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MBBS II ERS > L13 – Treatment of Pituitary Disorder > Flashcards

L13 – Treatment of Pituitary Disorder Flashcards

1
Q

Outline the effects of gonadotrophin deficiency in women?

A

 Amenorrhea (low menstrual cycle)

 No ovulation = infertility

 No FSH = no estrogen = regression of secondary sexual characteristics

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2
Q

Outline the effects of gonadotrophin deficiency in men?

A

 Impotence

 No spermatogenesis = infertility

 Testicular atrophy cause Regression of secondary sexual characteristics

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3
Q

List 2 treatment options for FSH deficiency?

A

Follitropin (recombinant human FSH)

Human menopausal gonadotrophins (HMG): purified extract of human postmenopausal urine, contains FSH and LH

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4
Q

List 3 treatment options for LH deficiency?

A

Lutropin α (recombinant human LH)

Human chorionic gonadotrophin (HCG): purified extract from placenta in urine of pregnant women

Choriogonadotropin α (recombinant HCG)***

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5
Q

Describe the preparation of hormone therapy for gonadotrophin deficiency?

A
  • Follitropin + Lutropin α/ Choriogonadotropin α

- Human menopausal gonadotrophins (HMG) + Lutropin α / HCG / choriogonadotropin α

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6
Q

MoA of gonadotrophin hormone replacement on women?

A

stimulate ovarian Graffian follicles development&raquo_space; produce estrogen:

  • thickening of endometrial wall
  • development of Secondary sexual characteristics

Stimulate ovulation&raquo_space; corpus luteum secretes progesterone to prepare implantation at endometrium

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7
Q

MoA of gonadotrophin hormone replacement on men?

A

stimulate spermatogenesis

testosterone production for secondary sexual characteristics

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8
Q

HMG has both FSH and LH activity so it can be used in isolation to treat gonadotrophin deficiency/ T or F?

A

False

LH activity is very low, still need LH therapy (lutropin α / HCG / choriogonadotropin α)

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9
Q

ADR of FSH and LH replacement therapy?

A

1) FSH and LH stimulate aromatase: convert testosterone to estrogen: gynaecomastia in men
2) ‘Ovarian hyperstimulation syndrome’
3) Fever
4) Multiple births

LH only:
Headache, depression, edema, precocious puberty

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10
Q

List some complications from Ovarian hyperstimulation syndrome.

A

1) Ovarian enlargement and burst > Hemoperitoneum

2) Ovary produces factors to increase BV permeability > edema:
a) Ascites
b) Hydrothorax
c) Hypovolemia leading to electrolyte imbalance and arterial thromboembolism

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11
Q

Compare the hormone therapy required in Hypopituitarism and Adrenocortical insufficiency.

A

Hypopituitarism:

  • Hydrocortisone only
  • Renin-angiotensin system maintain Aldosterone production = no need for Fludrocortisone

Adrencocortical insufficiency: e.g. Addison’s disease:
- hydrocortisone + fludrocortisone

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12
Q

Symptoms and signs of ACTH deficiency?

A

1) Hypoglycaema: less cortisol to elevate blood glucose

2) Impaired function of Adrenaline/ NE on heart, reduced vasocontriction:
a) Hypotension
b) Low blood flow to brain: fatigue, dizziness
c) Intolerance to stress, infection

3) Weight loss

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13
Q

List 2 treatment options for ACTH deficiency?

A
  • Hydrocortisone

- Cortisone (converted to hydrocortisone)

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14
Q

Can corticosteroids like prednisolone and betamethasone be used for ACTH deficiency?

A

NO

Those are too strong, only for anti-inflammatory immunosuppression

> > many adverse effects

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15
Q

How does hydrocortisone exert it’s effect on target cells?

A
  • Cross cell membrane and bind to intracellular steroid receptor
  • Steroid receptor complex into nucleus, bind to chromatin
  • trigger target gene transcription
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16
Q

List effects of hydrocortisone?

A
  • Increase blood glucose:
    a) decrease uptake in cells
    b) Increase gluconeogenesis
    c) increase proteolysis, lipolysis
    d) Increase liver glycogen stores
  • Increase β-adrenoceptors (permissive effect) = potentiates adrenaline, NE effects = maintain cardiovascular function
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17
Q

List effects of Fludrocortisone?

A

Acts on DCT of kidneys:
Increase Na reabsorption

Increase K/H secretion

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18
Q

ADR of hydrocortisone?

A

Iatrogenic Cushing’s syndrome**

Hyperglycaemia (DM) and hypertension **

Increase risk of infection **

Osteoporosis ** and muscle weakness

  • Growth suppression
  • Peptic ulcer
  • Cataracts
  • Psychological distubances
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19
Q

Describe changes induced by Iatrogenic Cushing’s syndrome?

A
  • Moon face
  • buffalo hump
  • Increase abdominal fat/ central obesity
  • Thin arm and legs
  • Thinning of skin
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20
Q

Stimulation and inhibition factors of Prolactin?

A

Stimulation = Prolactin- releasing factor/ hormone

Inhibition = tonic dopamine

21
Q

Symptoms and signs of hyperprolactinaemia?

A
  • Galactorrhoea

Inhibit GnRH, FSH and LH:
 Amenorrhoea (no menstrual cycle)
 Hypogonadism
 Infertility

22
Q

Treatment options for hyperprolactinaemia?

A

Dopamine receptor agonists – e.g. Bromocriptine, cabergoline

Cabergoline: longer t1/2 and higher selectivity for dopamine D2 receptor

23
Q

MoA of Bromocriptine/ Cabergoline?

A

1) Stimulate dopamine D2 receptors on anterior pituitary gland = inhibit prolactin production and lactation
2) Significant decrease size of prolactin-secreting adenomas

24
Q

ADR of bromocriptine/ Cabergoline?

A
  • Trigger D2 receptor in CTZ, nucleus of solitary tract = Nausea, vomiting**
  • Decrease parasympathetic activity in gut = Constipation**
  • Direct vasodilation: baroreceptor less sensitive to BP change = Postural hypotension = dizziness**
25
Q

Effects of Growth hormone hypersecretion during childhood and adults?

A

Childhood = pituitary gigantism

Adult = acromegaly

26
Q

Trigger and inhibitor of Growth hormone secretion?

A

Growth hormone releasing factor = stim

Somatostatin = inhibit

27
Q

Can somatostatin be used to treat GH hypersecretion?

A

No

Very short t1/2

28
Q

Treatment options for Acromegaly and GIgantism? (4)

A

Somatostatin analogues:
Octreotide, Lanreotide

Growth hormone receptor antagonist: pegvisomant

Dopamine D2 receptor agonists (e.g. bromocriptine, cabergoline)

29
Q

MoA of Lanreotide and Octreotide?

A

Inhibit release of growth hormone from anterior pituitary

Decrease pituitary tumor size in a minority of patients

30
Q

ADR of Lanreotide and Octreotide?

A

3 G’s:
GI disturbances: •Nausea & vomiting •Abdominal cramps •Flatulence •Steatorrhoea

Gallstones: Inhibition of gall bladder motility

Impaired Glucose tolerance: somatostatin inhibits pancreatic insulin secretion

31
Q

Explain how Lanreotide and Octreotide cause GI disturbance?

A

Octreotide inhibits secretion of gastrointestinal peptides (e.g. gastrin, vasoactive intestinal peptide, secretin, motilin, pancreatic polypeptide)

> > > inhibits digestion, motility of gut

32
Q

MoA of Pegvisomant?

A

Growth hormone receptor antagonist

Selectively blocks growth hormone receptor

> > interferes with Growth hormone signal transduction + Hepatic production of somatomedins

33
Q

ADR of Pegvisomant?

A

 Elevated liver enzymes (AST, ALT): damage liver, but no symptoms of liver failure / hepatotoxicity / hepatitis

 Nausea

 Diarrhoea

34
Q

MoA of Bromocriptine and Cabergoline to treat gigantism and acromegaly?

A

Normally = D2 receptor agonist stimulates growth hormone secretion

In Acromegaly = D2R agonist cause paradoxical decrease in growth hormone secretion

35
Q

Treatment against Cushing’s syndrome?

A

•Metyrapone •Trilostane

36
Q

MoA of Metyrapone and Trilostane?

A

Inhibit biosynthetic pathways of corticosteroids conversion (cortisol,aldosterone) (exam):

 Metyrapone inhibits 11β-hydroxylase

 Trilostane inhibits 3β-dehydrogenase

37
Q

ADR of Metyrapone and Trilostane?

A
  • Decrease cortisol = Hypotension
  • Nausea, vomiting
  • Headache and dizziness
  • Rash/ allergy
38
Q

Physiological effects of ADH?

A

1) Stimulate V1 receptor on vascular smooth muscles = vasoconstriction = increase BP
2) Stimulate V2 receptor on collecting ducts = increase expression and trafficking of AQP2 = increase water reabsorption

39
Q

Pathological effects of ADH deficiency?

A

Diabetes insipidus

Increase plasma osmolarity
Decrease blood volume
Decrease blood pressure

40
Q

Treatment options for ADH deficiency?

A

 Vasopressin (synthetic)

 Desmopressin: long-acting synthetic Vp analogue

41
Q

Desmopressin is V1 selective. T or F?

A

False

Desmopressin is More selective to V2 receptors in kidney (rather than blood vessels) = less vasopressor effect

42
Q

MoA of Vasopressin and Desmopressin?

A

Stimulate V2 receptor on renal distal tubules, collecting ducts

> > translocate AQP2 from cytoplasm to luminal membrane

> > increase permeability to water

43
Q

ADR of Vp and desmopressin?

A
  • Fluid retention and edema
  • Hyponatremia
  • Headache, nausea, allergy

Vp: stimulate V1R:

  • Vasoconstriction
  • Angina
  • Abdominal and uterine cramps
44
Q

What is pituitary dwarfism caused by?

A

Lack of GH

45
Q

Treatment option for pituitary dwarfism?

A

Somatropin (recombinant GH)

46
Q

MoA of somatropin?

A
  • Stimulate peripheral tissue growth + Amino acid uptake
  • Initial ‘insulin-like’ effect to increase glucose uptake, later peripheral insulin antagonistic effect with impaired glucose uptake and increased lipolysis
  • Stimulate Somatomedins (IGF-1) production from liver:
    i) uptake of sulphate into cartilage for growth
    ii) mediate bone growth
47
Q

Describe the early and later phase activity of somatotropin?

A

Initial ‘insulin-like’ effect:

  • Increase tissue uptake of glucose
  • Decrease lipolysis

After a few hours = peripheral insulin-antagonistic effect:

  • Impaired glucose uptake
  • Increase lipolysis
48
Q

ADR of Somatotropin?

A
  • Increase T4 to T3 conversion = quickly degraded = hypothyroidism
  • Activate Na channel in collecting ducts :
    a) peripheral edema
    b) Papilledema near optic nerve = vision chnage
    c) Raised ICP and headache
  • Impaired glucose tolerance (anti-insulin effect)

MBBS II ERS (37 decks)

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