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Medicine - Phase 1 > SUGER > Flashcards

SUGER Flashcards

1
Q

what are the layers of the glomerulus barrier?

A
  1. podocytes
  2. glomerular basement membrane
  3. fenestrated capillary endothelium
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2
Q

where does filtration of the blood take place?

A

glomerulus

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3
Q

which cell type in the glomerulus is responsibe for filtration of blood?

A

enodothelial cells

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4
Q

what is the name of the network of capillaries within the bowman’s capsule where blood filtration occurs?

A

glomerulus capillaries

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5
Q

what makes up the juxtoglomerular apparatus?

A

macula densa (from distal tubules)
juxtaglomerular cells (from afferent arteriole)

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6
Q

what do the juxtaglomerular cells from the afferent arteriole secrete?

A

renin in response to low BP

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7
Q

what is the average rate of urine flow?

A

1 ml/min

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8
Q

what % of cardiac output goes to the kidneys?

A

20%

brain 15%, muscles 20%, liver 25%

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9
Q

what gives rise to interlobular arteries?

A

arcuate arteries

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10
Q

what gives rise to the interlobular veins?

A

vasa recta

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11
Q

what is glomerular filtration?

A

passage of fluid from the blood into bowman space to form filtrate.
distal tubule responsible for secretion and reabsorbtion

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12
Q

what 5 factors determin glomerular filtration rate?

A
  1. pressure
  2. size of molecule
  3. charge
  4. rate of blood flow
  5. protein binding
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13
Q

which pressure forced favour filtration and which oppose filtration?

A
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14
Q

molecules up to what size can pass freely through glomerulus?
eg?

A

up to 10kDa
e.g. glucose, uric acid, potassium, creatinine
NOT plasma proteins (unless pathology!)

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15
Q

why can’t albumin, phosphate anf sulfate pass through the glomerulus?

A

the GMB is negatively charged so repells these negative anions

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16
Q

what happens to GFR when afferent resistance is increased?

A

reduced blood flow to glomerulus, reduced pressure in glomerulus, reduced GFR

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17
Q

what happens to GFR when efferent resistance is increased?

A

blood unable to exit. build up of blood in glomerulus, increased pressure, increased GFR

up to a point - then paradoxically this reverses (ACEi)

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18
Q

why cant albumin pass into the nephron tubule?

A

it has a weight of 66kDa and is negatively charged so cannot pass.

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19
Q

what protein might be find in the urine of a healthy individual?

A

no protein in urine of healthy individual
except Tamm Horsfall protein which is produced by the tubule

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20
Q

How is GFR calculated?

A
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21
Q

in practice, GFR is not measured directly. how is it normally calculated?

A
marker normally creatine
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22
Q

why is creatine normally used as a marker for GFR?

A

freely filtered
not secreted or absorbed (mostly)
not metabolised

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23
Q

what is the “gold standard” of a GFR marker?

A

inulin
- freely filtered]
- not secreted/absorbed
- not metabolised

time consuming though

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24
Q

what is a normal GFR?

A

125ml/min

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25
Q

what could affect a persons creatine levels?

A

dietary protein (+)
medications (+)
creatinine supplements (+)
age/gender/weight/ethnicity (-)

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26
Q

seven (!) things that regulate glomerular filtration

A
  1. renal autoregulation
  2. neural regulation
  3. hormone
  4. intrarenal baroreceptors
  5. extracellular fluid volume
  6. blood colliod osmotic pressure
  7. inflammatory mediators
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27
Q

what are the two mechanisms of renal autoregulation of GFR?

A

myogenic mechanism
tubuloglomerular feedback

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28
Q

how does the myogenic mechanism protect the GFR from high bp?

A

the myogenic mechanism is the intrinsic ability og renal arteriold to contrict/dilate

high BP
⇩
stretches blood vessel wall
⇩
opens stretch-activated cation channels
⇩
membrane depolarises
⇩
voltage gated channel open
⇩
calcium flows in
⇩
smooth muscle contraction
⇩
increase vascular resistance
⇩
minimises GFR chnages

only PREglomerular resistance vessels

can only protect up to a point.

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29
Q

how does the tubuloglomerular feedback influence afferent arteriolar resistance?

A
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30
Q

how does neural regulation affect GFR?

A

sympathetic nervous system - vasoconstricts afferent arterioles

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31
Q

what are the two mechanisms of hormone regulation of the GFR?

A

RAAS - renin released from JGA due to low bp/Na
and
ANP - from atria due to blood volume - vasodilation of afferent arteriole

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32
Q

how to intrarenal baroreceptors regulate GFR?

A

change diameter of afferent arterioles

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33
Q

how can extracellular fluid volume affect GFR?

A

changes in blood volum will affect hydrostatic pressure in glomerulus

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34
Q

how can blood colloid osmotic pressure affect GFR?

A

onctoic pressure of exerted by proteins

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35
Q

name some inflammatory mediators that affect the GFR

A

porstaglandins, NO, bradykinin histamine, cytokines

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36
Q

Name three homrones that reduce the GFR

A

norepinephrine
epinephrine
endothelin

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37
Q

which hormone prevents the decrease of GFR?

A

Angiotensin II

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38
Q

which two hormones increase the GFR?

A

enodothelial-derived nitric oxide
prostaglandins

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39
Q

how do NSAIDs affect GFR?

A

vasoconstricts afferent arteriole

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40
Q

how do ACEi affect GFR?

A

vasodilation of efferent arterioles

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41
Q

presentation of nephrotic syndrome

A

triad: oedema proteinuria low albumin

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42
Q

what is the most common cause of nephrotic syndrom in adults?

A

membranous pathology - thickening of GMB

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43
Q

which hormone regulates the diamter of the afferent and efferent arterioles to control the GFR?

A

renin

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44
Q

what is filtration fraction?

A

GFR/renal plasma flow

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45
Q

what is “clearance”?

A

the volume of plasma from which a substance is comletely removed by the kideny per unit time.

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46
Q

what is the definition of “rare” in disease?

A

1 in 2000 (europe)

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47
Q

what is the incidence of ADPKD?

A

1 in 500-1000

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48
Q

what is the second most common site of cysts in ADPKD?

A

the liver

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49
Q

what is an important extrarenal manifestation of ADKP, aside from cysts elsewhere?

A

intracranial aneurysms (8%)

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50
Q

what are the 2 genetic factors that cause ADPKD? which is “more serious”

A

Polycystin-1 and Polycystin-2

kidney will live longer in in PKD2 (80yr) than in PK1 (NT = 68/ T=56 yr)

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51
Q

what kind of tumour is often found in tuberous sclerosis?

A

AML tumour: AngioMyoLipoma - blood, muscle, fat

= cysts, adenomas on face, hypopigmentation

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52
Q

which gene most often causes tuberous sclerosis?

A

TSC2 (70-90%)

TSC prevalance = 1/1000

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53
Q

What causes androgen insensitivity syndrome?
presentation?

A

46 XY indivual with androgen receptor deficiency, tissues dont respond to androgens
Partial AIS - testosterone has some effect - apparant at birth
Complete AIS - no testosterone. Genitalia appear feamle, undiagnosed until puberty - no uterus

AMH still produced, mullerian duct regresses - no uterus

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54
Q

What is Acidemia?

A

Low blood pH

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55
Q

What is Alkalemia?

A

High blood pH

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56
Q

broadly, what are two factors that can affect blood pH?

A

Respiratory (CO2)
and
Metabollic (Inrinsic from metabolites, extrinsic from diet, buffers)

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57
Q

What is the Henderson-Hasselback Equation?

A
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58
Q

where is bicarb recyled?

A

in the kidneys

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59
Q

where is H+ secreted?

A

kidneys

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60
Q

Stewart’s strong ion difference is an alternative to the Henderson-Hasselbach equation…what does it look at?

why is is not used very often?

A

looks at what is driving thr changes in pH.
but more calculations = more analytical errors.

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61
Q

in an ABG, what is a the standard bicarbonate a measure/calculation of?

A

bicarbonate levels if patients’ CO2 was normal.

  • bicarb is affected by both resp and metabolic
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62
Q

what does a negative base excess in and ABG indicate?

A

Negtative base excess = acidosis
Base excess = alkalosis

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63
Q

Causes of metabolic Acidosis?

A

Failure of H+ excretion - renal, hypoaldosterone, renal tubular acidosis.
Excess H+ - lactic acidosis, ketoacidosis, ingest acids.
HCO3- loss - diarrohoea

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64
Q

clinical features of metabolic acidosis?

A

sighing respirations, tachypnoea

-compensatory hyperventilation

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65
Q

how can you investigate the causes of metabolic Acidosis?

A

using the anion gap - the difference between measured anions and cations.

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66
Q

what would a wide anion gap indicate?

A

metabolic acidosis - lactic acidosis, ketoacidosis, acid ingestions, renal failure

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67
Q

what would a narrow anion gap indicate?

A

metabolic acidosis - GI HCO3- loss, renal tubular acidosis

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68
Q

causes of metabolic alkalosis?

A

alkali ingestion
GI acid loss - vomiting
renal acid loss - hyperaldosteronism, hypokalaemia

compensatory hypOventilation - but this is limited by hypoxic drive.
compensatory renal bicarb excretion (removal)

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69
Q

causes of respiratory acidosis?

A

CO2 retention –> increased carbonic acid dissociation

Respiratory failure Type 1/Type 2

if Chronic - compensated by increased renal H+ excrretion (remove) and bicarb retention (keep)

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70
Q

in respiratory acidosis/alkalosis, when would renal metabollic compensation occur?

A

only if chronic

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71
Q

causes of respiaroty alkalosis?

A

CO2 depletion due to hyperventilation
Type 1 Resp failure, panic attacks

compensation - increased renal bicarb loss (if chronic)

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72
Q

what is this?

A
  • pH = low = Acidic
  • pCO2 = low = Alkaline
  • HCO3- = low = Acidic
  • Base excess = low = Acidic

= metabolic acidosis
with respiratory compensation.

  • likely diabetic ketoacidosis
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73
Q

what is the likely cause of this?

A
  • pH = high = alkaline
  • pCO2 = low = alkaline
  • HCO3- = normal
  • Base excess = normal

= respiratory alkalosis
no renal compensation ∴ acute not chronic

likely cause Type 1 Respiratory failure - CO2 still low

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74
Q

what is the likely cause of this?

A
  • pH = high = alkaline
  • pCO2 = normal
  • HCO3- = high = alkaline
  • Base excess = hight = alkaline

= metabolic alkalosis, no resp compensation.
likely cause = vomitting in pregnancy

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75
Q

what is the likely cause of this?

A
  • pH = low = acidic
  • pCO2 = high = acidic
  • HCO3 = high = alkaline
  • Base excess = high = alkaline

= respiratory acidosis
with renal/metabolic compensation ∴ chronic

COPD

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76
Q

what is the likey cause of this?

A

- pH = low = acid
- pCO2 = high = acid
- HCO3- = low = acid
- Base excess = low = acid

MIXED metabollic and respiratory acidosis

pneumonia = type II resp failure
sepsis = lactic acidosis

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77
Q

what is the rate of renal blood flow?

A

1250ml/min

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78
Q

what is the rate of renal plasma flow?

A

700ml/min

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79
Q

what is the glomerular filtration rate?

A

125ml/min

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80
Q

what is the urnie flow rate?

A

1ml/min

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81
Q
A
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82
Q

disorder associated with glucose reabsorbtion in the proximal tubule?

A

renal glycosuria

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83
Q

what is the defect in renal glyosuria?

A

sodium glucose transporter (SGLT2)
- failure of glucose reabsoribtion - benign

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84
Q

clinical features of renal glycosuria?

A

incidental finding on testing, benign

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85
Q

SGLT2 inhibitors have now been established as a treatment for?

A

type 2 diabetes - remove sugar and help lose weight
reduced mortality
reduced CV mortality
reduced heart failure hospitalisation

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86
Q

what disorder is associated with Amino Acid reabsorbtion failure in the proximal tubule?

A

Aminoacidurias - e.g. cysturia

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87
Q

what is the defect in Aminoaciduria: cystinuria?

A

Renal basic amino acid transported (rBAT)
= faillure of cystine reabsorbtion - more cystine in urine - kidney stones

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88
Q

clinical features of Aminoaciduria: Cystinuria?

A

Renal colic, recuttent kidney stones

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89
Q

Treatment of Aminoaciduria: Cystinuria

A
  • High fluid intake, lower cystine concentraion
  • Alkalinise urine (cystine crystallised better in acidic urine)
  • Chelation = prevents crystallising
  • surgery to remove stones
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90
Q

what disease is associated with phosphate reabsorbtion disorders in the proximal tubule?

A

Hypophosphateaemic rickets (usually cross-linked)
(XLH)

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91
Q

what is the defect associated with hypophosphateaemic rickets?

A

complicated - but essentially a chain of things that lead to dcreased expression and activity of Phosphate transporters (NaPi-II) in proximal tubules

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92
Q

clinical features of hypophosphataemic rickets?

A

same as Vit D deficiency rickets: Bow legged deformaty, impaired growth

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93
Q

treatment for hypophosphataemic rickets?

A

phosphate replacement

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94
Q

which disorder is associated with problems with bicarbonate reabsorbtion in the proximal tubule?

A

proximal renal tubule acidosis

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95
Q

what is the defect that causes proximal (type 2) renal tubular acidosis?

A

Na/H antiporter defect
= failure of bicarb reabsorbtion

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96
Q

what are the clinical features of Proximal (type 2) renal tubular acidosis?
treatment?

A

acidosis, impaired growth
treatment = bicarbonate supplementation

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97
Q

what can a genertic defect in carbonic anhydrase cause?

A

a mix of proximal/distal renal tubular acidosis
(Bicarb reaborbtion failure)
treated with - acetazolamide which induces metabolic acidosis to allow for mor rapid compensation of respiratory alkalosis

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98
Q

what defect can cause a mix of proximal and distal renal tubular acidosis?
how can this be treated?

A

genetic defects in carbonic anhydrase.

inhibited by acetazolamide = induced metabolic acidosis to induce rapid compensatory alkalosis. (used to treat altitude sickness)

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99
Q

what syndrome is associated with multiplle reabsorbtion issues in the proximal tubule?

A

Fanconi syndrome

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100
Q

causes of fanconi syndrome?

A

genetics, myeloma, lead poisoning, cisplatin. - generalaised proximal tubular dysfunction (failure to generate sodium gradient by pump)

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101
Q

clinical features of fanconi syndrome

A

glycosuria, aminoaciduria, phosphaturic rickets, renal tubular acidoses

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102
Q

what is the function of the thick ascending limb in the loop of Henle?

A

Primary site of Na reabsorbtion.
Thick ascending limb is impermeable to water.

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103
Q

How is Na+ reabsorbed in the thick ascending loop of Henle?

A

active transport - Na+ / K+ ATPase pumps 3 Na+ out and 2 K+ in.

Low Intracellular conc of Na+ creates a negative charge. Na+ then moves into cell from lumen through the NKCC2 transporter - one Na+, one K+, two Cl- in.

Potassium moved back into lumen through ROMK transporter.

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104
Q

what are the overall effects of Na+ reabsorbtion in the thick ascending limb of the loop of henle?

A
  • Na+ removed from lumen tubular lumen whilst retaining water (∴hypotonic soution arrived at the DCT)
  • Na+ pumped into the interstitial space (∴hyperosmotic environment in kideny medulla)
  • also magnesium, clacium, sodium and potassium paracellular reabsorbtion
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105
Q

What is Barrter’s syndrome?

A

a group of autosomal recessive conditions characterised by genetic mutations in the genes coding for the NKCC2 transporter, apical potassium channel or basolateral chloride ion channel.

NKCC2, ROMK, CICKa/b Barrtin

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106
Q

what is the mechanism of Barrter’s syndrome?

A

failure of sodium, potassium and chloride cotransport in thick ascending limb.
–> salt wasting –>hypokalaemic alkalosis due to volume contraction –> failure of coltage dependent calcium and magnesium absorbtion

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107
Q

symptoms of Barrter’s syndrome?

A

similar effects to loop diuretics:
hyponatraemia
hypokalaemia
metabolic alkalosis

prematurity, delayed growth, polyuria, polydipsia

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108
Q

what is the function of the distal tubule?

A

allow of “fine tuning” of sodium reabsorbtion, potassium and acid-base balance.

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109
Q

what is the function of the collecting duct?

A

mediates water reabsorbtion

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110
Q

name 4 distal tubule and collecting duct disorders

A
  1. Gitelman’s syndrome
  2. Distal (type 1) renal tubular acidosis
  3. Disorders resembling hyperaldosteronism
  4. Type 4 renal tubular acidosis
  5. Nephrogenic diabetes insipidus
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111
Q

of the three acid base regulation mechanisms the body has, what is the slowest but strongest?

A

renal regulation

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112
Q

what are the three types of chemical buffers?

A

Bicarbonate (ECF)
Phosphate (Urine ICF)
Protein (ICF) (Hb)

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113
Q

what two things can the kidney do to regulate acid-base balance?

A

HCO3- reabsorbtion
H+ excretion

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114
Q

which part of the nephron is not involved in acid-base regulation?

A

thin descending limb and thin ascending limb

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115
Q

where does HCO3- reabsorbtion take place?

A

early PCT (80%)

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116
Q

what facilitates the synthesis of H2CO3 from CO2 and H2O in the PCT cell?

what else does it do?

A

Carbonic Anhydrase.
synthesises H2CO3 from bicarb and H+ in the PCT lumen

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117
Q

how is bicarbonate reabsorbed into the capillery?

A

in the PCT, HCO3- is reabsorbed into the capillery with Na+ as cotrasnport.

later nephron, it is exhnaged for Cl-

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118
Q

During bicard reabsorbtion, how is H+ excreted into the lumen?

A

Na/H+ exchanger = secondary active transport

secondary to the Na/K/ATP pump pulling Na out of the cell

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119
Q

in HCO3- reabsorbtion, what is the net change in HCO3- and H+?

A

for every HCO3- reabsorbed into capillery, 1 H+ is excreted into PCT lumen.
BUT H+ binds to the HCO3+ already in the lumen so there is no net secretion of H+

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120
Q

what are the two methods that the kidneys can excrete H+?

A

via two urinary buffers:
* phosphate buffer
* ammonia

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121
Q

where in the nephron does H+ excretion take place?

A

alpha intercalated cells of the DCT and collecting ducts

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122
Q

how does H+ excretion via phosphate work?

A

H+ is excreted out of the lumen forcably using hydrogen-ATPase pumps on the lumen of late PCT alpha intercalated cells.
Excess luminal phosphate (only 85% of total phosphate is normally reabsorbed) can bind a large portion of hydrogen ions, buffering them as H2PO4– before excretion. This excretion of H+ ions increases blood pH.

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123
Q

how does H+ excretion via ammonia work?

A

glutamine is converted to glutamate and ammonium in the proximal convoluted tubule (PCT).
The ammonium dissociates to ammonia and H+ ions, allowing it to pass the through membrane and enter the lumen.
Once in the lumen, it reforms ammonium by picking up a luminal H+ ion. This allows hydrogen to be excreted as ammonium ions, increasing blood pH.
Furthermore, ammonia secreted at the PCT can be used further down to buffer and excrete H+ ions secreted by alpha-intercalated cells in the collecting duct. This is due to its ability to pass membranes and traverse the nephron.

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124
Q

outline the embryology of the pancreas.

when do exocrine functions begin?
when do endocrine functions begin?

A

at the junctiojof foregut and midgut, 2 pancreatic buds (dorsal and ventra) are genertated and eventually fuse.

exocrine functions begin at birth
endocrine functions begin from 10-15 weeks

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125
Q

exocrine activiry of the pancreas performed by what cells?

endocrine activity of the pancrease performed by what cells?

A

excocrine
- acinar cells = 99% of cells
- manufacture and secrete fluid and digestive enzymes - pancreatic juices into gut

endocrine
- iselt cells
- manufacture and release peptide hromones into portal vein

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126
Q

what are these cells? what is their function?

A

Islet cells of Langerhans
- site of insulin and glucagon secretion

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127
Q

what cells secrete insulin?

A

beta-cells of pancreatic iselts of Langerhans

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128
Q

what cells secrete glucagon?

A

alpha-cells of pancreatic iselts of Langerhans

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129
Q

what cells secrete somatostatin?

A

Delta cells in pancreatic islets of Langerhans

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130
Q

What is Insulin’s effect on:
* hepatic glucose output
* Glucose uptake
* lipolysis
* muscle breadown

A
  • Supresses hepatic glucose output - ↓ glycogenolysis, ↓ glyconeogensis
  • Increases glucose uptake to muscle and fat
  • Suppressed lipolysis
  • supressed breakdown on muscle (↓ketogenesis)
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131
Q

What is Glycogen’s effect on:

  • hepatic glucose output
  • Glucose uptake
  • Peripheral release of gluconeogenic precursors
  • lipolysis
  • muscle breadown
A
  • increases hepatic glucose output - ↑glycogenolysis, ↑glyconeogenesis
  • reduces glucose uptake peripherally
  • Stimulates peripheral release of gluconeogenic precursors (glycerol, AAs)
  • Stimulates lipolysis
  • Stimulates muscle glycogenolysis and breakdwon
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132
Q

what is insulin and what does it do?

A

polypeptide of 51 AAs.
- reduces glucose output by live, increases storage of glucose, fatty acids and AAs

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133
Q

what is glucagon and what does it do?

A

polypeptide of 29 AAs
- mobilises glucose, fatty acids and AAs from stores

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134
Q

How is insulin secreted by the 𝛃 cells?

A
  1. Glucose enters 𝛃-cell via GLUT2 glucose transporter
  2. Glucose metabolised in the cell, generating ATP
  3. The increase in ATP levels causes the cell’s potassium channels to close, leading to depolarization of the cell membrane
  4. Depolarisation opens voltage-gated calcium channels, calcium rushes in.
  5. The influx of calcium ions stimulates the beta cells to release insulin stored in small vesicles within the cell. These vesicles fuse with the cell membrane, releasing insulin into the bloodstream. Insulin is then transported throughout the body by the bloodstream.
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135
Q

what facilitates the movement of glucose into the 𝛃-cell through GLUT2 transporter?

A

glucokinase (= phosphorilator)

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136
Q

how can you tell if someone has been “killed” by insulin

A

when insulin is secreted from the cell, it is actually preleased as proinsulin which contains the A and B chains of insulin, and a C peptide.
Should be euqal amounts of insulin and C peptide, if C-peptide present, it is endogenous.

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137
Q

what are the two phases of Biphasic Insulin release

A

First phase repsonse (to high glucose) is rapid release of stored product
Second phase response is slower release of newly synthesised hormone

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138
Q

Explain insulin’s action in muscle and fat cells

A
  1. Insulin binds to insulin receptors on the surface of muscle and fat cells.
  2. This initiates intracellular signalling cascades that move the GLUT4 transporter proteins from intracellular vesicles to the cell membrane.
  3. GLUT4 then allows glucose to enter the cell
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139
Q

where can glucose sensors be found?

A

primary glucose sensors in pancreatic islets (𝛃-cells)
also medulla, hypothalamus and carotid bodies
also Input from senses and cells in gut wall

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140
Q

what is the short term glucose buffer of the body?

A

liver glycogen

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141
Q

what is the body’s short term response to hyperglycaemia?

A

make glycogen (glucose → glycogen = glycogenesis)

store the

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142
Q

what is the body’s short term response to hypoglycaemia?

A

Split glycogen (glycogen → gluocse = glycogenolysis)

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143
Q

what is the body’s long term effect to hyperglycaemia?

A

Make triglygeride (lipogenesis)

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144
Q

what is the body’s long term response to hypoglycaemia?

A

make glucose (gluconeogenesis) from AAs ansd Triglycerides

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145
Q

how does the route of getting glucose change insulin response?

A

insulin response is greater following oral glucose than intravenous glucose, despite similar plasma glucose concentrations.
this is due to INCRETIN = gut hormone stimulating insulin release

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146
Q

three mechanisms postprandial glucose levels are regulated by?

A
  1. ↑ Insulin
    ↳ rising plasma glucose stimulates pancreatic 𝛃 islet cells to secrete insulin
  2. ↓ Glucagon
    ↳Plasma glucose inhibits glucagon secretion by pancreatic 𝛂 cells
  3. ↓Gastric emptying
    ↳slowing gastric emptying is a major determinant of postprandial glycaemic excursion
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147
Q

How does incretin promote weight loss?

A

slows gastric emptying

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148
Q

Where does glucose come from whem the body is fasting

A

in the fasting state, all glucose comes from the liver : Glycogenolyis and gluconeogenesis (3 carbon precursors to synthesise glucose)
glucose to braind and RBCs

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149
Q

[?]% of ingested glucose goes to the liver
[?]% of ingested glucose goes to the periphery?

A

40% to the liver
60% to the periphery, mostly muscles

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150
Q

what is a common mutation found in type 1 diabetes in the pancreatic beta cells?

A

Mutation of the Kir6.2 Potassium/ATP channel
- channel stays open for longer than it should and needs higher than usualy blood glucose levels to close them
- treatment - sulphonylureas which clost the channels

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151
Q

explain the pathogenesis of diabetic ketoacidosis

A

Body cannot make insulin:
* no insulin = no glucose uptake into cells = high BMs
* no glucose uptake into cells = liver creates more glucose = higher BMs
* no glucose uptake into cells = body starts breaking down fats
* fat breakdown = liver produces ketones = acidotic

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152
Q

the kidney develops from what embryological germ layer?

A

intermediate mesoderm

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153
Q

name the three overlapping kidney systems develop from the intermediate mesoderm

A

pronephros
mesonephros
metanephros

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154
Q

when does the pronephros develop and what is its function?

A

4/40 (disappears by 5/40)
Non functional

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155
Q

when does the mesonephros develop and what is its function?

A

4/40
part of it persists in males

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156
Q

whehn does the metanephros develop and what is its function?

A

5/40 - functional at 12/40.
this becomes the definitive kidney

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157
Q

From the mesopnepros, excretory tubules develop with a group of capillaries. what will each of these become? what happens after these have formed?

A

tubules = bowman’s capsule
capillaries = glomerulus

then collecting duct called mesopheric duct forms and gonad starts to develop

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158
Q

what is the fate of the mesonephros in females?

A

tubules and mesophrenic ducts degenerate

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159
Q

what is the fate of the mesonephros in males?

A

a few tubules and the mesophreni duct remain:
* mesophrenic duct = vas def
* tubules = ducts of testes

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160
Q

where does the kidney develop (from the?)

A

in the peliv region (from the metanephros)

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161
Q

in the development of the kidney from the metanephros, the collecting systems and excretory system develop…?

A

differently

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162
Q

Development of the collecting system 1:
Develops from the [a]
The [a] grows out from the [b]
Covered over by a ‘cap’ of [c]
Bud grows into the cap = [d]

A

Develops from the ureteric bud
The ureteric bud grows out from the mesonephric duct
Covered over by a ‘cap’ of metanephric tissue
Bud grows into the cap = renal pelvis

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163
Q

Development of the Collecting systems 2:
Bud splits into two parts = [a]
Continued subdivision and formation of tubules = [b], [c], [d], [e]

A

Bud splits into two parts = major calyces
Continued subdivision and formation of tubules = ureter, renal pelvis, major and minor calyces, collecting tubules

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164
Q

Development of the Excretory system:
Develops from [a]
Development promoted by the developing [b]
Development of each is dependent on the other
Metanephric tissue forms [c]
Vesicles become tubular and capillaries develop = [d]
Form [e]

A

Develops from metanephric cap
Development promoted by the developing collecting tubules
Development of each is dependent on the other
Metanephric tissue forms renal vesicles
Vesicles become tubular and capillaries develop = glomerulus
Form nephrons

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165
Q

the uteric bud forms which parts of the renal and urinary system?

A
  • ureter
  • Renal pelvis
  • major and minor calcyces
  • collecting tubules
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166
Q

the metanephric tissue forms which parts of the renal and urinary tissue

A

Nephrons

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167
Q

during the ascent of the kidneys in utero, what happens to the vessels?
if this doesnt happen what occurs

A

During ascent, new vessels are derived from more proximal parts of the aorta and lower vessels regress.
if regression does not occur = Accessory Renal Vessels

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168
Q

when does the kidney start to function?

A

12/40

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169
Q

what happens to fetal urine?

A

excreted into amniotic fluid

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170
Q

what is this an example of?

A
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171
Q

what is this an example of?

A

Pancake kdiney: Fusion of the upper and lower poles of the kidney.

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172
Q

what is this called?

A

crossed renal ectopia

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173
Q

what is the cloaca?

A

common cavity for urogenital system and the gut

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174
Q

what goes on to separates the cloaca?

A

urorectal septum.
divide cloaca into urogenital sinys and anal canal

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175
Q

the bladder develops from?

A

the urogenital sinus

176
Q

the urogenital sinus gives rise to 3 parts:

A

Upper part = bladder
Middle / pelvic part = part of the male urethra
Phallic part = develops differently in males and females

177
Q

if the urorectal septum fails to close it sinus this leads to?

A

hypospadius

178
Q

what is this a case of and what has it resulted from?

A

exstrophy of bladder - rare
failure of anterior abdominal wall to close

179
Q

the ureter develops from?
when?

A

the ureteric bud.
Ureter directly enters the bladder after the distal part of the mesonephric duct merges into the bladder wall.

180
Q

what has this resulted from?

A

double ureter - ureter splits early in development

181
Q

what can the development of two uteric buds (for one kidney) result in?

A

ecopic ureter
One enters bladder
Other enters bladder, urethra, vagina or epididymal region

182
Q

all steroid hormones are synthesised from?

A

cholesterol

183
Q

catecholamines are synthesised from?

A

tyrosine

eg dopamine

184
Q

what is key for the synthesis of thyroid hormones?

A

iodine

185
Q

what are the fastest acting hormones?

A

catecholamines

dopamine / adrenaline

186
Q

what are the slowest acting hormones?

A

thyroid hormones

t3 / t4

187
Q

what are the action times of peptide hormones?

A

mins - hours

Human growth, prolactin, insulin

188
Q

what are the action times of steroids and pseudo steroids?

A

hours - days

cortisol, aldosterone

189
Q

how does insulin effect?

A

peptide hormones - cell surface receptors
Insulin doesnt go into the cell.
involves cascade and translocation of GLUT4 which allows glucose into the cell.

190
Q

how does cortisol effect?

A

steroid - intracellular
must get to cell nucleus
long 1/2 life and long mechanism of action

191
Q

basic action of thyroid hormone?

A

basal metabolic rate, growth (including brain)

192
Q

basic action of parathyroid hormone?

A

Calcium regulation

193
Q

basic action of cortisol hormone?

A

glucose regulation, inflammation

low = addisons disease

194
Q

basic action of aldosterone?

A

BP and Na regualtion

195
Q

basic action of Catecholamines?

A

BP and stress

196
Q

basic action of oestradiol?

A

mensturation

197
Q

basic function of testosterone?

A

sexual functions.
male feautures

198
Q

basic function of ANP?

A

Na+ regulation

199
Q

basic function of insulin?

A

glucose regulation

200
Q

basicl function of Vit D hormone?

A

Ca2+ regualtion

201
Q

three ways to meausre hormone concentrations?

A

Bioassays
Immunoassays
Mass Spec

202
Q

5 anterior pituitary hormones and their functions?

A
  1. ACTH - adrenal cortex regualtion
  2. TSH - thryoid regualtion
  3. GH - growth metabolism
  4. LH/FSH - Reproductive control
  5. PRL - breast milk
203
Q

2 posterior pituitary hormones?

A

ADH - water regulation
Oxytocin - breast milk

204
Q

draw out the HPT axis

A
205
Q

what is this patient suufering with?
what other symptoms might be present?

A

thyrotoxicosis
-bulging eyes
-irritability and anxiety
- sweating
-goiter

206
Q

what are these patients suffering with?

A

cushings disease - too much steroid due to pituitary tumor

207
Q

what is this and what is it caused by?

A

acromegaly.
too much growth hormone.

208
Q

a pituitary tumour can cause visual field defects because?

A

pressure on the optic chiasm

209
Q

symptoms of hypothyroidism?

A

Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation

can be primary or secondary

210
Q

weight of pituitary?

A

0.5g

211
Q

blood supply to anterior pituitary?

A

the anterior pituitary has no arterial blood supply but recieves blood thorugh a poral venous circulation from the hypothalamus.

212
Q

5 anterior pituitary hormones, their type and their function?

A
213
Q

What stiumlates the relase (hypothalamus) of Thyroid Stimulating Hormone in the pituitary?

A

Thyrotropin releasing hormone

214
Q

what stiumlates AdrenoCorticoTrophic Hormone release?

A

corticotropin releasing hormone

215
Q

what stiumlates FSH release?

A

Gonadotropin releasing hormone

216
Q

what stimulates LH release?

A

Gonadotropin releasing hormone

217
Q

what stimulates growth hormon release?

A

Growth releasing hormone

218
Q

the only anterior pituitary hormone that doesnt have negative feedback is?

A

prolactin

219
Q

draw out the HPA - cortisol axis

A
220
Q

ACTH acutley stimulates [?] release

A

cortisol
- about 20 mins behind

221
Q

this graph depict the sleep/wake cycle.
what is the likely y axis?

A

cortisol levels - circadian rhythm

222
Q

why is growth hormone difficult to measure?

A

pulsatile.
GH effect meidated by IGH1 in the liver = measured

223
Q

what stimulates growth hormone?
what suppresses it?

A

stim = low glucose, exercise, sleep
suppress = hyperglycaemia

224
Q

action of growth hormone?

A

linear growth in children (long bones)
- then sex hormones take over in puberty - axial

Stimulates:
- protein synthesis
- lipolysis
- gluocse metabolism

Regulation of body composistion
Psychological well-being

225
Q

draw out the GHRH HP axis

A
226
Q

draw out the thyroid stimulating hormone HPT axis

A
227
Q

what is responsible for the negative feedback in the LH/FSH H-P-Ovary axis?

A

inhibin

228
Q

draw out the GnRH, FSH/LH HPO axis (ovaries)

A
229
Q

Draw out the HPG axis for testes

A
230
Q

prolactin is synthesised in?

A

lactotrophs

231
Q

what negaitively inhibits prolactin?

A

dopamine

232
Q

draw out the prolactin axis

A
233
Q

what are the embryological origins of the posterior and anterior pituitary?

A

Neural ectoderm –> Posterior Pituitary
Oral ectoderm –> Anterior Pituitary

234
Q

what is the most commone cause of cushing’s disease?

A

cushings = high cortisol
high dose steroids, used to treat inflammation

235
Q

two hormones of the posterior pituitary?

A

Vasopressin (ADH)
Oxytocin (milk and labour)

236
Q

explain what happens to vasopressin levels during water defecit

A
237
Q

Action of Vasopressin:
1. Vasopressin binds to [?]
2. Receptor activates [?]
3. Cell inserts [?] into apicle membrane
4. Water is absorbed by [?] into the [?]

A

Action of Vasopressin:
1. Vasopressin binds to V2 membrane receptor
2. Receptor activates cAMP secondary messenger system
3. Cell inserts aqauporin-2 into apicle membrane
4. Water is absorbed by osmosis into the blood

ADH keep it in the blood, out of urine

238
Q

what regulates ADH release?

A

osmosreceptors
baroreceoptors

239
Q

what is normaly measured when calculateing plasma osmolality?

A

Na+ (x2)
Glucose
Urea

240
Q

name three things that could alter the relationship between plasma osmolality and vasopressing release

A
  1. drinking rapidly supresses vasopressin release and thirst
  2. pregnancy decreases the osmotic threshold for vasopressin release
  3. plasma vasopressin concentrations increase with age
241
Q

what is AVP-D and AVP-R?

A

Vasopressin deficiency = cranial
Vasopressing Resistance = nephrogenic (diabetes insipidus)

242
Q

causes of AVP deficiency?

A

idiopathic
tumours
trauma]infections - TB
familial (rare)

243
Q

how is VPD/VPR measured?

A

hypertonic saline stimulation
- meausre copeptin

244
Q

causes of AVP Resistance?

A

diabetes mellitus
duges
chronic renal failure

245
Q

what is SIADH
what are its symptoms?

A

Syndrome of inappropriate antidiuretic hormone secretion
Too much AVP = low blood conc, low osmolaity, low plasma sodium
high urine conc
euvolaemia

246
Q

outline the essential criteria for SIADH

A
  1. Hyponatraemia
  2. Plasma hypoosmolality
  3. High urine osmolality
  4. High Na in urine
  5. euvolaemia - no clinical signs or hyper/hypovolaemia
247
Q

what should you be cautious of in treating hypernatraemia secondary to SIADH?

A

<12mmol/l incerease in Na+ per 24 hours
otherwise risk of central pontine myelinolysis.

248
Q

what are the three layers of skin?

A

Epidermis
Dermis
Subcutis

249
Q

three things that allow skin to be waterproof?

A
  1. tight junctions between cells in stratum granulosum
  2. epidermal lipids in statum corneum
  3. keratin in stratum corneum

waterproof in and out

250
Q

why does skin wrinkle when wet

A

to improve grip
sympathetic vasoconstriction in dermis

251
Q

what features of skin allow it to be a physical barrier?

A

stratified epithelium = resist abrasion
Fat in subcutis = shock absorber

252
Q

outline the process of vitamin d synthesis and storage

A

7 dehydrocholesterol in plasma membranes of epidermal keratinocytes and dermal fibrobalsts converted to previtamin D3 (cholecalciferol) by UVB

253
Q

Vitamin D is [a] so can be stored in [b]

A

[a] lipid soluble
[a] subcutis adipocytes

254
Q

skin as a site of endocrine action-
* Androgens act on [?]
* Thyroid hormones act on [?]

A
  • Androgens act on follicles and sebaceous
  • Thyroid hormones act on keratinocytes, follicles, dermal fibroblasts, sebaceous glands, eccrine glands
255
Q

effects of hypothyroidism on the skin?

A

epidermal - course, thin and scaly
dermis - myxoedema
hair and nail- dry and brittle
sweat glands - decreased sweating

256
Q

4 hormones synthesised at the skin?

A
  1. Vitamin D
  2. 17𝛃- Hydroxysteroid dehydrogenase
  3. 5𝛂-reductase
  4. IGF binding protein 3
257
Q

where is 17𝛃- Hydroxysteroid dehydrogenase and 5𝛂-reductase found?

A

17𝛃- Hydroxysteroid dehydrogenase - sebocytes
5𝛂-reductase - dermal adipocytes

258
Q

function of 17𝛃- Hydroxysteroid dehydrogenase and 5𝛂-reductase?

A

convert dehydroepiandrosterone (DHEA) into androstenedione and 5 𝛂-dihydrotestosterone

259
Q

where is insulin like growth factor binding protein 3 synthesised?

A

dermal fibroblasts

260
Q

which type of UV light damages the skin

A

both!
UVA and UVB

261
Q

how does UV light damage the skin?

A
  • burns
  • spresses langehans cells (immune)
  • photo-aging
  • DNA damage
262
Q

Skin colour depends on [a] which is synthesised in [b] within [c] from [d].
Transported via [e] to adjacent keratinocytes.

A

[a] Melanin
[b] melanosomes
[c] melanocytes
[d] tyrosine
[e] dendrites

263
Q

red hair containt more of which melanin

A

pheomelanin.

264
Q

all skin types contain more of which melanin

A

eumelanin

265
Q

melanin is prone to photodegradiation which may generate what?

A

ROS

266
Q

what type of melanin increases the release of histamine?

A

pheomelanin

267
Q

more/less melanin reduces ability to utilize light to make vitamin D

A

more

268
Q

a range of peptides synthesised by [?] have antimicrobial properties

A

granular layer keratinocytes

269
Q

where are Langerhans cells found?
what are they?

A

Epidermis
antigen-presenting and secrete cytokines

270
Q

what immune cells are found within the dermis?

A
  • Regulatory T cells
  • Natural killer
  • dendritic
  • Macrophages
  • Mast cells
271
Q

keratinocytes secrete [?] and [?] that maintain populations of leucocytes in skin

A

cytokines
chemokines

272
Q

when skin is challenged (immune) what happens? (x3)

A
  • leucocytes migrate to dermis and lymph nodes and activate a T cell respones
  • Keratinocytes proliferate and secrete cytokines
  • leucocytes enter skin from the blood
273
Q

what cells found within the skin allow it to function as a sensory organ?

A

Merkle cells - light touch (basal epidermis)
Pacinian corpuscles - pressure/vibration (dermis)
Meissner corpuscles - touch (dermis)
nerve endings - pain, itch, temp (dermis)

274
Q

what is meant by endothermic homeotherms

A

heat generated through metabolism

275
Q

vasoconstriction and vasodilation are under what kind of control?

A

all sympathetic!
vasoconstriction = sympathetic alpha-noradrenergic
vasodilation = sympathetic cholinergic

276
Q

what muscles cause goosebumps?
innervation?

A

arrector pili muscles
sympathetic 𝛂1 - adrenergic fibres

277
Q

functions of subcutaneous fat?

A

insulator
shock absorber, energy store.

278
Q

label the arrows on the histological zones of the adrenal including what is made where

A
279
Q

how does the fetal adrenal differ to the adult adrenal?

A

fetal zone —> zona reticularis

280
Q

what does the adrenal glands develop from embryologically?

A

urogenital ridge 4/40

281
Q

what is the precursor of all adrenal steroids?

A

cholesterol

282
Q

describe the atomical structure of corticosteroids

A

cyclopentanoperhydrophenanthrene structure
- three cyclohexane rings (A, B, and C)
- single cyclopentane ring (D)

283
Q

corticosteroids can pass through membranes because they are?

A

lipid soluble
Intracellular receptors —> alter gene indirectly/directly

284
Q

what are the three classifications of steroids?

A
285
Q
A
286
Q

what is made in the zona glomerulosa?
what is the function?
what triggers its secretion?

A

mineralocorticoids - regulate body’s electrolytes via aldosterone
secretion triggered by renin

287
Q

outline how mineralcorticoids are synthesised in the zona glomerula

A
288
Q

what is synthesised in the Zona fasciculata?
what is its action?

A

glucocorticoids - sugar regulation and stress response. - acts on most tissues!

289
Q

outline how glucocorticoids are synthesised.
what stimulates this syhtnesis

A

synthesis stoumlated by ACTH

290
Q

what is synthesised in the zona reticularis?

A

weak androgens - sex hormones

291
Q

outline how andorgens are synthesised in the zona reticularis

A
292
Q

how are glucocorticoids transported around the body?

A

90% bound to Corticosteroid-Binding Globin
5% bound to albumin
5% “free”

only “free” = bioavailable.
Breakdown of CBG to free up more when needed

293
Q

what regulates glucocorticoid synthesis?

A

ACTH

circadian rhythm, stress can also impact.

294
Q

name two mineralcorticoids, which is more potent?

A

aldosterone and DOC
DOC has 3% activity of aldosterone

295
Q

aldosterone acts where?
explain its action

A

distal convoluted tubule
* increases ENaC expression apically
* Increases Na/K/ATPase expression basolaterally
∴ INCREASES NA+ IN BLOOD, INCREASE K+ IN URINE

296
Q

draw out RAAS

A
297
Q
A
298
Q

name to adrenal androgens, which is more potent?

A

Dehydroepiandrosterone (DHEA) most abundant adrenal steroid but very weak androgen
Androstenedione more androgenic but only 1/10th that of testosterone, but major source of androgens in women
- converted to testosterone in peripheral tissues.

REGULATED BY ACTH

299
Q

what is synthesised in the adrenal medulla?

A

catecholamines
Adrenaline (80%) and Noradrenaline (20%)

300
Q

what enzyme, present in the adrenal medulla, converts noradrenaline to adreniline?

A

Phenylethanolamine-N-methyl

301
Q

Catecholamine synthesis is dependent on?

A

cortisol levels.

302
Q

action of catecholamines

A

Catecholamines released during “flight or fight”
-gluconeogenesis in liver and muscle
-lipolysis in adipose tissue
-Tachycardia and cardiac contractility
-Redistribution of circulating volume

303
Q

which gene determines how the bipotential gonads differentiate?

A

SRY gene
SRY + → male
SRY - → female

304
Q

what does the presence of the SRY gene lead to the development of?

A

testes at 9/40

305
Q

what does the absence of SRY gene lead to the development of?

A

ovaries 11/40

306
Q

what migrates to the urogenital ridge in 6/40?

A

Primordial germ cells → oocytes and spermatogonia

307
Q

What hormones will testes produce in reprodctive embryological development?
What do they produce, and what is their function?

A

Leydig cells = testosterone
= promotes Wolffian duct development
= dihydrotestosterone (DHT) = male external genitalia

Sertoli Cells = anti mullerian hormone = inhibits Mullarian duct development

308
Q

What hormones will the ovaries produce in reproductive embryological development?

A

Follicular cells = Oestrogen = External Female Genitalia
Lack of testes = lack of anti mullerian hormone

309
Q

what is the mesophrenic duct and what does it lead to the development of?

A

Mesophrenic = Wolffian = male structures
* ejaculatory duct
* epididymis
* prostate
* vas deferens
* seminal vesicle

310
Q

what is the paramesophrenic duct?
what does it develop into?

A

paramesophrenic duct = Mullerian duct = female reporductive strcutures
* fallopian tuube
* uterus
* upper 2/3 of the vagina

311
Q

what develops into the lower 1/3 of the vagina?

A

urogenital sinus (from cloaca) –> sinovaginal bulbs –> lower vagina

312
Q

What hormone controls the development of external male genitalia? How is this hormone produced?

A

dihydrotestosterone (DHT)
5𝛂reductase converts testosterone to DHT

313
Q

the genital tubercle becomes what in males and what in females?

A

males: Genital Tubercle –> Glans
females: Genital Tubercle –> clitoris

314
Q

The genital fold develops into?
This goes on to develop into what in females and males?

A

genital fold –> Urethral fold
females: urethral fold –> labia minora
males: urethral fold –> fuse into penile urethra/shaft

315
Q

what does the genital swelling differentiate into in males and females?

A

females –> labia majora
males —> scrotum

316
Q

overview of what is made in each zone of adrenals.

A
317
Q

What can Androgen insensitivity Syndrome lead to?

A

Androgen receptors not responding to androgens.

Clinical and biochemical phenotype
* Very high testosterone and dihydrotestosterone levels * Internal genitalia male (due to AMH production)
* External genitalia and external appearance female
* Gender identity female
=> Diagnosis often because of primary amenorrhoea

318
Q

how do the body proportions of a newborn differ from that of an adult?

A
  • Newborns:largerhead,smallermandible,shortneck, chest rounded, abdomen prominent, limbs short
  • Adults:relative growth of limbs compared to trunk
319
Q

in the Infancy-Childhood-Puberty Model, where does growth occur the fatsest?

A

Infancy - rapid until 2-3 years. determined by nutrition - long term growth faiulure if underfed in infancy

320
Q

what does growth in the childhood component of the INFANCY-CHILDHOOD-PUBERTY MODEL depend on?

A

– switch from nutritional to hormonal dependence – height velocity slows 2-3 yrs to puberty

321
Q

what does growth in the puberty component of the INFANCY-CHILDHOOD-PUBERTY MODEL depend on?

A

Growth Hormone and
sex hormones (oestrogen and testosterone)

322
Q

how does growth end?

A

with fusion of epiphyses due to influence of oestrogens in boys and girls
* Boys convert testosterone to oestrogens in fatty tissues

323
Q

on average how much taller are boys than girls?

A

12.5cm.
13.becuase girly start pubert 2-3 years before boys, with a shorted maxiumum growth spike

324
Q

what are some determinants of growth?

A
  • Parental phenotype and genotype * Quality and duration of pregnancy * Nutrition
  • Specific system and organ integrity * Psycho-social environment
  • Growth promoting hormones and factors
325
Q

all growth disorders originate from or affect {?}

A

the growth plate - chondrogenesis

326
Q

Disproportion can give clues to diagnosis
Short limbs –>
Short back & long legs –>

A

Disproportion can give clues to diagnosis
Short limb —> hypochondroplasia
Short back & long legs —> delayed puberty

327
Q

outline the growth hormone axis

A
328
Q

GHRH is regulated by?

A

food, sleep, steroids

329
Q

what is the most abundant hormone?

A

Growth hormone

330
Q

where is growth hormone synthesised?
by what cells?

A

somatotroph cells = 40-50% of total cells in anterior pituitary

331
Q

when is growth hormone at max?

A

night (pulsatile)

332
Q

what is growth hormones effect on glucose use. lipolysis and muslce mass?

A

decrease glucose use;
increase lipolysis andmusclemass

333
Q

what stimulates growth hormone?

A

Exercise
Stress
Hypoglycaemia
Fasting
High protein meals
Perinatal development
Puberty

334
Q

what supresses growth hormone?

A

Hypothyroidism
Hyperglycaemia
High carbohydrate meals
Glucocorticoid excess
Aging

335
Q

what is puberty?

A
  • Describes the physiological, morphological, and behavioural changes as the gonads switch from infantile to adult forms.
  • Definitive signs:
    – Girls - Menarche – first menstrual bleeding. – Boys - first ejaculation, often nocturnal.
    – These do not signify fertilityv
336
Q

what are the secondary sexual characteristics of female puberty and what hormones control them?

A
  • Ovarian oestrogens regulate the growth of breast and female genitalia
  • Ovarian and adrenal androgens control pubic and axillary hair
337
Q

what are the secondary sexual characteristics of male puberty and what hormones control them?

A
  • Testicular androgens
    –External genitalia and pubic hair growth
    –enlargement of larynx and laryngeal muscles = voice deepening
338
Q

mean age of breast development in girls?

A

Breasts - 8.87 (african), 9.96 (white)

339
Q

what is precocious puberty?

A

onset of secondary sexual characteristics before 8 yrs (girl), 9 yrs (boy)
* Menarche before 9 yrs may lead to short stature

340
Q

what is characterised as delayed puberty?

A

Delayed puberty: absence of secondary sexual
characteristics by 14 yrs (girl), 16 yrs (boy)
* Delayed puberty leads to reduced peak bone mass and osteoporosis

341
Q

outline the female HPG axis

A
342
Q

outline the male HPG axis

A
343
Q

Physical changes controlled by gonadal and adrenal
sex steroids is regulated by?

A

the gonadotrophins, LH and FSH

344
Q

Hypothalamic regulation of GnRH is increased by?
and decreased by?

A

GnRH secretion
(+) Glutamate and kisspeptin
(-) GABA and opioids

345
Q

what is adrenarche?

A

gradual “maturation” of the adrenal gland, development of pubic and axillary hair, body odour and acne

346
Q

what percentage of cardiac output do the kidneys receive?

A

20-25%
= 1200ml/min of blood flow

347
Q

where is the medulla and where is the cortex?

A

Cortex above dashed line
Medulla below dashed line

348
Q

suprise histology slide

A
349
Q

another suprise histology slide

A
350
Q

label the part of the tubule

A
351
Q

What does the proximal convoluted tubule absorb?

A

glucose
amino asids
phosphate
bicarb

352
Q

how is bicarb reabosorbed in the PCT?

A
353
Q

glucose is only absorbed where?
how?

A

PCT - only site of glucose reabsorbtion
Co-transported with Na via sodium glucose transporter 2 (SGLT2)
Defect → failure of glucose reabsorption (glucose in urine)

354
Q

Loop of Henle generates a concentration gradient in the medulla via?

A

countercurrent system

355
Q

What is absorbed in the thick ascending limb of the loop of Henle?

A

Na - active transport

356
Q

What cells line the thin descending limb of the loop of henle?
What about the thin ascending and thic ascending?

A

thin descending - simple squamous
thin ascending - simple squamous
thick ascending - simple cuboidal or low columnar with prominant folding and no microvilli +++ mitochonndria for active transport

357
Q

what occurs in the distal convoluted tubule?

A

Distal tubule and cortical collecting ducts allow “fine tuning” of sodium reabsorption, potassium and acid-base balance

358
Q

the distal convoluted tubule is impermeable to?

A

to passive movement of water and sodium

359
Q

the distal convoluted tubule can reabsorb approx 5% of Na…how?

A

Impermeable to passive movement of water and sodium
Uses NCCT co transporter to reabsorb 5% of sodium

360
Q

what cells line the distal convoluted tubule?

A

Epithelial cells
- Simple cuboidal epithelium with tall microvilli
- Numerous mitochrondria
Basal striations
Tight junctions

361
Q

how is salt and water abrobed in the DCT

A
362
Q

what is the function of the collecting duct?

A

Collecting duct mediates water reabsorption and maintains acid base homeostasis

363
Q

what are the two cells important in the collecting duct and what is their functions?

A

Principal cells - Na and water reabsorption and K excretion (simple cuboidal epithelium)

Intercalated cells (alfa and beta) – secrete H or HCO3
Essential for acid base homeostasis

364
Q

how does ENaC and Aldosterone effect the principle cells of the collecting duct?

A

ENaC – specific sodium transporter , main site of Na regulation
Aldosterone – increases the number of open ENaC channels regulating Na absorption

365
Q

how does the collecting duct reabsorb water?

A

Reabsorption of water due to action of ADH and aquaporins

ADH acts on tubule (principle cells
-Binds V2 receptor
-Activates adenylyl cyclase increasing cyclic AMP
-Vesicles containing aquaporin 2 channels deposit contents into apical membrane

ADH produced in hypothalamus, stored in posterior pituitary gland

366
Q

SIADH caused by?

A

Excess ADH released
Excessive dilution of blood lowering sodium concentration
Fluid retention
Consequent reduced aldosterone further reducing sodium uptake

367
Q

label which dieretic affect which part of the tubules and what they affect

A
368
Q

The defect in Barrter’s syndrome is similar to which diuretic’s mechanism of action:
A. Chlorthialidone (thiazide like diuretic)

B. Furosemide (loop)

C. Spironolactone (mineralocorticoid receptor antagonist)

D. Acetazolamide (carbonic anhydrase inhibitor)

A

B. Furosemide (loop)

369
Q

Which cell in the collecting duct functions in maintaining acid-base balance?
A. Intercalated cells

B. Enterochromaffin cells

C. Parietal cells

D. Principal cells

A

A. Intercalated cells

370
Q

In renal tubular acidosis type 1 (distal), which of the following statements is true?
A. Bicarbonate reabsorption is impaired

B. Hydrogen ion secretion is impaired

C. Urinary pH is acidic (<5.5)

D. Aldosterone action is impaired

A

B. Hydrogen ion secretion is impaired

371
Q

Amino acids are transported via specific transporters that are present in which region?
A. Proximal tubules

B. Loop of Henle

C. Distal tubules

D. Collecting ducts

A

A. Proximal tubules

372
Q

About 80% of filtered bicarbonate is reabsorbed in proximal tubules, which enzymes are involved?

A

Na/K ATPase enzymes on basolateral surface

Na/K ATPase enzymes on luminal surface

Carbonic anhydrase enzymes

373
Q

Thiazide diuretics inhibit the reabsorption of sodium and chloride by inhibiting the Na-Cl cotransporter present in…?
A. Proximal tubules

B. Loop of Henle

C. Distal tubules

D. Collecting ducts

A

C. Distal tubules

374
Q
A
375
Q

bloody supply to the thyroid?

A
376
Q

where is the thyroid?

A

in the neck
25-30g, surrounded by thin fibrous capsule

377
Q

the major cellular stuctures in the thyroid is/

A

follicles
-follicular cells

thyroid hormones stored in he colloid
378
Q

what do c cells in the thyroid produce?

A

calcitonin

379
Q

outline the role of thyroid hormones

A
  • Control of metabolism: energy generation and use
  • Regulation of growth
  • Multiple roles in development - up to 2yo = major in brain development
380
Q

outline the HPT axis

A
learn it
381
Q

outline thyroid hormone synthesis

5 steps

A
382
Q

with underfunction of the thyroid, what would you expect TRH and TSH to be?

A

TSH high because trying to stiumlate more thyroid

383
Q

which enzyme facilitates
tyrosine –> diiodotyrosine—> thyroxine?

A
384
Q

what is the biologically active thyroid hormone?

A

T3

385
Q

what is the most abundant thyroid hormone?

A

T4

386
Q

how is T3 produced?

A

Produced by mono-deiodination of T4

387
Q

Thyroid hormones are Produced by [a]
Synthesised from the [b] which requires [c]
[] [ is absorbed from bloodstream and concentrated in follicles

A

Produced by follicular thyroid cells
Synthesised from the thyroglobulin precursor
Iodine is absorbed from bloodstream and concentrated in follicles

388
Q

if thyroglobulin detected, this might indicate?

A

cancer

389
Q

[a] binds iodine to tyrosine residues in thyroglobulin molecules to form [b]

A

Thyroperoxidase binds iodine to tyrosine residues in thyroglobulin molecules to form MIT + DIT

390
Q

MIT + DIT =

A

T3

391
Q

DIT + DIT =

A

T4

392
Q

name three thyroid hormone binding proteins

A

TBG
Transthyretin
Albumin

Free thyroid is what is measured clinically

393
Q

Thyroid hormones are a different class of hormones.
They require a [a] to enter cell (dont use extracellular receptor)
But then, once in the cells, act like a steroid hormone which use [b]

A

[a] Transmembrane reporters
[b] nuclear receptors

394
Q

thyroid hormone transport in the CNS depends on which transporters? (2)

A

MCT8
OATP1C1

395
Q

What serum levels would you expect to find with primary hyperthyroidism

A

↓ Serum TSH
↑Serum free T4
↑Serum free T3

396
Q

What serum levels would you expect to find with primary hypothyroidism

A

↑ Syrum TSH
↓Serum free T4
↓Serum free T3

different if pituitary is problem - secondary

397
Q

hyperthyroidism prevalence?
incidence?

A
  • prevalence: 2.7%
    - incidence: 0.1%/yr (♀> ♂ )

Prevalence: ♀: 20/1000 ♂: 2/1000

398
Q

hypothyroidism prevalence? incidence?

A
  • prevalence:1.9%
    - incidence: 0.4%/yr (♀> ♂ )

Prevalence 40/1000 females
5% of over 60’s

399
Q

goitre prevalence and incidence?

A
  • prevalence 24.4 %
    - incidence: 0.2% (♀> ♂ )
400
Q

name some causes of hyperthyroidism

A
  • Graves’ hyperthyroidism - autoantibodies against TSHR
    - Toxic nodular goitre (single or multinodular)
    - Thyroiditis (silent, subacute): inflammation
401
Q

cardiovascular symptoms of hyperthyroidism

A

Tachycardia (rapid heart rate)
AF (atrial fibrillation)
Shortness of breath
Ankle swelling

can be a CV Killer!

402
Q

GI symptoms of hyperthyroidism

A

Weight loss
Diarrhoea
Increased appetite

403
Q

neuro signs of hyperthyroidism

A

Tremor
Myopathy (muscle weakness)
Anxiety
“can be properly bonkers”

404
Q

Eyes/skin signs of hyperthyroidism

A

Sore, gritty eyes
Double vision
Staring eyes
Pruritus (itching)
Feeling warm all the time

405
Q

name some causes of hypothyroidism

A

Autoimmune – Hashimoto’s thyroiditis (TPO and Tg antibodies - genetic predisposition)
After treatment for hyperthyroidism
Subacute/silent thyroiditis
Iodine deficiency
Congenital (thyroid agenesis/enzyme defects)

406
Q

CV signs of hypothyroidism

A

Bradycardia (slow heart rate)
Heart failure
Pericardial effusion

407
Q

GI signs of hypothyroidism

A

Weight gain - only around 5kg
Constipation

408
Q

skin signs of hypothyroidism

A

Myxoedema
Erythema ab igne
Vitiligo

409
Q

neuro signs of hypothyroidism

A

Depression
Psychosis
Carpal tunnel syndrome - always check thyroid

410
Q

how many parathyroid glands?

A

4

411
Q

what does the parathyroid gland do?

A

Regulate calcium and
phosphate levels

Secrete parathyroid hormone
(PTH) in response to:
Low calcium or
High phosphate

412
Q

action of PTH?

A

Increases calcium reabsorption in renal distal tubule
Increases intestinal calcium absorption (via activation of vitamin D)
Increases calcium release from bone (stimulates osteoclast activity)

Decrease phosphate reabsorption

413
Q

what % of calcium is soluble?
what is it necessary for?

A

1%

414
Q

which enzymes control Endocrine control of extracellular calcium homeostasis

A

Parathyroid hormone
Vitamin D
Calcitonin, FGF23

415
Q

calcium absorbtion in the kidney depends on what hormones?

A

Parathyroid hormone
Vitamin D
FGF23

416
Q

what are normal serum calcium levels?

A

2.1-2.6

417
Q

what % of serum calcium is free?

A

50% of serum calcium ‘free’ (ionised)
50% bound to albumin (so cannot diffuse into cells)

418
Q

what systems are involved in calcium homeostasis?

A
419
Q

what happens during hypocalcaemia to maintain homeostasis?

A
420
Q

what happens during hypocalcaemia to maintain homeostasis?

A
421
Q

what happens to urinary phosphate and urinary calcium in hypocalcaemia?
What happen in the intestine?

A

Kidney: Reabsorb calcium, pee phosphate out (if not, kidney stones)
Intestine: Reabsorb calcium AND phosphate

422
Q

PTH mainly binds to?

A

Binds to G protein coupled receptors mainly in kidney and osteoblasts

423
Q

Primary hyperparathyroidsm causes?

A

Primary HPT:
parathyroid tumour (usually benign adenoma)
Causes hypercalcaemia and low serum phosphate
Loss of negative feedback from hypercalcaemia
(Treatment is surgery)

424
Q

secondary hyperparathyroidism causes?

A

Secondary HPT:
renal disease (increased phosphate, decreased activation of vitamin D) = loss of negative feedback
(Treatment with phosphate binders or vitamin D analogues)

425
Q

causes of tertiart hyperparathyroidism

A

Tertiary HPT:
long-standing secondary HPT leads to irreversible parathyroid hyperplasia. Usually seen when renal disease corrected e.g. by transplantation
(Treatment is surgery)

426
Q

where is calcitonin produced?
when is it released?
What does it do?

A

Produced by thyroid c-cells (parafollicular)
Calcitonin released in hypercalcaemia
Inhibits bone resorption (by direct effect on osteoclasts)

Not essential to life (post thyroidectomy no calcium problems)
Two calcitonin genes products from a single gene and primary RNA transcript

427
Q

what occurs during hypercalcaemia to maintain homeostasis?

A
428
Q

uric acid is derived from?

A

purine

429
Q

the enzyme involved in uric acid synthesis is?

A

xanthine oxidase

430
Q

Purine intake is from?

A

diet (meats esp.)
nucleotide breakdown
body synhesis

431
Q

what hormone promotes uric acid excretion

A

oestrogen
therefore gout rare in premeno women

432
Q

what is gout caused by

A

too much uric acid
ususally due to reduced uric acid excretion

433
Q

if untreated, gout can cause?

A

damage to joint
infections
nerve damage

434
Q

what can reduce uric acid excretion

A

thiazide diuretics
reduced kidney function
metabolic syndrome
alcohol (also increases uric acid synthesis)

435
Q

how doe the medication allopurinol treat gout?

A

inhibits xanthine oxidase

436
Q

Lesch Nyhan syndrome is a rare inherited disease caused by high uric acid levels.
behavioural problems; biting fingers and lips (severe).

what causes it?

A

lack of HPRT.
(no backwards recycling or purines into nucleotides
∴ more uric acid)

Medicine - Phase 1 (16 decks)

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