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Year 1 Medicine > Week 128 - Gen Endocrinology > Flashcards

Week 128 - Gen Endocrinology Flashcards

1
Q

What is Cushing’s Syndrome? (name the 3 types)

A

Cushing’s Disease - ↑ACTH, due to pituitary

ACTH dependent Cushing’s - ↑ACTH, due to ectopic production

non-ACTH dependent Cushing’s - ↑Cortisol, ↓ACTH, due to adrenal tumour

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2
Q

What is Nelson’s disease

A

Increased pigmentation due to ↑ACTH

Associated with enlarging pituitary tumour

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3
Q

What can the Dexamethasone Suppression Test show?

A

With:
Ectopic ACTH production - no change in Cortisol levels
Pituitary-dependent disease - ↓Cortisol

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4
Q

What is Congenital Adrenal Hyperplasia?

A

Autosomal Recessive deficiency of 21 hydroxylase
Resulting in: ↓Cortisol, ↑ACTH

Diversion of steroid precursors occurs –> ↑17-hydroxyprogesterone and ↑testosterone levels

Clinical Features: sexual ambiguity, adrenal failure, hypotension, salt-losing state, primary amenorrhoea

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5
Q

What is Primary Hypoadrenalism : Addison’s disease?

include clinical features and investigations

A

Autoimmune disease ( 21 hydroxylase = common antigen)

↓Cortisol, ↑CRH, ↑ACTH

Clinical Features: pigmentation, postural systolic hypotension (Na+ loss), fatigue, weight loss

Investigations: Tetracosactide (Synacthen) = confirms presence of hypoadrenalism

Management: hydrocortisone, fludrocortisone, education

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6
Q

What is Conn’s Syndrome?

include investigations and treatment

A

Adrenal adenoma –> ↑aldosterone
↑Na+, ↓K+

Investigation: ↑aldosterone : renin ratio, CT scan, Adrenal Venous Sampling

Treatment: Laparoscopic adrenalectomy, low sodium diet, spironolactone

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7
Q

What is Phaechromocytoma?

A

Adrenal Medulla tumour (sympathetic NS) secreting catecholamines

Clinical Features: Headaches, Sweating, Anxiety, Palpitations, Poorly controlled hypertension, weight loss, chest pain, nausea, vomiting

Investigations: Urinary catecholamines + metabolites, plasma catecholamines, clonidine suppression test, CT

Management: ↑salt diet, phenoxybenzamine (α-blockade), propranolol (β- blockade), laparoscopic adrenalectomy.

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8
Q

What happens in Primary Hypogonadism (male)?

A

Testicular Failure
↓ Testosterone
↑FSH & LH

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9
Q

What happens in Secondary Hypogonadism (male)?

A

Hypothalamic-pituitary Failure
↓ Testosterone
↓FSH & LH (or inappropriately low)

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10
Q

What are the clinical features of androgen deficiency (hypogonadism-male)?

A 
Small or absent testes
Gynacomastia
Infertility, sexual dysfunction
Small prostate
Reduced hair growth
Eunuchoid (if pubertal deficiency)
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11
Q

What are the normal testicular sizes?

A 
Pre-pubertal = 1 - 6 ml
Pubertal = 8 - 15 ml
Adult = 15 - 25 ml
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12
Q

What investigations should be carried out for Androgen Deficiency?

A

Morning Testosterone x2

LH, FSH & seminal analysis x2

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13
Q

Name the common causes of Primary Hypogonadism

A 
Klinefelter's Syndrome
Surgical castration or trauma
Infections - orchitis
Drugs, alcohol, chemotherapy, radiotherapy
Chronic liver & kidney disease
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14
Q

Name the common causes of Secondary Hypogonadism

A 
Constitutional delayed puberty
Cushing's Syndrome
Drugs, opiates, anabolic steroids
Chronic disease, liver, kidney, HIV, diabetes
Obesity
Hypopituitarism
Hyperprolactinaemia
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15
Q

What is Kallmann’s Syndrome?

A

Genetic syndrome resulting in suppressed gonadotrophins

In males: absent facial hair, poor musculature, gynaecomastia, infertility, eunochoid body proportions, ANOSMIA, COLOUR BLINDNESS

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16
Q

What is Foetal Androgen Deficiency?

include clinical features

A

5-α reductase deficiency
Clinical Features: blind vagina, small clitoris, testis present (phenotypically female), bilateral inguinal hernia, primary amenorrhoea, ↑testosterone levels

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17
Q

What is precocious puberty?

A

Oestogen secretion or cyclical ovarian activity before 7-8 years in girls
or
Androgen secretion & spermatogenesis before 9-10 years in boys

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18
Q

What investigations would you carry out for precocious puberty?

A

LHRH/LH, FSH test, MRI pituitary, oestradiol, ovarian ultrasound, free T4, bone age

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19
Q

What is Pseudoprecocious puberty?

A

Adrenal & gonadal disease, hCG-secreting tumours
–> premature epiphyseal fusion & short stature
Investigations: DHEAS, 17-α OH-progesterone, hCG

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20
Q

What are the causes of primary amenorrhoea?

A

Primary ovarian failure (hypergonadotrophic hypogonadism)
Hypothalamic/pituitary failure
Excess sex steroid hormone production (CAH, adrenal tumours)
Turner’s Syndrome

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21
Q

In what conditions will you find androgen excess?

A 
PCOS
Non-classical adrenal hyperplasia (CAH)
Ovarian tumours
Adrenal tumours
Drugs
22
Q

What are the clinical features of PCOS?

include investigations

A

ovulatory dysfunction –> ↑testosterone ↓SHBG
hirsuitism, acne
insulin resistance
raised LH/FSH ratio
?raised prolactin
Investigations: LH:FSH ratio, testosterone, prolactin, T4 & TSH, 17-α OH-progesterone, ovarian ultrasound.

23
Q

What cells secrete PTH?

A

Chief cells

24
Q

What is the effect of PTH?

A

↑ [Ca] plasma
↓ [PO4] plasma
Enhances renal tubular reabsorption; osteoclast bone resorption; ↑25(OH)vitD –> 1,25(OH)vitD

25
Q

What is the effect of calcitonin?

A

↓ [Ca] plasma

↓ [PO4] plasma

26
Q

What is the effect of vitamin D?

A

↑ [Ca] plasma

↑ [PO4] plasma

27
Q

What are the main causes of Hypercalcaemia?

A

Primary hyperparathyroidism

Malignancy

28
Q

What are the causes of Primary Hypeparathyroidism? (include symptoms)

A

Adenoma, hyperplasia, carcinoma
Can be familial: MEN type 1, 2a
Generally asymptomatic, but may present with renal stones, musculoskeletal, GI or neuro problems

29
Q

What are the causes of Secondary Hypeparathyroidism?

A

compensatory, elevated PTH level secondary to hypocalcaemia with parathyroid gland hyperplasia

30
Q

What are the causes of Tertiary Hypeparathyroidism?

A

Autonomous secretion of PTH following long term hypocalcaemia

31
Q

Treatment of Hyperparathyroidism?

A 
?Tumour ablation
i.v. fluids
Diuretics
Bisphosphonates
Glucocorticoids
Calcitonin
32
Q

What are the causes of Hypocalcaemia?

A

Hypoparathyroidism
Impaired PTH secretion
Target organ resistance
Vitamin D-related disorders (diet, liver/kidney malfunction)

33
Q

What is the Clinical Presentation of Hypocalcaemia?

A

Chvostek’s sign (angle of jaw)
Trousseau’s sign (BP cuff)
ECG abnormalities, prolonged QT
Laryngeal spasm, tetany, paraethesia

34
Q

What is the treatment for Hypocalcaemia?

A

i.v. Calcium infusion
?magnesium infusion
oral (Ca, vitD, magnesium)

35
Q

What are the causes of Hypocalcaemia?

A 
Post surgical
Post radioactive iodine
Polyendocrine deficiency syndromes
Hypomagnaesaemia (e.g. PPI use)
Metastases, haemochromotosis, chemotherapy, PTH resistance
36
Q

What is Pseudo Hypoparathyroidism (PHP)?

A

Deficient Gα activity in renal tubules, erythrocytes, platelets, lymphoblasts
-> Hormone resistance (TSH, FSH, LH)
Investigation: ↓plasma cAMP
Albright’s Hereditary Osteodystrophy - cluster of symptoms (short stature, round face, short metacarpals (4), subcutaneous calcification)

37
Q

In the development of pituitary gland, what two segments come together in week 11 to form the pituitary gland?

A

Ectoderm & the hypophyseal diverticulum (Rathke’s pouch) AND Neuroectoderm and the neurohypophyseal diverticulum (infudibulum)

38
Q

Name the hormones secreted by posterior pituitary

A

Oxytocin, Vasopressin (ADH)

39
Q

Where does the thyroid gland develop from?

A

Foramen caecum (part of developing tongue)

40
Q

What duct may persist and cause problems after the thyroid gland descends?

A

The thyroglossal duct may persist and appear as a midline cyst

41
Q

Describe the development of the parathyroid gland

A

Ultimobrachial body arises from 4th pharyngeal pouch (neural crest) become C cells (parafollicular cells) that make calcitonin.
Inferior parathyroid glands come from 3rd pharyngeal pouch
Superior parathyroid glands come from 4th pharyngeal pouch

42
Q

What are neurohormones?

A

Released from synapses and travel via bloodstream

43
Q

Name some PEPTIDE hormones

A

GH, Prolactin, Insulin, ACTH, LH, FSH

44
Q

Name some STEROID hormones

A

Cortisol, Aldosterone, Testosterone, Oestrogen

45
Q

Name some AMINO ACID hormones

A

Thyroxine, Adrenaline, Noradrenaline

46
Q

Name some Lipid hormones

A

Prostacyclin, Prostaglandins, Thromboxanes, Leukotrienes

47
Q

Name some hormones secreted by the thymus

A

Thymosin, Thymopoietin, Thymulin

48
Q

What hormones are derived from Tyrosine?

A

Thyroid hormones, Catecholamines

49
Q

How is testosterone modified in different tissues?

A

testosterone (5α reductase) -> skin,external genitalia -> dihydrotestosterone
testosterone (aromatase) -> bone,brain -> estradiol

50
Q

What is the effect of T3 & T4?

A

Breakdown of carbohydrates and fats, synthesise proteins

Hormones made by follicular cells and carried in the blood bound to TBG

51
Q

What are the effects of Cortisol?

A

↑ amino acids in blood, ↑gluconeogenesis, ↑use of fat

Year 1 Medicine (12 decks)

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