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Metabolic - Urology > PPT2 > Flashcards

PPT2 Flashcards

1
Q

Outline some of the disorders of micturition

A
  1. Urgency urinary incontinence: associated with overactive bladder syndrome
  2. Stress urinary incontinence: due to urethral sphincter incompetence
  3. Mixed urinary incontinence: stress + urgency urinary incontinence
  4. Overflow incontnence: with continuous urine leakage, resulting from hypotonic bladder or bladder outlet obstruction producing urinary retention
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2
Q

Which group of patients are more prone to urge incontinence?

A

Older women

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3
Q

What is urge incontinence?

A

Sudeen , strong need to urinate AKA overactive bladder

Thought to occur due to detrusor overactivity leading to involuntary detrusor muscle contractions during bladder filling

Causes a strong urge to urinate and involuntary urination

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4
Q

What are the pharmacological options for urge incontinence?

A
  1. Muscarinic receptor antagonists: oxybutinin, tolterodine - inhibit actions of acetylcholine which functions via the parasympathetic nervous system to cause bladder contraction
  2. B3 adrenoceptor agonists: mirabegron
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5
Q

Discuss neurotransmitter release in the parasympathetic and sympathetic nervous systems

A

Parasympathetic nervous system: ACETYLCHOLINE pre and post ganglionic

Sympathetic nervous system: ACETYLCHOLINE pre ganglionic and NORADRENALINE post ganglionic

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6
Q

Which is the main muscarinic receptor subtype in the bladder?

A

M3 - acetylcholine binds to M3 receptors and causes contraction of the detrusor muscle

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7
Q

How does mirabegron work?

A

Stimulates B3 adrenoreceptors in the bladder trigone which flattens and lengthens the bladder base which facilitates urine storage

Adverse effects: increase in BP and HR - mirabegron is contraindicated in people with severe hypertension

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8
Q

What are the adverse effects of muscarinic blockade?

A

Dry mouth

Tachycardia

Constipation

Blurred vision

Urinary retention if there is bladde outflow obstruction

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9
Q

What type of incontinence occurrs when a person coughs or sneezes?

A

Stess incontinence

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10
Q

What is the cause of stress incontinence?

A

Urethral sphincter incompetence

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11
Q

What would be initially reccommended to a patient suffering with stress incontinence?

A

Pelvic floor muscle training for 8-12 weeks

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12
Q

When would drug therapy be recommended for stress incontinence?

A

If surgical treatment is not suitable

Drug therapy for stress incontinence is limited

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13
Q

Which surgical procedures are avalaible for stress incontinence?

A
  • Surgical sling procedures: sling placed around the neck of the bladder to support it
  • Colposuspension: stitches to vagina to hold it and support external sphincter when stress is placed upon it e.g. when sneezing
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14
Q

Which drugs are used to treat stress incontinence?

A

Duloxetine (SNRI)

  • Reduces the frequency of incontinence episodes in 50% of those treated, recommended to those who are poor candidates for or averse to surgery

Enhances glutamatergic activation of the pudendal motor nerve which innervates the external urethral sphincter - allows for stronger external urethral sphincter contraction and therefore more pressure needed to overcome it

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15
Q

How can the severity of BPH be assessed?

A

International prostate severity score

Questions relating to: incomplete empyting, frequency, intermittency, urgency, weak stream and straining - rated 0-5

0-7 = mildly symptomatic

8-19 = moderately symptomatic

20-35 = severely symptomatic

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16
Q

What is the first therapeutic intervention for BPH?

A

Alpha blocker - tamsulosin

Alternatives: alfuzosin, doxazosin, terazosin

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17
Q

What is the mechanism of action of alpha blockers in BPH?

A

Most drugs in this class are highly selective for the a1 adrenoreceptor which are mainly found in the smooth muscle of blood vessels and the bladder (particularly the bladder neck and prostate)

Stimulation of the a1 adrenoreceptors causes smooth muscle contraction and blockade causes relaxation

Alpha1 blockers cause a reduced resistance to bladder outflow

They also cause vasodilation and thus a reduction in blood pressure

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18
Q

What can be offered in addition to alpha blockers for BPH?

A

5-alpha reductase inhibitor e.g. finasteride or dustasteride

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19
Q

What is the mechanism of action of 5-alpha reductase inhibitors?

A

Reduce the size of the prostate

5-alpha reductase usually converts testosterone to dihydrotestosterone which leads to prostate hypertrophy - blocking this leads to prostate shrinkage

Takes 6-12 months to provide symptomatic relief, more effective in men with larger prostates

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20
Q

What are the side effects of 5-alpha reductase inhibitors?

A
  • Breast enlargement
  • Breast tenderness
  • Reduced libido
  • Ejaculation disorders
  • Impotence
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21
Q

Which drugs do 5-alpha reductase inhibitors interact with?

A

Verapamil and diltiazem - increase the concentrations of dultasteride (yellow alert)

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22
Q

What is an important consideration when prescribing 5-alpha reducatse inhibitors?

A

Pregnant women should not handle broken or damaged tablets and should not have unprotected sex with a man taking the tablets

Exposure of a male foetus to 5-a reductase inhibitors can cause abnormal development of the external genitals

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23
Q

What drugs can be used for prostate cancer?

A

Antiandrogens: flutamide

Gonadorelin analogues: leuprolide, goserelin, buserelin

Chronic administration of gonadorelin analogues results ina sustained suppression of pituitary gonatotropins, serum testosterone falls to levels comparable to surgical castration

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24
Q

What is the preferred initial approach for systemic therapy in patients with metastaic bladder cancer?

A

Platinum based chemotherapy

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25
Q

Which chemotherapy is urothelial cancer most sensitive to?

A

Cisplatin-based combination chemotherapy

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26
Q

Which drugs are used to treat renal cell carcinoma?

A

Tyrosine kinase inhibitors: sunitinib, sorafenib

mTOR inhibitors: everolimus

Tyrosine kinase receptor inhibitors: bevacizumab

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27
Q

In what forms can oral iron be given?

A
  1. Ferrous sulphate
  2. Ferrous fumarate
  3. Ferrous gluconate

*little difference in Hb regeneration between the three so choice is made based on incidence of side effects and cost

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28
Q

What are the forms of parenteral iron?

A

Iron dextran

Iron sucrose

Ferric carboxymaltose

Iron isomaltoside 1000

*reserved for patients who cannot tolerate oral iron or if there is continuing blood loss or malabsorption

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29
Q

Discuss iron absorption

A
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30
Q

What transports iron from the enterocyte into the circulation?

A

Ferroportin protein

31
Q

What regulates iron transport from enterocytes?

A

Hepcidin - peptide hormone (synthesised in the liver)

When circulating and tissue iron levels are high hepcidin synthesis is increased, it binds to ferroportin and leads to its degredation

Hypoxia, increased erythropoiesis and iron deficiency lead to the suppression of hepcidin and thus promote iron absorption

32
Q
A
33
Q

What are ferric iron ions bound to in the blood?

A

Aptotransferrin (a globulin)

34
Q

How is the majority of iron stored?

A

Complexed with aptoferritin and stored as ferritin

35
Q

What is haemosiderin?

A

An iron storage complex

insoluble aggregates of degraded forms of ferritin

36
Q

What proprtion of iron is found in RBCs?

A

2/3

1/2 of the remainder is found in macrophages, reticuloendothelial cells and hepatocytes, the rest is present in myoglobin in muclse cells

37
Q

Through which system are ageing RBCs broken down?

A

Reticuloendotheial system

Most of the released iron is recycled via macrophages

38
Q

How is iron lost from the body (apart from bleeding)?

A

Iron loss from the body rarely happens, when it does occur it is mainly via shedding of mucosal cells that contain ferritin

39
Q

What are the adverse effects of oral and parenteral iron?

A

Constipation, diarrhoea, epigastric pain, faecal impaction, GI irritation, nausea

40
Q

What are the drug inractions of iron?

A

Iron reduced the absoprtion of:

Levothyroxine

Bisphosphonates

Ciprofloxacin

Tetracyclines

Calcium and zinc salts

*advise patients to take this medications at least two hours before they take oral iron

41
Q

What should the daily dose of elemental iron be?

A

100-200mg dialy

Ferrous fumarate 200mg = 65mg elemental iron

Ferrous gluconate 300mg = 35mg elemental iron

Ferrous sulphate 200mg = 65mg elemental iron

42
Q

By how much should oral iron supplements raise blood Hb?

A

20g/L over the first 3-4 weeks and then 10g/L per week thereafter

Oral iron should be conitnued for 3 months after the Hb conc. has been restored in order to replenish iron stores

43
Q

What is the difference bwteen folate and folic acid?

A

Folate: water soluble vitamine B9 that occurs naturally in foods such as beef liver, leafy veg, oranges, legumes

Folic acid: synthetic form of folate found in food supplements and added to fortified foods

44
Q

Why is folic acid supplementation recommended to proegant women or women planning to get pregnant?

A

Reduces risk of neural tube defects

Folid acid may enchance cell proliferation for neural closure

45
Q

What is folate required for?

A

DNA synthesis

Cell replication

Formation of RBCs

46
Q

What form is folate in in the circulation?

A

5-methyltetrahydrofolate (5-MeTHF)

47
Q

Which women are most at risk of having a child with a neural tube defect?

A
  • Previous child with a NTD
  • Taking anti-convulsants such as valproate and carbamazepine

BUT 95% of those who have children with a NTD are not in the high risk group

48
Q

Discuss folate supplementation in women at high risk of having a child with a NTD

A

Pre-conception: 5mg daily

then 5mg daily until week 12 of pregnancy

Reduces the risk by ~70%

49
Q

Discuss folate supplementation in females wanting to get pregnant

A

400ug daily before conception up to week 12 of pregnancy

50
Q

Folic acid supplementation and sickle cell disease

A

Patient should continue taking folic acid (5mg) before conception and throughout pregnancy

51
Q

Why is folic acid supplementation advised for all women of childbearing age?

A

Most pregnancies are unplanned

52
Q

What is subacute combine ddegeneration of the cord?

A

AKA Lictheim’s disease - degeneration of posterior and lateral columns of the spinal cord due to B12 deficiency

Usually presents with loss of vibration and proprioception of hands and feet and eventual total sensory loss, features of dementia may also be present

* if treating a macrocytic anaemia where there may be a B12 deficiency, always give B12 before starting folic acid

53
Q
A
54
Q

When treating a macrocytic anaemia due to B12 deficiency, how is hydorxycobalamin given?

A

IM - the vast majority of vitamin B12 deficiency is due to the inability to absorb B12 in the terminal ileum

55
Q

Oxybutinin

A
56
Q

Tolterodine

A
57
Q

Doxazosin

A
58
Q

Tamsulosin

A
59
Q

Dutasteride

A
60
Q

Finasteride

A
61
Q

Cisplatin

A
62
Q

Sunitinib

A
63
Q

Bevacizumab

A
64
Q

Goserelin

A
65
Q

Cyproterone acetate

A
66
Q

Sildafenil

A
67
Q

Tadalafil

A
68
Q

Alprostadil

A
69
Q

Ferrous sulfate

A
70
Q

Iron sucrose

A
71
Q

Hydroxycobalamin

A
72
Q

Folic acid

A
73
Q

Darbepoetin

A

Metabolic - Urology (10 decks)

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