic ones are used to induce labour
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57
Q

Cardiovascular changes in pregnancy

A
  • CO increases
  • there is reduced total peripheral resistance
  • this reduces systemic blood pressure
  • there is much increased uterine blood flow
  • increased stroke volume
  • increased heart rate
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58
Q

changes to blood chemistry during pregnancy

A
  • increased number of blood cells
  • increased clotting factors
  • increased fibrinolytic activtity
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59
Q

changes to the respiratory system during pregnancy

A
  • diaphragm displaced superiorly
  • decreased functional reserve capacity
  • increased risk of apnea and dyspnea
  • hyperventilation
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60
Q

changes to the GI system during pregnancy

A
  • Nausea and vomiting
  • heart burn and acidity
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61
Q

visible weight changes during pregnancy

A
  • varicose veins
  • linea negra
  • weight gain
    • foetal
    • amniotic
    • maternal
    • placental
    • breast size
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62
Q

Changes to breasts during pregnancy

A
  • increase in size
  • nipples increase in size
  • areolas become larger and darker
  • montgomery’s tubercles become more active and secrete substances to lubricate the nipples
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63
Q

fundal height

A
  • measured from the top of the uterys to the symphosis pubis with a tape measure
  • in cm it roughly corresponds to the age of the baby in weeks
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64
Q

early embrylology diagram - can you describe what happens on days:

  • 7
  • 12
A
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65
Q

common maternal probelms that can affect the outcome of pregnancy

A
  • Malnutrition
  • extremes of maternal age
  • an underlying medical condition
  • drug misuse
  • hemorrhage
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66
Q

common fetal problems

A
  • Miscarriage
  • abnormal development
  • disordered foetal growth:
    • too big
    • too small
  • Premature birth and consequences of that
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67
Q

Growth of the uterus

A

there’s both hypertrophy and hyperplasia

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68
Q

what is the myometrium

A

smooth muscle cell bundles in the uterus that contract during parturition to expel the foetus

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69
Q

what does the endometrium become

A
  • it becomes the decidua which is the maternal part of the placenta
  • together with the chorion it forms the placenta
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70
Q

cervical ripening

A
  • this is the remodelling of the cervix in the final three months of pregnancy to prepare for labour
  • it is promoted by the release of prostaglandin, relaxin and placental oestrogen
  • collagen concentration drops
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71
Q

4 phases of pregnancy

A
  • phase 0: myometrial repression - no labour
    • promoted by progesterone
  • phase 1: myometrial activation - results in labour
    • promoted mainly by oestrogen
  • phase 2: biochemical activation - together with myometrial activation results in labour
    • promoted by cytokines and prostaglandins
  • phase 3: permanent changes associated with labour
72
Q

prostaglandins and parturition

A
  • synthesised by all uterine tissues
  • main ones are E2 and F2alpha
  • they increase the sensitivity of the myometrium to oxytocin
  • positive feedback: as the head of the baby presses on the cervix this stimulates the production of PGEs
73
Q

How is the foetus adapted for birth?

A
  • joints of the skull are soft and sutures can overlap while the head is passing through the birth canal
  • the head also flexes to reduce its diameter
74
Q

Uterine contractions

A
  • there are braxton-hicks contractions throughout pregnancy that don’t amount to labour
  • Ca2+ influx to the cell results in excitation relaxaction coupling
  • the uncoupling leads to relaxation
  • contractions must be coordinate to result in the safe birth of a baby
  • if they are inco-ordinate then it won’t be as effective
75
Q

the initation of labour

A
  • There are foetal, maternal and placental components to the initiation of labour
  • the drop in progesterone coupled with the rise in oestrogen results in increases in:
    • uterine sensitivity to oxytocin
    • increased release of prostaglandins
    • softening of the cervix
  • this all leads to uterine contractions and labour
  • oxytocin does the final job of ensuring that the uterus contracts
76
Q

Oxytocin in labour

A
  • the number of oxytocin receptors changes a lot throughout pregnancy
  • PGEs increase number of receptors on decidua and myometrium
  • Distention of uterus near term does the same thing
  • uterine contractions are elicited when the number of receptors reaches a critical point
77
Q

what position is the baby’s head in during birth ?

A

Occipital-anterior position

78
Q

phases of labour

A
  • defined by the amount of cervical dilatation
  • there is a phase where there is not much dilation happening
    • this is the latant phase
  • then there is a phase when dilation begins to happen much more quickly
    • active phase
    • this is when you want to me managing the labour
79
Q

the stages of labour

A
  • 1st stage: the time of established labour until the cervix is fully dilated
  • 2nd stage: the time between full dilation and delivery
  • 3rd stage: the time of full delivery of the baby until full expulsion of the placenta
80
Q

placental structure

A
  • maternal surface:
    • cobblestone appearance
    • covered with maternal decidua basalis
  • embryonic side
    • umbilical cord attachment
    • umbilical vessels branch into chorionic vessels which anastomose within the placenta
81
Q

Implantation

A
  • the outer layer of the blastocyst forms the trophoblastic cell mass (TCM)
  • The TCM infiltrates the endometrium and degenerates
  • implantation is the first stage of the development of the placenta
  • there’s a differentiation of the cells forming:
    • trophoblast –> placenta
    • embryoblast –> baby
82
Q

what are the vessels in the umbilical cord?

A
  • two arteries out of baby
  • one vein into baby
83
Q

Placental function:

A
  • remember that the placenta has functional reserve so a lot of it needs to be damaged to cause problems
  • placenta has 3 main functions:
    • metabolism
      • synthesises glycogen, cholesterol and fatty acids
    • transport
    • endocrine
      • produces some important hormones
84
Q

what hormones does the placenta produce

A
  • hCG - which supports the corpus luteum
  • Relaxin
  • Progesterone
  • Oestrogen
  • Human chorionic somatommotropin (hCS)
85
Q

What is placenta accreta

A

abnormal adherance with absense of decidua basalis

86
Q

placenta praevia

A
  • the placenta overlies the internal os of the uterus
  • blox exit
  • may cause abnormal bleeding
87
Q

Development of internal genetalia

A
  • If the testis are present:
    • leydig cells make testosterone
      • so the wolffian system develops into:
        • epididymis
        • vas deferens
        • seminal vesicles
        • ejaculatory ducts
    • sertoli cells secrete AMH which causes mullerian system to regress
  • If there are no leydig cells then the mullerian cells develop into:
    • fallopian tubes
    • uterus
    • upper third of the vagina
88
Q

Development of External Genetalia

89
Q

Layers of the Adrenal Gland and what they produce

90
Q

when does puberty growth end?

A

when oestrogen causes the epiphysis in the legs to fuse

NB boys have oestrogen too they convert testosterone to oestrogen in fatty tissue

91
Q

the growth plate

A
  • its the growing bit of bone
  • each long bone has a growth plate at either end
  • growth from here is chondrogenesis
  • because building materials are needed every day, there is a direct effect of nutrition and calcium / phosphate supply on bone architecture
92
Q

regulation of growth hormone secretion: can you draw the diagram?

93
Q

the hypothalamus and growth hormone

A
  • GHRH cell bodies in the arcuate nucleus project into the portal capillaries of the anterior pituitary gland
  • Negative feedback is by:
    • IGF-1 (insulin like growth factor 1)
    • Somatostatin (SST)
    • GH
94
Q

where is human growth hormone (GH) synthesized

A
  • Synthesized in the somatotroph cells
    • these are 40-50% of the anterior pituitary
95
Q

Human Growth Hormone

A
  • Pulsatile secretion (bursts)
  • mainly secreted at night
  • stimulates insulin like growth factor 1
  • has a direct effect on the growth plate of bones
  • decreases glucose use
  • increases lipolysis
  • increases muscle mass
96
Q

what factors suppress GH secretion?

A
  • aging
  • high carbohydrate meals
  • hyperthyroidism
  • hyperglycaemia
97
Q

what factors stimulate growth hormone secretion?

A
  • hypoglycaemia
  • stress
  • high protein meals
  • perinatal development
  • fasting
  • exercise
98
Q

IGF-1

A
  • GH stimulates the production of Insulin like Growth Factor 1
  • this is what mediates some of the growth
  • if there is IGF deficiency then there will be short stature
99
Q

Factors that can cause overgrowth with impaired final height

A
  • Precocious puberty
    • menarche before 9 leads to short stature
  • congenital adrenal hyperplasia
  • Hyperthyroidism
100
Q

factors that can cause overgrowth with increased final height

A
  • androgen/oestrogen deficiency
  • GH excess
  • Klinefelter syndrome (XXY)
  • Marfan syndrome
101
Q

definitive signs of puberty in both sexes

A

Girls: menarche

Boys: ejaculation

NB neither of these signify fertility

102
Q

female secondary sexual characteristics and what they’re controlled by

A
  • Ovarian oestrogens control growth of breasts and female genetalia
  • Ovariana and adrenal androgens control pubic and axillary hair
103
Q

male secondary sexual characteristics and what they’re controlled by

A
  • Testicular androgens control the development of:
    • external genetalia
    • pubic hair
    • enlargement of larynx
104
Q

factors that influence timing of puberty onset

A
  • genetics
  • nutrition
  • environment
  • leptin
  • adrenarche
    • the gradual maturation of the adrenal gland
    • comes with development of pubic hair, axillary hair, body odour and acne
105
Q

difference between precocious puberty and precocious pseudopuberty

A
  • pseudopuberty doesn’t have hypothalamus or anterior pituitary involvement and the gonadal effects are mediated by something else
  • the difference between them can be checked by stimulating them with GnRH and seeing how much gonadotropin (LH and FSH) they produce
    • if it’s true puberty they should produce lots
106
Q

what is androgen

A

it’s an oestrogen precursor

107
Q

3 key points about pancreas embryology

A
  • at the junction of the foregut and the midgut, 2 pancreatic buds (dorsal and ventral) are generated and fuse to form the pancreas
  • exocrine functions begin after birth (pancreatic juices etc)
  • Endocrine functions (hormones) begin from 10-15 weeks
108
Q

key anatomy points of the pancreas

A
  • retroperitoneal
  • posterior to the greater curvature of the stomach
  • 12-15cm long
  • head tucks into the C portion of the duodenum
  • has 5 parts
    • uncinate process
    • head
    • neck
    • body
    • tail
  • exocrine secretions pass from small ducts into two larger ducts
  • these larger ducts join the common bile duct and enter the duodenum as the hepatopancreatic ampulla
    • aka the ampulla of Vater
  • this ampulla has a sphincter (sphincter of Oddi)
109
Q

exocrine function vs endocrine function

A
  • 98-99% of cells are in clusters called acini
    • exocrine activity secretes pancreatic juice which includes:
      • amylase - carbs
      • trypsin, elastase - protein
      • Lipase - triglycerides
      • all become active once in lumen of small gut
  • endocrine activity is performed by islet cells
    • hormones secreted into the portal vein
110
Q

cells in the islets of langerhans

A
  • Beta cells are the most common (60-70%)
    • secrete insulin
  • Alpha cells (20%)
    • secrete glucagon
  • Delta cells (5%)
    • secrete somatostatin
  • there’s cross talk between alpha cells and beta cells
    • i.e. insulin secretion inhibits glucagon secretion
111
Q

brief outline of the effects of insulin

A
  • suppresses hepatic glucose output
    • inhibits glycogenolysis
    • inhibits gluconeogenesis
  • increases glucose uptake by somatic cells
    • GLUT4 on transport vesicles is transported to the membrane when insulin binds the membrane receptors
  • suppresses use of bodily stores for energy
    • inhibits lipolysis
    • inhibits ketogenesis
    • inhibits muscle breakdown
112
Q

brief outline of the effects of glucagon

A
  • increases hepatic glucose output
    • activates glycogenolysis
    • activates gluconeogenesis
  • reduced peripheral glucose uptake
  • stimulates release of gluconeogenic precursors
    • this includes amino acids and glycerol
    • activates lipolysis
113
Q

Insulin secretion by the B cell

A
  • glucose crosses GLUT2 transporters on B cells at a rate that reflects the blood glucose concentration
  • intracellular metabolism of this glucose results in production of ATP
  • ATP closes a potassium channel on the cell which stops the efflux of K+
  • the membrane is depolarised which results in the opening of voltage-dependent Ca2+ channels
  • rapid influx of calcium triggers exocytosis of insulin from secretory granules
114
Q

how can you check if there is endogenous insulin production

A
  • the presence of C peptide
  • a peptide that linked A and B chains of pro-insulin
  • they are secreted together in equimolar concentrations
  • helps physicians to distinguish between endogenous and exogenous insulin
115
Q

two phases of insulin release

A
  1. rapid release of stored insulin
  2. slower process of synthesising and releasing insulin
116
Q

Incretins

A
  • these are hormones secreted by sensory cells in the gut wall that also stimulate insulin release
  • insulin response is greater following oral glucose than IV glucose
  • this difference is due to the incretin effect
  • incretins to remember:
    • Glucagon-Like Peptide 1 (GLP-1)
    • Glucose-dependent insulinotrophic peptide (GIP)
117
Q

GLP-1

A
  • Glucagon-Like peptide-1
  • has a short half life as it is cleaved by protein DPPIV
    • this prevents hypoglycaemia
118
Q

Carb metabolism in the fasted state

A
  • all glucose comes from the liver through:
    • breakdown of glycogen
    • gluconeogenesis
      • from alanine, lactate or glycerol
  • this glucose is then delivered to the tissues
  • muscles use FFA for fuel
  • insulin levels are low
  • glucose is delovered
119
Q

CHO metabolism in the fed state

A
  • Rising glucose causes increase in insulin and suppression of glucagon
  • ingested glucose replenishes glycogen stores in the muscle and the liver
  • excess glucose is converted to fat
  • lipolysis is inhibited and level of FFAs falls
120
Q

summarise diabetic ketoacidosis

121
Q

zones of the adrenal gland

A
  • there’s an outer capsule, a cortex and a medulla
  • the cortex has three layers:
    • the zona glomerulosa
      • mineralcorticoids (aldosterone)
    • the zona fasciculata
      • glucocorticoids (cortisol)
    • the zona reticularis
      • androgens (DHEA)
  • the medulla produces catecholamines
122
Q

corticosteroids overview

A
  • includes mineralocorticoids and glucocorticoids
  • cholesterol is the precursor for them all
  • they’re lipid soluble
  • bind specific intracellular receptors
  • alter gene transcription
    • directly or indirectly
  • some key ones are cortisol and aldosterone
123
Q

effect on corticosteroid synthesis of ACTH

A
  • it massively stimulates it
  • in ACTH excess the adrenal gland becomes enlarged
124
Q

glucocorticoids

A
  • synthesised int he zona fasciculata and reticularis
  • essential for life
  • important for homeostasis
  • increase glucose metabolism
    • increased lipolysis
    • augment gluconeogenesis
  • maintain circulation
    • salt/water balance
    • vascular tone
  • immunosuppression
125
Q

glucocorticoid transport

A
  • these proteins are heavily bound
    • 90% to corticosteroid-binding globulin (CBG)
    • 5% to albumin
    • 5% free
  • only the free ones are bioavailable
  • CBG is cleaved during inflammation
  • so when CBG decreases due to inflammation (e.g. due to sepsis) the % free cortisol increases
  • more glucocorticoid can enter cells
126
Q

Factors that regulate glucocorticioid synthesis

A
  • ACTH does!!!
    • it acutely stimulates cortisol release
    • it also stimulates corticosteroid synthesis
    • it does this by binding a receptor on the surface of a cell in the zona fasciculata
    • this produces a cAMP response within the cell that triggers steroidogenesis
  • CRH from hypothalamus stimulates ACTH release from pituitary
  • cortisol in turn has a negative feedback mechanism on the ACTH and CRH production
127
Q

diurnal rhythms and cortisol

A
  • just know it’s quiet when you’re asleep and then released mainly between waking up and breakfast
  • also know that stresses such as trauma or sepsis will heighten it
    • CBG is broken down so more free cortisol
128
Q

Mineralocorticoids overview

A
  • Aldosterone and DOC are the main ones
  • they’re synthesised in the zona glomerulosa
  • they’re essential for life
129
Q

where does aldosterone act

A
  • acts on the distal conveluted tubule and the cortical collecting duct
  • it acts on intracellular receptors
  • these upregulate transcription of proteins that modulate the activity of ion transport systems in the apical and basolateral membranes
    *
130
Q

which transporters does aldosterone result in the stimulation of

A
  • ENaC on apical surface
    • more Na+ out of lumen and into cells
  • Na+K+ATPase on basolateral surface
    • more Na+ out of cell and into interstitium
    • more K+ into cell and out of interstitium
      • this then leaves the cell and enters the urine through ROMK
  • Plasma: sodium up, potassium down
  • Urine: sodium down, potassium up
131
Q

how are mineralocorticoids regulated?

A
  • e.g. aldosterone
  • not regulated via the hypothalamus, pituitary, adrenal system
  • YOU DO NOT GET SALT LOSS AS A SYMPTOM OF SECONDARY ADRENAL INSUFFICIENCY
  • the juxtoglomerular apparatus sense the bp of the afferent arterioles
  • if blood pressure drops they secrete renin
  • this kicks off RAAS
132
Q

RAAS

A
  • secretion of renin by JGA can be activated by:
    • drop in bp
    • prostaglandins
    • beta adrenergic action
  • renin cleaves angiotensinogen (produced by the liver) into angiotensin I
  • angiotensin I is cleaved by ACE (angiotensin converting enzyme) in the lung to angiotensin II
  • angiotensin II binds angiotensin II receptor in the adrenal leading to the synthesis and release of aldosterone from the zona glomerulosa
  • aldosterone works on the kindey by binding the mineralocorticoid receptor
  • once extracellular potassium drops there’s a direct negative feedback on the adrenal to halt aldosterone production
133
Q

other organs affected by mineralocorticoids

A
  • pancreas
  • sweat glands
  • colon

in these places there is the same effect of sodium retention

134
Q

what is cortisone?

A
  • the inactive form of cortisol
  • cortisol is present at high levels but can also bind the mineralocorticoid receptor
  • this is a problem because aldosterone is present at very low levels
  • so in order for aldosterone to be able to bind its receptor and be effective, cortisol must be inactivated
  • so every tissue that expresses the mineralocorticoid receptor also expresses the enzyme which inactivates cortisol to cortisone
  • if you inhibit this enzyme then you induce severe hypotension because aldosterone can no longer bind
135
Q

adrenal androgens

A
  • androgens are produced in the ovaries and the testis too
  • females have them but at lower levels
    • in women the adrenal is a major source of androgen
  • adrenal androgens
    • Dehydroepiandosterone (DHEA) is the most abundant adrenal steroid but it is a very weak androgen
    • Androstenedione is stronger but still only a 1/10th as strong as testosterone
    • production is regulated by ACTH not gonadotrophins
136
Q

The Adrenal Medulla

A
  • produces catecholamines like adrenaline
  • is part of the autonomic nervous system
  • has specialised ganglia supplied by preganglionic neurones from the spinal cord
  • these preganglionic neurons produce noradrenaline
  • the medulla has the enzyme to convert noradrenaline to adrenaline but the neurons don’t
  • so catecholamine synthesis is regulated by the sympathetic nervous system
137
Q

catecholamine synthesis

A
  • they are synthesised from tyrosine
  • sympathetic stimulation is important for some of the enzymes
  • cortisol stimulates the final enzyme which makes adrenaline from noradrenaline
    • so without cortisol you will not produce adrenaline
138
Q

catecholamines effect on fight or flight

A
  • gluconeogenesis in liver and muscle
  • lipolysis in adipose tissue
  • tachycardia and increased cardiac contractility
139
Q

where does the posterior pituitary recieve its stimuli from?

A
  • through the hypothalamic hypophysial tract
  • from the paraventricular nucleus and the supraoptic nucleus of the hypothalamus
  • the hormones are transported in the large neurons of these nuclei to the posterior pituitary where they are released
140
Q

what two hormones are secreted by the posterior pituitary?

A
  • Vasopressin
    • AKA ADH
    • stimuli from supraoptic nuclei
  • Oxytocin
    • promotes onset of labour
    • promotes expression of milk
    • stimuli is from the paraventricular nuclei
141
Q

Summarise water distribution in the human body

142
Q

what are the main extracellular ions?

A
  • Na+
  • Ca2+
  • Cl-
  • HCO3-
143
Q

What are the main intracellular ions

A
  • K+
  • Mg2+
  • PO3-4
144
Q

vasopressin’s effect on the kidney

A
  • binds V2 receptors on the renal collecting duct principal cells
  • it triggers and intracellular signalling cascade that results in the transport of AQP2 containing vesicles to the apical surface of the cell
    • aquaporins are transmembrane channel proteins for water
  • this results in net movement of water into the cell and through into the blood stream
  • this decreases plasma osmolality
145
Q

Osmolality

A
  • concentration of particles per kilo of liquid
  • v similar to osmolarity in plasma
  • size of particle is not relevant, just the numbers of them
146
Q

Oxytocin

A
  • synthesised in both sexes but well known effects are only in women
  • action
    • secretion of milk
    • contraction of myometrium
    • onset of labour
  • together with oestrogen it causes cervical dilation
  • both suckling and uterine contraction have a positive feedback effect on the PVN to produced more oxytocin
147
Q

what is the purpose of the urea cycle and where does it occur

A
  • mainly to rid the body of nitrogenous waste
  • it does this by converting ammonia and ammonium to the less toxic urea
  • urea is water soluble and can be excreted through the kidneys
148
Q

Draw out the urea cycle

149
Q

briefly summarise the function of the proximal tubule

A
  • bulk reabsorption
    • Na+
    • Cl-
    • amino acids
    • HCO3-
150
Q

label this

151
Q

Fill this table in (SH should be TSH)

152
Q

what are the two posterior pituitary hormones? Which hypothalamic nuclei are they associated with?

A
  • Oxytocin: paraventricular nucleus
  • Vasopressin (AKA ADH): supraoptic nucleus
153
Q

what 3 hormones does the thyroid produce?

A
  • Tri-iodo-thyronine (T3): major thyroid hormone
  • Thyroxine (T4): reservoir for T3
  • Calcitonin: involved with Ca2+ homeostasis
154
Q

can you draw the thyroxine secretion and feedback flow diagram?

155
Q

what does calcitonin do?

A
  • increasing plasma Ca2+ levels causes the thyroid gland to produce calcitonin.
  • Calcitonin has two effects to reduce plasma calcium
    1. It inhibits bone resorption by osteoclasts
    2. it decreases reabsorption of calcium in the kidneys.
156
Q

what is calcitriol and how is it produced?

A
  • it is the active form of vitamin D
  • sunshine converts 7 dehydroxy cholesterol in the skin into vitamin D3
  • In the liver this vitamin D3 is converted to 25, hydroxy VD3
    • aka calcidiol
  • Calcidiol is converted to 1,25 dihydroxyvitamin D3 (Calcitriol) in the kidney by enzyme 1 alpha hydroxylase
157
Q

calcium homeostasis: can you draw the diagram?

158
Q

How does parathyroid hormone mediate calcium resorption? can you draw the diagram?

A
  • even though osteoblasts are principally responsible for building bone, they have an important role in activating osteoclasts which are responsible for bone resorption
  • Parathyroid hormone binds to PTH receptor on osteoblasts and mediates 3 effects on it:
    1. osteoblast proliferation
    2. upregulation of cell surface RANKL
    3. stops production of OPG
  • OPG inhibits activity of RANKL binding
  • This means that RANKL can now bind RANK on pre-osteoclasts.
  • RANK-RANKL binding allowsthe pre-osteoclast to proliferate and differentiate into a mature osteoclast
  • This will result in increased bone resorption
159
Q

Summarise the effects of Insulin:

Can you draw the diagram?

A
  • Reduced glucose produced by the liver
    • less glycogenolysis
    • les gluconeogenesis
  • Increases movement of glucose to tissues
    • Glycogen and protein synthesis in the muscle
    • Triglyceride synthesis in the adipocytes
  • Suppresses:
    • ketogenesis
    • lipolysis
    • muscle breakdown
  • Insulin also draws potassium into cells
160
Q

label this doogroom

161
Q

where does aldosterone act?

A

distal conveluted tubule and the collecting duct

162
Q

what are the actions of aldosterone

A
  1. acts on the principle cells of the collecting duct and the distal tubule to up regulate the Na+/K+ pump
    • more Na+ enters the interstitium
    • therefore more Na+ reabsorbed down concentration gradient
    • K+ is pumped into the urine in exchange
  2. upregulates ENaC Na+ transporter on the apical surface of cells lining the collecting duct and the colon
163
Q

Draw out RAAS

164
Q

what are the functions of cortisol?

A
  1. Metabolism
    • Protein –> amino acids
    • Triglyceride –> glycerol and fatty acids (lipolysis)
    • Glycogen –> glucose (gluconeogenesis)
  2. Circulation
    • increases vasoconstriction
  3. Decreases inflammation and the specific immune response
  4. Decreases non-essential functions like reproduction and growth
165
Q

cortisol secretion: can you draw the diagram?

166
Q

How does the anterior pituitary recieve info from the the hypothalamus?

A

Through the hypothalamic-hypophyseal portal system into which the neurosecretory neurons secrete releasing hormones.

167
Q

what is the releasing hormone of thyroid stimulating hormone (TSH)?

A

thyrotropin releasing hormone (TRH) released from hypothalamus

168
Q

what is the adrenocorticotrophic hormone (ACTH) releasing hormone?

A

Corticotropin releasing hormone (CTH) released from the hypothalamus

169
Q

where is gonadotropin releasing hormone released from and where does it act and what does it cause the release of

A

it is released by neurosecretory neurons in the hypothalamus. It travels in the hypothalamic-hypophyseal portal system to the anterior pituitary where it causes the release of follicle stimulating hormone (FSH) and Leutenising Hormone (LH)

170
Q

what are the releasing hormones of growth hormone (GH) and what might inhibit its release?

A

growth hormone releasing hormone (GHRH) released by the hypothalamus

GH release is inhibited by somatostatin

171
Q

what inhibits prolactin release

A

dopamine release by the hypothalamus causes inhibition of prolactin release

172
Q

what is the difference between primary, secondary and tertiary problems with hypothalamic/pituitary/tissue axis

A

primary is always a problem with the final gland (i.e. with cortisol it would be a problem with the adrenal)

secondary is always a problem with the pituitary

tertiary is always a problem with the hypothalamus

173
Q

what is the most abundant hormone in the anterior pituitary?

A

growth hormone

174
Q

what is the male hypothalamus pituitary gonad axis

A
  • GnRH release from hypothalamus
  • GnRH causes release of LH and FSH
  • LH stimulates leydig cells in interstitium to produce testosterone
  • FSH stimulates sertoli cells to produce androgen binding globulin and inhibin
    • ABG binds testosterone and localises it to the seminiferous tubules for spermatogenesis
    • Inhibin supports spermatogenesis and inhibits FSH, LH and GnRH production
175
Q

Female HPG axis

A
  • Hypothalamus secretes GnRH
  • The AP releases FSH and LH
  • LH and FSH reach the ovaries where they cause the production of oestrogen, progesterone and inhibin
  • Inhibin inhibits activin which is responsible for stimulating GnRH
176
Q

effects of oestrogen at low and high levels

A
  • Low levels
    • stimulates FSH release
    • inhibits LH release
  • High levels
    • stimulates LH release
    • inhibits FSH release
177
Q

Cortisol functions

A
  • Metabolism
    • protein –> amino acids
    • triglycerides –> FFAs and glycerol (lipolysis)
    • glycogen –>glucose (glycogenolysis)
  • Circulation
    • vasoconstriction
  • Inhibits inflammation and specific immune response
  • Inhibits non-essential functions like reproduction and growth

EM: (14 decks)

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