Others e.g. glomerulonephritis, erectile problems etc Flashcards

1
Q

What is involved in the process of an erection (neurovascular phenomenon under hormonal control)

A

Arterial dilation
Smooth Muscle relaxation
Activation of the corporeal veno occlusive mechanism

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2
Q

What are the 3 shafts of the penis

A

2 corpora cavernosa

Corpus spongiosum

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3
Q

What covers the corpora cavernosa

A

Tunica albuginea

corpus spongiosum has a similar thinner tunica

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4
Q

What is contained in the 2 Corpora Cavernosa

A

Spongy vascular erectile tissue - trabeculated smooth muscle lined by endothelial cells

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5
Q

What structure is found in the Corpus spongiosum

A

Urethra

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6
Q

Describe arterial supply of the penis in order

A

Internal Iliac
-Internal pudendal artery:
Dorsal penile artery, Cavernosal artery (deep penile arteries), Bulbar artery

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7
Q

Describe venous drainage of the penis sinusoids

A

Subtunical plexus:

to circumflex veins to deep dorsal vein

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8
Q

Describe venous drainage of the corpora cavernosa

A

Cavernous veins:

to crural veins to internal pudendal veins

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9
Q

Autonomic supply of penis

A

Parasympathetic - erectile S2-4

Sympathetic - T11 to L2

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10
Q

What nerve carries both types of fibres that supply penis

A

Cavernous nerve (passes posterolateral to prostate thus risk damage in prostatectomy)

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11
Q

Describe physiology of flaccid state of penis

A

sympathetic tone
arterioles constricted
Sympathetic nerve terminal releases neuropeptide Y and noradrenaline
Vascular endothelium releases endothelin and prostanoids
all act on smooth muscle cells

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12
Q

Describe physiology of erect state

A

Parasympathetic stimulation – arteriolar dilatation, trabecular smooth muscle relaxation
Parasympathetic nerve terminal releases Vasoactive intestinal polypeptide, Nitric oxide that act one smooth muscle cells
Parasympathetic nerve terminal also releases Acetylcholine and Calcitonin gene related peptide. ACh inhibits sympathetic nerve terminal and (like calcitonin gene related peptide) increases production of nitric oxide from vascular endothelium.
Prostanoids also secreted by vascular endothelium and act on smooth muscle cell

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13
Q

Where is the central control of erections

A

Higher stimuli:
Hypothalamus, oxytocin pro-erectile pathways
Spinal reflex

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14
Q

Give example of a hormone required for normal erectile function

A

Testosterone

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15
Q

Examples of testosterone deficiency

A

Acquired: Primary or Secondary

Congenital e.g. Kleinfelters

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16
Q

Where is problem in primary testosterone deficiency

A

Pituitary gland or Hypothalamus

17
Q

Where is problem in secondary testosterone deficiency

A

Testes - tumour, injury, drugs

18
Q

Describe the peripheral control of erections

A

Smooth muscle mediated - arteriolar dilation and trabecular relaxation
Nitrous oxide release

19
Q

Why is the release of nitrous oxide important

A

Acetylcholine effect on endothelium
In smooth muscle cell stimulates Guanylate Cyclase enzyme which converts GTP to cGMP. This then stimulates the enzyme protein kinase G (PKG) to close L-type calcium channels and open Potassium channels.
Results in decreased cytoplasmic calcium concentration and smooth muscle relaxation.

20
Q

How does phosphodiesterase work?

A

Returns penis to flaccid state

21
Q

Example if Phosphodiesterase inhibitor

A

Sildenafil (Viagra)

22
Q

Define erectile dysfunction

A

The persistent inability to attain and maintain an erection sufficient to permit satisfactory sexual performance.

23
Q

Risk factors of ED

A
Lack of exercise
Obesity
Smoking
Hypercholestrolaemia
Metabolic syndrome (diabetes at x3 risk)
24
Q

Surgical cause of ED

A

Post-radical prostatectomy

25
Q

Indicators of psychological aetiology

A

Sudden onset of ED
Good nocturnal and early morning erections
Situational ED
Younger patient

26
Q

Assessment of ED

A
Bloods and Examination often normal
Sexual Hx (International Index for Erectile Function)
Physical examination - BP, HR, Hepatosplenomegaly, Genitalia (Peyronies disease), Prostatic enlargement or cancer, Hypogonadism (small testes or other)
27
Q

Lab testing of ED

A

Fasting glucose
Lipid profile
Morning testosterone (if low then perform prolactin, FSH, LH)

28
Q

Treatment of ED (non-pharmacological)

A

Identify and treat reversible causes of ED
Lifestyle and risk factor modification
Patient and partner involvement in education and counselling

29
Q

When is ED curable

A
Hormonal causes such as testosterone deficiency, thus testosterone replacement
Psychosexual counselling (variable results)
30
Q

Treatment of ED (pharmacological)

A

Lifestyle and risk factor modification should accompany ED treatment. If a cause of ED is detected it should be treated first.
1st line = Phosphodiesterase (PDE5) inhibitors
2nd line = Apomorphine SL; Intracavernous injections; Intraurethral alprostadil; vacuum devices

31
Q

Describe physiology of first line therapy of ED

A

PDE5 inhibitors result in increased arterial blood flow, vasodilatation, and erection
Action on Nitric oxide
3 PDE5 inhibitors have been approved. Not initiators of erections – require sexual stimulation