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Yr 2 EOYS ^2 > MET EOYS4 > Flashcards

MET EOYS4 Flashcards

1
Q

What effect does increasing FGF23 have on:

Serum phosphate levels [1]
Phosphate excretion [1]
1a hydroxylase activity [1]

A

High FGF23:
* increase fractional phosphate excretion
* Reduce serum phosphate levels
* Reduce 1α-hydroxylase activity

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2
Q

Which of the following secretes FGF-23

osteoblast
osteoclast
chondrocyte
osteocyte

A

Which of the following secretes FGF-23

osteoblast
osteoclast
chondrocyte
osteocyte

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3
Q

Explain what happens when have hypercalcemia and diabetes? [2]

A

Nephrogenic Diabetes Insipidus:
* Ca2+ binds to CaSR in nephrone, which down regulates NaKCL2 symporter
* Renal stones & Renal failure due to XS Ca2+ in urine

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4
Q

Parathyrodism diagnosis

Explain the mechanism of a MIBI scan [1]

A

The parathyroid scan uses the radioisotope, technetium-99m sestamibi (or MIBI), which is injected into the body and absorbed by the overactive parathyroid mitochondria.

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5
Q

State the vertebral levels for each of the following:

Iliohypogastric [1]
Ilioinguinal [1]
Genitofemoral [1]

A

Iliohypogastric: L1
Ilioinguinal: L1
Genitofemoral; L1 & L2

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6
Q

Which type of diuretic may be used to treat kidney stones?

Loop diuretics
Thiazide like diuretics
K sparing diuretics
Carbonic anhydrase inhibitors

A

Which type of diuretic may be used to treat kidney stones?

Loop diuretics
Thiazide like diuretics: cause hypercalcemia
K sparing diuretics
Carbonic anhydrase inhibitors

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7
Q

Which areas of nephron cause reabsorbtion of Ca2+ dependently / independently of PTH? [3]

A

PCT: independent
LoH: independent
DCT: PTH dependent

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8
Q

Explain how Ca2+ is reabsorbed at PCT [2]

A

At PCT:
- independent of PTH
- Driven by NaKCl2 channel causing a voltage gradient paracellularly which Ca2+ flows (coupled with Na+ reabsorbtion)

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9
Q

Explain how Ca2+ is reabsorbed at LoH [2]

A

Driven by voltage gradient: Para/transcellular
Coupled with Na+ reabsorbtion: NKCC2 channel

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10
Q

Why do thiazide diuretics raise serum calcium?

A

Increase Ca2+ reabsorbtion into the blood / raises Ca2+ serum levels:

  • Blocks Na/Cl symporter on luminal side
  • This drops the Na conc. In tubular cell
  • This creates Na diffusion gradient
  • Na diffusion increases from capillary into tubular
    cell - across Na/Ca exchanger -> takes Na into cell and transports Ca2+ into blood. -> increase in blood Ca levels.
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11
Q

The conversion of vit. D to WHAT is regulated? [1]

The conversion of vit. D to WHAT is unregulated? [1]

What are the enzymes used for each? [2]

A

Conversion of vit D to 25(OH)D in the liver is an unregulated process, under the action of p450 enzymes. The half life of 25(OH)D is 2-3 weeks.

The conversion of vit D to 1,25(OH)D is highly regulated, via 1αhydroxylase

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12
Q

How does negative feedback of activation of vitamin D receptor work?

A

In most cells there is a negative feedback inhibition: activation of the VDR inhibits the action of 1α hydroxylase (which converts vit D to active form), therefore reducing the amount of activated vitamin D able to bind to the VDR.

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13
Q

Why would chronic infection (e.g from sarcoidosis / TB granuloma) cause hypercalcemia?

A
  • Macrophages produce vitamin D
  • Release of vitamin D is converted to 1 25 dihydroxyvitamin dby 1α hydroxylase
  • Causes increase in serum calcium
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14
Q

What does the hormone FGF23 do? [1]
Which cells are they secreted from? [1]
What does FGF23 do to 1-a-hydroxylase? [1]

A

What does the hormone FGF23 do? [1]
Reduces serum P levels USED FOR WHEN GET P EXCRETED FROM FROM BONE BUT NEED TO EXCRETE VIA RENAL SYSTEM
It inhibits renal tubular reabsorption of phosphate

Which cells are they secreted from? [1]
Secreted by osteocytes

What does FGF23 do to 1-a-hydroxylase? [1]
reduces 1-a-hydroxylase: less activated vit. D

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15
Q

Explain 3 classes of symptoms seen in hypercalcemia

A

Hypercalcemia
Symptoms

Neuropsychiatric disorders: due to reduced membrane excitibility causing reduced nerve transmisison in the brain

GI abnormalities:
* Constipation / pancreatitis: reduced membrane excitibility causes less muscle contraction

Renal dysfunction:
* Nephrogenic Diabetes Insipidus: Ca2+ binds to CaSR in nephrone, which down regulates NaKCL2 symporter
Renal stones & Renal failure due to XS Ca2+ in urine

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16
Q

How do you treat hypercalcemia?

A

Expand plasma volume IV saline: reduces voltage gradient in tubular cells -> less Ca ++ reabsorbed
Reduce Ca release from bone
Treat underlying cause

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17
Q

What are primary, secondary and tertiary causes of hyperparathyroidism?

A

Primary: Parathyroid adenoma/carcinoma/hyperplasia

Secondary: Physiological compensation for hypocalcemia or Vitamin D deficiency. Can create tertiary

Tertiary: Autonomous PTH production following chronic secondary.

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18
Q

How can you ID if have primary Hyperparathyroidism? [4]

A

Neck USS
MIBI scan
CT scan
Parathyroid Venous Sampling

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19
Q

kidney, [] converts 25-hydroxyvitamin-D into 1,25-dihydroxyvitamin-D

A

kidney, 1-α-hydroxylase converts 25-hydroxyvitamin-D into 1,25-dihydroxyvitamin-D

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20
Q

Label A-E

A

A: Renal artery
B: Segmental arteries
C: Interlobar arteries
D: Arcuate arteries
E: Interlobal arteries

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21
Q

What are the 3 main nerves associated with the kidney? [3]

A

Iliohypogastric
Ilioinguinal
Genitofemoral

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22
Q

Label each colour

A

Purple: psoas major
Green: Quadratus lumborum m
Red: Transversus abdominis m.
Blue: diaphragm

23
Q

Where are the 3 places that kidney stones get stuck in the ureters? [3]

A

Uteropelvic junction
Pelvic inlet (and iliac vessels)
Uterovesical junction

24
Q

Ureter nerve supply:

Which nerves are nerve due to kidney stones referred along? [2]

Where is the pain common felt? [1]

Why does the referred pain change? [1]

A

The loin pain is referred along the ilioinguinal and the iliohypogastric nerves (L1)

As the stone descends the patient may start to feel pain descend over the groin and scrotum/labium majora (“from loin to groin”)

This is because of the changing nerve segments and the pain is now referred through the genitofemoral nerve (L1,2)

25
Q

Different role of internal and external urethral sphincter in males? [2]

A

Internal urethral sphincter (males): involuntary sphincter at the bladder-urethra junction (preventing retrograde ejaculation)

External urethral sphincter: voluntary sphincter surrounding the urethra as it passes through the urogenital diaphragm

26
Q

What is sympathetic innervation of bladder from? [1] What is the effect? [1]

What is parasympathetic innervation of bladder from? [1] What is the effect? [1]

What is somatic innervation of bladder from? [1] What is the effect? [1]

A

Sympathetic (hypogastric n; T12-L2)
Stimulate contraction (closure) of the internal urethral sphincter
Inhibit the detrusor muscle (prevents contraction and bladder emptying)

Parasympathetic (S2-S4)
Stimulate the detrusor muscle to contract
Inhibits (opens) the internal urethral sphincters

Somatic - external urethral sphincter (Pudendal n.S2-S4

27
Q

Vit D —(1)—> X —(2)—> Y

Name 1, 2 and X and Y [4]

A

Vit D—> 25(OH)D (25-hydroxyvitamin D₃) —-> 1,25-dihydroxvitamin D(3)

1: P450 enyzmes (In the liver)
2: 1 alpha hydroxylase

28
Q
A
29
Q

Which drug class would cause prostate to shrink?

alpha blockers

5-alpha reductase Inhibitors

phosphodiesterase-5 (PDE5) inhibitors

Antimuscarinics

A

5-alpha reductase Inhibitors

Both normal and abnormal prostate growth is driven by the androgen dihydrotestosterone (DHT), which is formed from testosterone under the influence of 5-alpha reductase.

30
Q

Dexamethasone Suppression Test is used to diagnosis

Addisons disease
Cushing syndrome
Conns syndrome
Graves disease

A

Cushing syndrome

Dexamethasone at night (i.e. 10pm) and their cortisol and ACTH is measured in the morning (i.e. 9am). The intention is to find out whether the dexamethasone suppresses their normal morning spike of cortisol.

31
Q

Short synacthen test is used to diagnose

Addisons disease
Cushing syndrome
Conns syndrome
Graves disease

A

Short synacthen test is used to diagnose

Addisons disease

The test involves giving synacthen, which is synthetic ACTH. The blood cortisol is measured at baseline, 30 and 60 minutes after administration. The synthetic ACTH will stimulate healthy adrenal glands to produce cortisol and the cortisol level should at least double. A failure of cortisol to rise (less than double the baseline) indicates primary adrenal insufficiency (Addison’s disease).

32
Q

Which drug targets B3 receptors in urge incontinence

Mirabegron
Finasteride
Oxybutynin
Botox

A

Which drug targets B3 receptors in urge incontinence

Mirabegron

Mirabegron is a beta-3 receptor agonist which will cause detrusor muscle relaxation

33
Q

What is the name for the nerve that supplies the sympathetic action of the hindgut? [1]

A

Lumbar splachnic nerve

34
Q

Which diagnostic score would use to assess micruition? [2]

What would scores be for mild, moderate and severe? [3]

A

Internation Prostate Symptom Score (IPSS)

Mild: 0-7
Moderate: 8-19
Severe: 20-35

AND

Input / Output Chart = voiding diary to create a frequency / volume chart

35
Q

What does a normal flow-rate recording look like? [1]

What ([] ml/s) would demonstrate unobstructed flow-rate [1]

A

Fast and short
20 ml/s = unobstructed

36
Q

Explain drugs used to treat bladder problems / LUTS [4]

A

alpha blockers(‘stretchers’): stretch prostates open

5-alpha reductase Inhibitors: (‘shrinkers’) shrink prostates

phosphodiesterase-5 (PDE5) inhibitors: PDE5 inhibitors facilitate smooth muscle relaxation through the NO/cGMP pathway, with effects in the bladder, prostate, and urethra.

Antimuscarinics (for OAB)

Combination

37
Q

Explain how stress incontinence occurs

A

weaking of pelvic floor or urethral sphincter

support is diminished, this causes intra-abdominal pressure to push more urine into urethra

38
Q

Explain how urge incontinence occurs

A

Larger squeezes on bladder muscle occur

overcomes sphincter and urine comes out urethra

39
Q

Explain 3 drug classes used for urge incontinence / OAB [3]

A

.

40
Q

The EAS is supplied by which nerve?
The IAS is innervated by which NS?
- What are sympathetic and parasympathetic nerve roots?

A

EAS: supplied by inferior branch of the pudendal nerve

IAS: Enteric NS
- Sympathetic: L1-L2 via hypogastric nerves (excitatory)
- Parasympathetic: S2-S4: pelvic nerves (inhibitory)

41
Q

Explain how the closing reflex occurs

A

Last bolus of stool is passed and then the ‘closing reflex’ of the EAS is stimulated by the releases of traction.

Upon voiding, receptor adaptation in ampulla recti removes inhibitory drive to IAS - thus contraction of IAS

Voluntary contraction of EAS closes anus off.

Smooth muscles in sigmoid relax (enteric nervous system) re-establishing of reservoir function.

42
Q

What is the definition of constipation?

A

purely symptomatic – not at diagnosis

infrequent stools (more than 3 per week) OR

passage of hard stools (less than 25% of the time) OR

a sensation of incomplete evacuation (>25% of the time) or

43
Q

What is primary constipation? [1]

Name 3 types of primary constipation [3]

A

Primary constipation: no identifiable organic cause include:

  • normal transitconstipation: due to inadequate calorie, fibre, or water intake, difficulty with defecation and hard stools, overlap with IBS-C since pain and bloating are common.
  • slow transitconstipation: infrequency and slow movement of stool
    due to bloating, abdominal pain and infrequent urge to defecate (ineffective colonic propulsion due to deficit and abnormalities of the enteric system that has a control on the motility of the large)

- pelvic floor dyssynergia.

44
Q

What does High Resolution Anorectal Manometry measure / ID? [2]

A

Pressure / time graphs of sphincter or rectum

Sphincter function: Resting pressure, Squeeze pressure, Endurance Squeeze, Rectoanal inhibitory reflex (RAIR)

Rectal sensation:
* hypersensitivity (associated with faecal incontinence)
* hyposensitivity (associated with constipation)

45
Q

What are the triad of symptoms for minimal change disease? [3]

A

Nephrotic syndrome - triad of proteinuria, hypoalbuminaemia and oedema

Minimal change disease is a relatively common cause of nephrotic syndrome and has its name due to renal changes not being seen on a standard microscope. However, under an electron microscope, effacement of the podocyte foot processes can be observed. In minimal change disease, the permeability of the glomerular basement membrane increases, allowing albumin to leak into the urine, causing proteinuria.

46
Q

Do you use surgery or medication for urge incontinence? [1]
Do you use surgery or medication for stress incontinence? [1]

A

medication for urge incontinence
surgery for stress incontinence

47
Q

Stimulation of which receptor would treat urinary incontinence?

Beta 1

Beta 2

Beta 3

M3

A

Stimulation of which receptor would treat urinary incontinence?

Beta 1

Beta 2

Beta 3

M3

48
Q

Which nerve carries sympathetic innervation to the bladder?

Ilioinguinal nerve

Hypogastric nerve

Pudendal nerve

Pelvic nerve

A

Which nerve carries sympathetic innervation to the bladder?

Ilioinguinal nerve

Hypogastric nerve

Pudendal nerve

Pelvic nerve

49
Q

Which of the following is correct regarding muscle activity during the storage phase of micturition?

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous contraction of the internal and external urethral sphincters.

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous relaxation of the internal and external urethral sphincters.

Storage requires contraction of the detrusor muscle of the bladder and simultaneous contraction of the internal and external urethral sphincters.

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous relaxation of the internal and external urethral sphincters.

A

Which of the following is correct regarding muscle activity during the storage phase of micturition?

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous contraction of the internal and external urethral sphincters.

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous relaxation of the internal and external urethral sphincters.

Storage requires contraction of the detrusor muscle of the bladder and simultaneous contraction of the internal and external urethral sphincters.

Storage requires relaxation of the detrusor muscle of the bladder and simultaneous relaxation of the internal and external urethral sphincters.

50
Q

Relaxation of the detrusor muscle and contraction of the internal urethral sphincter (IUS) is under the control of which receptors respectively?

B2-adrenoreceptors and A1-adrenoreceptors respectively

B3-adrenoreceptors and A1-adrenoreceptors respectively

A1-adrenoreceptors and B3-adrenoreceptors respectively

A1-adrenoreceptors and B2-adrenoreceptors respectively

A

Relaxation of the detrusor muscle and contraction of the internal urethral sphincter (IUS) is under the control of which receptors respectively?

B2-adrenoreceptors and A1-adrenoreceptors respectively

B3-adrenoreceptors and A1-adrenoreceptors respectively

A1-adrenoreceptors and B3-adrenoreceptors respectively

A1-adrenoreceptors and B2-adrenoreceptors respectively

51
Q

A spinal cord lesion (above T12) would cause which of the following deficits regarding storage and voiding of the bladder?

Inability for the detrusor muscle to relax, inability for the internal sphincter to relax, and constant relaxation of the external urethral sphincter.

Inability for detrusor muscle to relax, inability for the internal urethral sphincter to contract, and constant relaxation of the external urethral sphincter.

Inability for the detrusor muscle to contract, inability for the internal urethral sphincter to contract, and constant relaxation of the eternal urethral sphincter.

Inability for the detrusor muscle to contract, inability for the internal urethral sphincter to relax, and constant relaxation of the external urethral sphincter.

A

Inability for detrusor muscle to relax, inability for the internal urethral sphincter to contract, and constant relaxation of the external urethral sphincter.

After a spinal cord lesion above T12, sympathetic input to the bladder is lost, leading to an inability of the detrusor muscle to relax, and an inability of the internal urethral sphincter to contract. Afferent signals via the sensory pelvic nerve are also unable to reach the brain, so the external urethral sphincter remains constantly relaxed.

52
Q

What is the action of B3-adrenoreceptor agonists on the control of micturition?

Bind to B3-receptors on the detrusor muscle to cause contraction, promoting the voiding of urine.

Bind to B3-receptors on the internal urethral sphincter to cause contraction, preventing the voiding of urine.

Bind to B3-receptors on the internal urethral sphincter to cause relaxation, promoting the voiding of urine.

Bind to B3-receptors on the detrusor muscle to cause relaxation, increasing the bladders storage capacity.

A

What is the action of B3-adrenoreceptor agonists on the control of micturition?

Bind to B3-receptors on the detrusor muscle to cause contraction, promoting the voiding of urine.

Bind to B3-receptors on the internal urethral sphincter to cause contraction, preventing the voiding of urine.

Bind to B3-receptors on the internal urethral sphincter to cause relaxation, promoting the voiding of urine.

Bind to B3-receptors on the detrusor muscle to cause relaxation, increasing the bladders storage capacity.

53
Q

Which receptors, when stimulated, cause detrusor muscle contraction?

5-alpha-reductase

Acetylcholine

β3-adrenoreceptors

M3 muscarinic receptors

A

M3 muscarinic receptors

β3-adrenoreceptors cause relaxation of the detrusor rather than contraction.

54
Q

What is the typical male urinary flow rate?

15-20ml/s

20-25ml/s

25-30ml/s

30-35ml/s

A

What is the typical male urinary flow rate?

15-20ml/s

20-25ml/s

25-30ml/s

30-35ml/s

Yr 2 EOYS ^2 (42 decks)

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