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IPFC 3 Midterm 2 > Men's health Pathophysiology > Flashcards

Men's health Pathophysiology Flashcards

1
Q

Define male hypogonadism

A

Clinical syndrome resulting from failure to produce testosterone OR normal amounts of sperm or BOTH
- needs both

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2
Q

What enzyme used to turn testosterone to dihydrotestosterone DHT? What is DHT responsible for? (2)

A

5a-reductase

Responsible for:
1. External genitalia
- differentiation during gestation
- maturation during puberty
- adult prostatic disease

  1. Hair follicles
    - increased growth during puberty
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3
Q

What enzyme used to turn testosterone to estradiol? What is estradiol responsible for? (2)

A

CYP19 (aromatase)

Responsible for:
1. Bone
- ephiphyseal closure
- increased density

  1. Libido
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4
Q

What is testosterone alone used for without getting converted into anything (4)

A
  1. Internal genitalia
    - wolffian development during gestation
  2. Skeletal muscle
    - increased mass and strength during pubery
  3. Erythropoiesis
  4. bone growth
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5
Q

Differentiate between primary and secondary hypogonadism
Disease type?
low test + LH/FSH levels?
Fertility?

A

Primary
- Disease of testes
- LH/FSH levels high
- Fertility cannot be restored, seminiferous tubules damaged

Secondary
- Disease of hypothalamus or pituitary
- LH/FSH levels low or normal
- Fertility CAN be restored, using GnRH therapy

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6
Q

Define late-onset male hypogonadism

A
  • clinical and biochemical syndrome characterized by an unequivocally and consistent deficiency of testosterone WITH symptoms and signs that can be caused by testicular and/or hypothalamic dysfunction
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7
Q

What age group would you suspect primary hypogonadism? Secondary?

A

From 20-50
- likely primary

50+
- more often secondary but primary still occurs

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8
Q

What is the age-related defects that occur at the hypothalamic-pituitary-testicular axis?
Which is likely the main cause of declining androgen levels?

A
  • Pulsatile GnRH secretion effect reduced
  • LH response to GnRH is reduced
  • Testicular response to LH impaired
    (likely the main cause of declining androgen levels)
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9
Q

What are the MOST specific symptoms of late-onset hypogonadism? (3)

A
  • Decreased libido
  • ED
  • Decreased frequency of morning erections
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10
Q

What are less-specific symptoms of late-onset hypogonadism

A
  • decreased energy
  • decreased motivation
  • changes in mood (depression,anger)
  • Impaired memory
  • inability to concentrate
  • sleep disturbances
  • hot flushes
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11
Q
A
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12
Q

What are signs of late-onset hypogonadism

A
  • decreased body/facial hair
  • central obesity
  • decreased testicular volume
  • decreased muscle mass
  • increased body fat
  • gynecomastia (large breasts)
  • osteoporosis
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13
Q

Is there evidence for testosterone treatment to help with decreased muscle mass, higher visceral fat mass, insulin resistance etc..

A

Low total and Free testosterone levels are weakly associated with multiple adverse outcomes

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14
Q

When should you measure testosterone levels?

A

Measure in morning between 7 - 11
OR
3 hours after you wake up

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15
Q

How much % of testosterone is bound to serum proteins?
Which protein is testosterone bound to that does not make it bioavailable?

A

98% is bound to serum proteins
- 44% is bound so SHBG (not bioavailable)

Sex hormone binding globulin increases with aging

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16
Q

When do we measure free testosterone (3)

A
  1. when SHBG may be decreased
  2. when SHBG may be increased
  3. Total testosterone is borderline/low normal
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17
Q

What conditions and drugs decrease SHBG?

A

Conditions
- obesity
- diabetes
- hypothyroidism
- nephrotic syndrome
- polymorphisms in SHBG gene

Drugs
- glucocorticoids
- progestins
- androgenic steroids

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18
Q

What conditions and drugs increase SHBG?

A

Conditions
- Aging
- HIV
- Cirrhosis and hepatitis
- hyperthyroidism
- polymorphisms in the SHBG gene

Drugs
- anticonvulsants
- estrogens

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19
Q

What is the pathogenesis of androgenetic alopeica? (3)

A

Androgen dependent trait that requires a genetic predisposition.
- Located on the X chromosome

thinning starts in the crown

number of hair follicles and growth steps (cycle) remain constant
- BUT the anagen or growth stage is shorter (length of growth period is shorter)
- causes a shorter and thinner hair shaft

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20
Q

What is are the 3 key pathophysiologic features of alopecia pathogenesis

A
  1. Alteration in hair cycle development
    - anagen phase decreases but the telogen (shedding) phase remains the same length
    - anagen phase becomes so short that it does not reach the skin
  2. Follicular minimization
  3. Inflammation
    - sebacious glands and other secretions can build up overtime and cause this
    - not really studied
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21
Q

do males castrated before puberty or patients with androgen insensitivity develop alopecia?

22
Q

Which hormone plays a role in alopecia

A

Dihydrotestosterone
- binds to androgen receptor activating genes involved in hair follicles

23
Q

Which enzyme is used in alopecia? What are the 2 isoforms types in scalp hair follicles

A

5-alpha-reductase

2 isoforms
Type 1 in
- sebaceous glands
- epidermal and follicular keratinocytes
- dermal papillae cells
- sweat glands

Type 2 in (MAIN DRIVER)
- outer sheath of hair follicles
- Plus epididymis, vas deferens, seminal vesciles and prostate

24
Q

Is it common to have symptoms of BPH before age 50?

25
What are risk factors of BPH
- high levels of endogenous test, DHT, estradiol, insulin, inflammatory markers - Obesity - Diabetes - Lot of alcohol - Physical inactivity
26
Prostate growth phase in men
Size of 1g until puberty 1. grows to chestnut sized by 25-30 2. Second growth spurt at age 40 where prostate can quadruple in size
27
What fluids do prostates secrete (4)
1. Citrate (nutrient source) 2. Proteolytic enzymes to liquefy coagulated sperm 3. Seminal plasmin 4. Relaxin to enhance sperm motility
28
How much do prostatic fluid contribute to total semen volume
1/3 (30%) rest is - seminal vesicles (65%) - Testicles (5%)
29
What are the 3 types of tissues in the prostate
1. Epithelial tissue - produces secretions 2. Stromal tissue or smooth muscle tissue - contains alpha-1 adrenergic receptors - normal prostate to stromal tissue ratio is 2:1, in BPH is 5:1 3. Capsule - has fibrous connective tissue and smooth muscle - also contains alpha-1 adrenergic receptors
30
Which hormone and enzyme play a central role in BPH
DHT Type II 5-alpha-reductase
31
What is the pathogenesis of BPH 2 components? What causes them?
Static component - Proliferation of the stromal (smooth) and epithelial cells of the prostate - via DHT / 5-a reductase enzymes - ANATOMIC enlargement - PHYSICALLY blocks bladder neck and obstructs urinary flow Dynamic component - increase in smooth muscle tone in the prostate and bladder neck - via alpha-adrenergic receptors
32
What is the relationship between BPH and prostate cancer? how?
Strictly association and not causation - BPH proliferation occurs in transitional or central zone - prostate cancer occurs in the peripheral zone
33
BPH pathogenesis progression (3)
1. BPH 2. BP enlargement 3. BP obstruction - chronic bladder overfilling
34
What are some obstructive symptoms in lower urinary tract symptoms?
- slow urinary flow - intermittent urinary stream - straining to void - occasional mid-stream stoppage - post-void dripping
35
What are some irritative symptoms in lower urinary tract symptoms?
- increased daytime frequency - increased nocturia - increased urgency - increased retention - UTI - Urinary incontinence
36
What are MANDATORY investigations for BPH (3)
1. History - medical conditions - meds bladder contractility (anticholinergic agents) OR urinary outflow (sympathomimetic agents, phenylephrine ICU type meds) 2. Urinalysis - to rule out infection - to detect presence of blood 3. Digital rectal exam - normal prostate is firm and nontender
37
What are RECOMENDED investigations for BPH (2)
1. Symptom survey - american urological symptom score 2. Prostate specific antigen PSA - measure prior to treatment with 5-alpha-reductase inhibitor
38
What are the OPTIONAL investigations?
- Serum creatinine (if high could be bladder obstruction) - Urine cytology (screen for bladder cancer or irritative symptoms) - Uroflow (if less than 15ml/sec) - Voiding diary - Post-void residual (PVR) concerning if over 200ml - Sexual function questionnaire
39
What is the ED definition
Persistent failure to achieve a penile erection for a minimum of 3 months
40
What are some causes of erectile dysfunction? (5)
Psychogenic - performance anxiety Organic - vascular - neurologic - hormonal - locale penile factors - drug induced
41
What drugs induce ED (7)
- Antidepressants (SSRIs, MOAIs, TCAs) - Antihypertensives (beta-blockers) - Cardiac (digoxin amiodarone) - Diuretics - Hormones (corticosteroids, ketoconazole, antiandrogens) - H2RAs - Recerational drugs (alcohol, marijuana, cocaine)
42
What 3 systems are affected in erection
1. Vascular system 2. Nervous system 3. Hormonal system
43
What is the physiology of the vascular system
Flaccid state - arterial blood flow into and out of corproa cavernosa Erect state - decrease in venous outflow from the corpora - inc in ARTERIAL flow into corpora via Ach vasodilation
44
What is the physiology of the nervous system
Sacral nerve reflex arc external stimuli integration vs hypothalamus - dopamine exerts erectile effects - Alpha-2-adrenergic is anti erectal effects
45
What is the physiology of the hormonal system
testosterone stimulate sexual drive - androgen receptors may increase NO nitric oxide
46
What is it called if there is no organic cause and no response to psychogenic stimuli ?
psycjogenic erectile dysfunction
47
How much % of cases is drug-induced erectile dysfunction responsible for?
10-25%
48
What is ED a potential marker for?
arteriosclerosis or CV disease
49
What are Symptoms (2), signs (6), and lab values (3) for ED
Sx - ED +/- decreased libido or other sexual disorders Signs - Low satisfaction with erection quality - comorbidites (diabetes) - signs of hypogonadism - abnormall curved penis - decreases pulses in pelvic region - decreased anal sphincter tone Tests - testosterone - Digital rectal exam - Can also order PSA
50
ED investigations (5)
1. Sexual history 2. Medical history (any vascular comorbidities) 3. Medication history 4. Physical exam - abnormal penile anatomy (curved or weak pulses) - signs of reduced nerve function via anal sphincter tone 5. Lab tests (FBG, A1C, lipids) - serum testosterone if 50+ or if decreased libido

IPFC 3 Midterm 2 (7 decks)

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