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Endocrine disorders Flashcards

1
Q

Describe the HPA axis

A

HPA axis

  • FSH and LH are hormones in reproductive pituariary
  • act on ovary
  • LH acts on theca cells → these make androgens
    • peak in LH mid-cycle causes ovulation
  • androgens produced get to oestrogen in granulosa cells
  • oestrogen feeds back to pituitary

You have negative and positive feedback in this cucle

as you produce more oestrogen it dampens down FSH and LH

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2
Q

what happens if you give continous GnRH

A
  • you suppress FSH and LH
    • supresses ovulation
  • gove opportunity to give exogenous FSH and control teh growth of follicles without the risk of sponetonous ovulation

would use a GnRH agonsist

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3
Q

Whats the difference between central and gondal pathlogies

A
  1. Central pathology
    • piruariatry gland and cerebal thing
    • Lack of secretion of LH and FSH
      • hypo hypothalamic and gonadal
        • get no oestrogen → so no cycle
    • Hypothalamic/pituitary disease
  2. Gonadal damage (secondary)
  • Failure of germ cell production
  • Lack of sex steroid production
    • like oestrogen, failure of ovaries

Central and gondal can be congenital or acquired

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4
Q

What are the causes of ammonhera

A
  • Pregnancy – always exclude
    • make sure to always check
  • Central causes
    • Hypothalamic - weight loss (anorexia), excessive exercise, stress
      • problems with FSH, LH
    • Pituitary – hyperprolactinaemia (lactation), pituitary tumours
      • can be life-threatening if it affects the eyes
    • Hypogonadotropic hypogonadism (failure of LH, FSH secretion)
  • Ovarian causes
    • Turner’s syndrome (45 X0)
    • Premature ovarian failure
  • Polycystic ovary syndrome
    • common cause outside of pregnancy
  • Miscellaneous – thyrotoxicosis, chronic disease, local uterine problems
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5
Q

What are the causes of hypothalamic amenorrohea and why are the presentations differeng

A

anoxeria, excerise, bulimia

  • people have different baslines when they get amenorrhea
  • there’s a cut of when pituarity gland gets cut off
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6
Q

What is lepin

how does it work etc

A

-Leptin is a peptide hormone released by adipocytes
-Regulates appetite, neuroendocrine function, and energy homeostasis

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7
Q

What is congential leptin defieceny

A

signs
severe obesity, hyperphagia, hypogonadotropic, hypogonadism

leptin levels fall, food intake foes up, energy expenditure goes down, and reproductive function decreases

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8
Q

What is prolactin

A

hormone that stimulates lactation

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9
Q

what inhibits prolactin

A

dophamine

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10
Q

In women that need to breastfeed, what medication can we give to promote this

A

be given dopamine antagonist to try and promote lactation

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11
Q

When does prolactin levels increase

A
  • Physical or psychological
    • breast examination, after exercise
  • Post seizure
  • Greater increase in women
    • reference range for women is different
    • if its very high the investigate
  • PRL peaks during sleep

- Rarely exceeds 850-1000 mU/L

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12
Q

Clinical features of hyperprolactinaemia

pre menopausal women

A
  • Hypogonadism
    • Oligo/amenorrhoea
    • symptoms of estrogen deficiency – associated problems
      • vaginal dryness etc
  • Galactorrhoea – spontaneous/expressible from breas
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13
Q

Clinical features of hyperprolactinaemia

Post menopausal women

A

Due to hypogonadal status – they dont get the same features as premenopausal women

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14
Q

what can prolactin inhibit

A

Prolactin inhibits LH & FSH.
So if you have high PRL you will have decreased FSH & LH & Oestrogen/Testosterone production – end up hypogonadal

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15
Q

What is patholgical hyperprolcatnima caused by

A

Can be due to:
PRL-secreting pituitary tumours - prolactinomas
-Microadenomas (< 1 cm diameter)
-Macroadenomas (≥ 1 cm diameter)
Loss of inhibitory effect of hypothalamus-derived DA (dopamine agonist)
-This is due to Pituitary stalk compression/pituitary disconnection
Drugs – DA antagonists
-Phenothiazines, metoclopramide, TCAs, verapamil
Hyperthyroidism
-Increase in TRH ->increase TSH which can then increase prolactin.

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16
Q

How can we treat patholgical hyperproclatneima

A

Dopamine agonists to supress PRL, Surgery (to remove pituitary tumour)

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17
Q

What is meant by premature ovarian insuffuicency

A

when ovaries cannot function well

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18
Q

How do people with POI present

A
  • Amenorrhoea
  • Oestrogen deficiency
  • Elevated LH, FSH (>30 IU/L) all < 45 years of age
    • FSH of 25 would be concerned
    • must always repeat after 6-week intervals
    • don’t do this test over age of 45
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19
Q

What are the causes of POI

A

-Turners -> congential
- Autoimmune (nb thyroid, Addisons, diabetes)
- Iatrogenic – chemotherapy and radiotherapy, surgery
- Mutations in FSH receptor, galactosaemia, FMR1 gene premutation (fragile X→ more disposed to this deficiency, can get bigger down generations)

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20
Q

Tuners

symptoms

A

what is it
1:2500 live births 45XO

symptoms
- Short stature and gonadal dysgenesis (streak ovaries)
- Webbed neck,
- cubitus valgus,
- congenital heart disease,
- hypothyroidism
- lymphoedema
- gains weight easily

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21
Q

How can autoimmune conditions cause POI

A
  • mechanism of autoimmune POI is likely to be due to inflammatory infiltration of follicles and production of anti ovarian Ab,
  • this may cause apoptosis and atrophy
  • sharing of auto antigens between the ovary and adrenals may explain the link with POI and Addison’s

egg frezzing-> addisons
POI -> precedes addiosns by 8-14 years

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22
Q

POI

Fragile X premutation

what is it, who gets it, what is the mutation etc

A

1 in 200 females has the genetic change that leads to FXPOI.
FXPOI accounts for about 4 to 6 % of all cases of POI in women.
Mutations in the FMR1 gene increase a woman’s risk of developing FXPOI.
It is inherited – so gets worse with going down the generation.
FXPOI is inherited in an X-linked dominant pattern therefore one copy leads to the condition

23
Q

How do we diagnose and manage POI

A
  • Diagnosis on serial FSH and E2 levels
    • do them 6 weeks apart
  • Karyotyping and FMR-1 premutation analysis
  • Screening for autoimmune diseases:
    • anti–adrenal, TPO, ovarian Abs
  • Anti Mullerian Hormone (AMH)
    • produced by granulosa cells
    • produced by resting follicles
    • can be used to diagnose women with low ovarian reserve
    • can be useful for menopause
  • DEXA scan: POI carries 50% risk of osteopenia
    • do after 23 which is when we reach
  • Manage with oestrogen replacement – need progesterone added if still has a uterus
    • oestrogen: bones
    • progesterone: protects endometrium

basically hormone replacment for managment

24
Q

How common is PCOS

A

Commonest endocrine condition affecting 10% of all pre- menopausal women

25
Q

What are the signs of PCOS

A
  • Oligoamenorrhoea (80%)
  • Hirsutism (30%)
  • Obesity (40%)
  • Infertility (30%) – anovulation
  • Polycystic ovaries on ultrasound
26
Q

Why do people with PCOS get hyperandrogenism

A

due to Increased testosterone, androstenedione, (DHEA)

  • Increased LH/FSH ratio
    • more LH, remember LH stimulates androgens
    • levels are normal
    • but the ratio between the same is different
27
Q

People with PCOS are not oestrogen deficent, so what needs to be done

like what do you need to make sure happens and why

think about what oestrogen does physiologically

A
  • NOT oestrogen deficient (prog withdrawal bleed)
    • if they are not having periods, need to make sure there’s progesterone release
    • helps protect the endometrium
    • protects from endometrium abnormalities
    • need to have 4 withdrawal bleeds a year
    • use a minipill
28
Q

What is rotterdams critera

A

Oligo-amenorrhea
clinical or biochemical signs of hyperandrogenameia
polysitic ovaries

2 out of 3 means PCOS

remember to exculde POI, cushings, adrenal tumors, CAH,

29
Q

What are the clinical features of PCOS

A
  • anovulation
  • insulin
  • androgen excess
  • obesity

all of these things feed into each other -> weight loss may help

30
Q

PCOS

What sign is a marker of insulin resistance

A

Acanthosis nigrinacans

31
Q

What are the risks of PCOS and pregnancy

Oligo-/Amenorrhea & Infertility commonest clinical problem

A
  • Risk of gestational diabetes and pregnancy-related hypertension is ten times increased
  • IVF: increased risk of Ovarian Hyperstimulation Syndrome (OHSS) although this can be avoided by using an antagonist

IVF protocol with a GnRH trigger injection for egg maturation

32
Q

How to treat PCOS

A

Obesity, oligo/ammenohera: metaformin, lifestyle, bariatric surgery

anvolution
-> metformin + IVF

hirtusim: Yasmin, vaniqua cream, cosemtic removal, sprinolactone

33
Q

What can people buy over the counter to increase insulin sensitivity

A

Myo-inositol

can help regulate cycles

34
Q

What anti-androgenic oral contraceptives can you take

A

dinette → better ones but no longer first line anymore
zoely
Yasmin

35
Q

What are the two types of 21 hydroxylase defienecy

what symptoms can you get

A
  • classical form pick up as neonate
    • salt wasting
    • andorgen excess
  • non classical happens at puberty
    • can look like PCOS
    • premature puberty, hirsutism
    • can be subtle

can mimic PCOS

36
Q

When trying to diagnose PCOS what other thing do you need to check

A
  • do 17 OH progesterone when diagnosing PCOS
    • if it’s high means that it’s not being converted into cortisol or aldoestrone
37
Q

What is complete 46XY

what are the features ans

used to be called Testicular Feminisation

A
  • Female external genetalia
  • Short, blind-ending vagina
  • No uterus, may have abdominal/inguinal testes
    • need to remove testes
    • these testes are more at risk of testicular cancer
  • Absent prostate, axillary (pubic) hair
  • Gynaecomastia – impressive breast development
38
Q

How do people with 46 XY present

A

May present as “inguinal hernia” but it is actual testes
Primary amenorrhoea

39
Q

What are the signs of 46 XY

A
  • Bloods: Elevated LH, Testosterone and E2
  • Oestrogen from aromatisation of Testosterone and LH- driven gonad secretion
  • T secretion 50% increased vs normal
40
Q

What condition is hard to differeniate with 46 XY and why

A

people with 5 alpha reductase deficiency

  • cant convert testosterone into DHT
  • so tissues cant convert it…
  • appear female but have abdominal testes
  • present with primary ammenhorrea
41
Q

Describe the hypothalamic testes axis in males

A

LH/FSH drives things

Leydig cells produce testosterone, LH acts on these

Sertoli cells produce AMH, inhibition

you also get spertamgenous

testosterone gives negative feedback to reduce FSH and LH

- testosterone decreases with age

42
Q

How can hypogonadism present in men

A

Delayed puberty

  • Psychological effects
    • Loss of libido and reduced sexual behaviour
    • Lack of sex drive versus erectile impotence
  • Gynaecomastia
  • Loss of body hair, reduced shaving frequency, thin skin
  • Decreased muscle mass, female fat distribution
  • Osteoporosis
  • Infertility +/- reduced testicular volume
43
Q

Causes of

Primary gonadal failure

A

Primary gonadal failure

  • Trauma – surgery and torsion
  • Chemotherapy and radiotherapy
  • Undescended testes (cryptorchidism) (10% at birth)
  • Infections, Inflammation & Infiltration
  • Orchitis (mumps)
    • can cause insufficiency
  • Iron overload
    • inhertied disease
  • Varicocele
    • warm up testes and cause spermatic damage
  • Chromosomal abnormalities
    • Klinefelter’s syndrome
  • Systemic diseases
    • Liver cirrhosis
    • Renal failure
    • Thyroid dysfunction
    • Myotonic dystrophy
44
Q

what causes secondary gondal failure

A

– Pituitary tumours

– Hyperprolactinaemia

-Hypothalamic disorders:
like, Craniopharyngioma (brain tumour)
Kallman’s syndrome
GnRH therapy

-Systemic disease
-Obesity (lots of oestrogen production which may inhibit FSH and LH)

-Androgen use & abuse

45
Q

How do we investigate hypogondism

what tests, exmaination

A
  • LH, FSH, Testosterone
    • Is Testosterone low? (Remember age)
      • Negative feedback

– High LH, FSH indicates primary gonadal failure

– Low LH, FSH suggests secondary cause

  • Further investigations to establish cause
  • eg Liver function, prolactin, karyotype (looking at chromosomes), imaging etc
46
Q

Klienfelters syndrome

how common, what chromsomes, what symptoms

A

Affects 1:1000 males
47 XXY
Leads to Primary hypogonadism – “firm pea-sized” testes
Feminisation – Azoospermia (no sperm in sample),
Gynaecomastia
Reduced secondary sexual hair
Osteoporosis
Eunuchs – tall stature
Reduced IQ in 40%
20-fold increased risk of breast cancer

47
Q

muscular dystrophy

talk about symptoms, genetics etc

A
  • Autosomal dominant
  • Progressive muscular weakness
  • Myotonia
  • Mental impairement
  • Frontal baldness
  • Cataracts
  • Primary gonadal failure
48
Q

Kallmans

talk about common, genetics, symptoms

A
  • Idiopathic hypogonadotropic hypogonadism
  • 1:10,000 - M:F = 4:1
  • Anosmia in 75%
  • Failure of migration of GnRH neurons to hypothalmus

Genetics
* X-linked, autosomal recessive or autosomal dominant
* Mutations in Kal-1, FGF-Receptor 1, prokineticin
* GnRH-Rec and G-protein coupled receptor 54 (normosmic)
*

49
Q

How can we treat men with fertlity problems

A

**Testoerone replacement
**
- can give tablets
- give injections 3 monthly (intramsuclar)
- patches are withdrawn
- subdermal implants every 6 months (on abdomen or buttocks)

50
Q

What are the conerns around testosterone replacement

A

-Behaviour: High testosterone can result in person becoming aggressive
-Need to do Annual PSA, FBC (can get high levels of red cells in blood), Lipids (can get high),
-BP monitors over 50 yrs
-High PSA can lead to prostate hyperplasia and prostate cancers.

Need to make sure testosterone is in normal range

51
Q

What can androgen abuse cause

A

Hypogonadism
-Side effect of androgen abuse is very small testicles.
-Exogenous testosterone will inhibit FSH and LH production – this means you do not get sperm production

other side effects
Psychological changes (aggression, sex drive)
Prostate cancer
Atrophy of testes
Azoospermia - infertility
Polycythaemia (too many red cells)
Cardiovascular death

Men how are not proudcing LH, FSH will be given hormones stimulate spermatgoensis + produce testostrone

Exogneoius testsotorne is given to protect cCV system and bones -> but they will not make sperm due to supression

52
Q
A
53
Q

What do you need to look at when investigating endocrine causes of male infertlity

A

assessment – history + examination

  • Seminal Fluid analysis
  • LH, FSH, Testosterone
  • Increased FSH – germ cell failure – numbers game, IVF, ICSI etc (may need endocrine input if primary gonadal failure)
  • Normal FSH, normal sized testes – think of obstructive uropathy
  • Low FSH, LH, Testosterone – ENDOCRINE causes
    • Pituitary/hypothalamic disease
    • Replace with LH (HCG 2000units/twice weekly and FSH 75IU x3/week – injections)
    • Spermatogenesis may take >12 months

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