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Year 3 > Week 9 Endoncrinology > Flashcards

Week 9 Endoncrinology Flashcards

1
Q

Pituitary tumours

A

Non-functional (most common) - don’t secrete hormones

Cause: Bitemporal hemianopia

Headaches

Functional - secrete hormones

Prolactinoma (most common)

GH adenoma - acromegaly

TSHoma

ACTH - Cushing’s

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2
Q

Prolactinoma

A

Pituitary tumour that secretes prolactin

Symptoms: - Golactorrhoae and ammenorrhoea (as prolactin causes decreased GnRH hence decreased LH, FSH)

  • Decreased libido in males
  • Headaches

Investigations:

Serum prolactin

MRI pituitary

Treatment:

Dopamine agonists e.g. bromocriptine, carbergoline

Surgery

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3
Q

Acromegaly

A

Pituitary tumour secreting GH

Other causes: GH cell adenoma, MEN 1, Increased GHRH (ganglioneuroma)

Gigantism in children

Acromegaly in adults

Symptoms:

Increased size in hands/feet, cardiomyopathy (LV dysfunction decreased), peripheral neuropathy, HTN

Increased inter-dental spaces Investigations:

Glucose tolerance test (as glucose normally suppresses GH)

IGF-1 levels (increased in acromegaly)

MRI Treatment:

1st line: surgery

Somatostatin analogues

  • Ocreotide

GH receptor antagonists - Pegvisomant

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4
Q

Cushing’s disease

A

Pituitary tumour secreting ACTH

Main cause of Cushing’s syndrome

Symptoms: moon face, weight gain, thin skin, increased BP

Diagnosis:

Dexamethasone suppression test

Treatment:

1st line: surgery

Bilateral adrenalectomy

Ketoconazole Radiotherapy

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5
Q

TSHoma

A

Pituitary tumour releasing TSH

Causes increased T4

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6
Q

Hypopituitarism

A

Tumour - Pituitary adenoma

Radiotherapy

Infarction/haemorrhage (apoplexy)

  • post partum: Sheehan’s syndrome
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7
Q

ADH

A

Post. pituitary

Diabetes insipidus

ADH deficiency (cranial or nephrogenic - due to impaired renal response to ADH))

Cranial

Causes:

Idiopathic

Pituitary tumour

Trauma

Sarcoidosis

Investigations

Water deprivation test (unable to concentrate urine)

Treatment: Desmopressin (analogue ADH)

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8
Q

Anterior Pituitary

A

GHRH - GH - Somatotrophs (50%) - multiple organs

GnRH - LH/FSH - Gonadotrophs (10-%) - ovaries/testes

CRH - ACTH - Corticotrophs (10%) - adrenal gland

TRH - TSH - Thyrotrophs (5%) - thyroid gland

Prolactin - dopamine (-ve) - Lactotrophs (20%) - breast/uterus

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9
Q
A

Follicular cells (produce T3 and T3)

Parafolliclar cells secrete calcitonin

Colloid (thyroglobulin) in middle

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10
Q
A
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11
Q

Actions of thyroid hormones

A

Increaeses metabolic rate

Increases glucose, protein synthesis

Grwoth and development

Increases catecholamine effect

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12
Q

Hypothyroidism

A

Causes: Iodine deficiency (common cause worldwide)

Iatrogenic - radiotherapy, drugs e.g. litium, amiodarone

Congenital hypothyroidism/cretinism

Pituitary macroadenoma

Clinical features: developmental delay, large fontenelle, dry skin

Autoimmune - Hashimoto’s thyroiditis (autoimmune disease leading to destruction of thyroid gland)

Symptoms:

Cold interolance, Weight gain, Constipation, Goitre (swelling in neck due to enlarged thyroid) , Heavy menstrual periods

Signs:

brittle hair with loss of outer eyebrows, dry skin, bradycardia, cold peripheries

Investigations

TSH, T4, (T3 unhelpful as there is increased conversion of T4 to T3)

Primary hypo: High TSH, Low T3/T4

Secondary hypo: Low/normal TSH, Low T3/T4

Subclinical hypo: High TSH, Normal T3/T4

Antibodies (Hashimoto’s)

Anti-thyroglobulin antibody

Anti-tyrosine perxodiase antibidy

US goitre

Treatment: Levothyroxine (acts like T4, gets converted into T3. Increases metabolic rate of all tissues)

Side effects: Tacycardia, chest pain, diarrhoea

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13
Q

Hyperthyroidism

A

Primary causes (due to thyroid):

Grave’s disease

Toxic multinodular gotire

Toxic adenoma

Secondary:

Pituitary adenoma - TSHoma

Gestational thyroxcisos - high hCG

Drugs - amiodarone:

  • inhibits conversion T4 to T3 (leads to increased TSH)
  • causes hypothyroidism
  • causes hyperthyroidism by Jod Basedow (due to increaesed iodine) or destructive thyroiditis

Grave’s:

Autoimmune disease where IgG stimulates TSH receptor of the thyroid gland, causing T4 release

  • Triad of thyroid eye disease (peri-orbital oedema, proptosis, lid retraction), gotire, thyrotoxicosis
  • Pretibial myoxedema (thyroid dermopathy)
  • Clubbing (thyroid acropachy)
  • Smooth, diffuse gotire

Symptoms: Weight loss, heat intolerance, diarrohea, ammenorhoea, anxiety

Signs: Tremor, Tachycardia, sweaty skin

Investigations:

Primary: low TSH, T3/T3 high

Secondary: high TSH: T3/T4 high

Subclinical hyperthyroidism: low TSH, Normal T3/T4

TSH receptor antibodies

TPO antibody

Iodine (I23) uptake scan

Diffuse with reduced backgroud: Grave’s

Irregular - toxic multinodular goitre

Hot nodule - toxic adenoma

Reduced uptake - Thyroiditis

Treatment:

Carbimazole/Propylthiouracil:

  • Inhibits production of tyrosine peroxidase, required for production of thryoid hormones and inhbits conversion of T4 to T3

PTU used if pregnancy planned/pregnant

Side effects: agranulocytosis, rash

Beta-blocker e.g. propanolol

Radioactive iodine - contraindicated in pregnancy, lactation, tyroid eye disease

Indicated for toxic multinodular goitre

Surgical - failed medical treatment

Complications: hypothyroidism, recurrent laryngeal damage (hoarse voice), damage parathyroid glands (hypocalcaemia)

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14
Q

Iodine induced hypo and hyperthyroidism

A

Jod Basedow - iodine induced hyperthyroidism

Wolff Chaikoff - iodine induced hypothyroidsm

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15
Q

Amiodarone

A

Type I - Autoimmune thyrotoxicosis (increase thyroid hormone synthesis due to increaesd iodine)

Treatment: High dose carbimazole

Type II - destructive thyroiditis (desrtruction thyroid gland leading to T3/T4 release)

Treatment: Glucocorticoids

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16
Q

Thyroid cancer

A

Follicular cell - benign adenoma, follicular cancer

Cancer of parathyroid cells - medullary cancer

familail medullary thyroid ca. - assoc with RET (proto-oncogene)

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17
Q

PTH

A

Stored in chief cells of parathyroid gland

Controlled by calcium sensing receptor (CaSR)

When there is increased Ca:

  • inhibits secretion of PTH
  • increases breakdown of PTH

Loss of function assoc. with familaim hypocalciuric hypercalcaemia

  • increases Ca2+ and Mg2+ excretion in kidneys
  • stimulates calcitonin release in thyroid gland
18
Q

Hyerpcalcaemia

A

PTH mediated (high Ca2+, high PTH)

Primary hyperparathyroidism

Familial hypocalciuric hypercalcaemia

PTH independent (high Ca2+, low PTH)

Malignancy

  • osteolytic metastases
  • tumour secreting PTHrP e.g. squmous cell lung carcinoma
  • tumour secreting Vit D e.g. lymphoma

Vit D toxicity (increases bone resorption, gut absorption)

Drugs e.g. thiazide

Milk-alkali syndrome (taking too much Ca2+. Hypercalcaemia, renal insuffiency, metabolic alkalosis)

Symptoms:

Moans - confusion

Groans - abdo pain, short QT

Stones - nephrolithiasis

Bones - bone pain

Treatment:

Rehydration (dilute Ca2+ level)

Loop diuretics (with saline to increase excretion of Ca2+)

Bisphosphonates (inhbits bone resorption)

Calcitonin (increases urinary Ca2+ excretion)

Steroids (Vit D toxicity)

19
Q

Primary hyperparathyroidism

A

Causes: Parathyroid adenoma

Parathyroid hyperplasia - assoc. with MEN

Common in post menopausal women

End-organ damage:

Bone - OP

Kidneys - nephrocalcinosis

Can cause brown tumours - collection of osteoclasts leading to poorly mineralised bone, brown due to haemosiderin deposition

Investigations

U and Es, PTH, urine calcium:creatnine ratio, Vit D

Treatment

1st line: Parathyroidectomy

Complications: vocal cord paresis, haematoma compressing trachea

Bisphosphonates

Cinalcalet (calcium sensing receptor agonist. Decreases PTH, decreases serum calcium)

20
Q

Vit D deficiency

A

Causes:

Decreased sunlight exposure

Malabsorption

Renal disease - (as can’t hydroxlyate 25-OH)

Osteomalacia

Assoc with decreased vit D

Can’t ossify adult bones

Symptoms: bone pain, proximal myopathy, hypocalcaemia

Low Ca, ALK phos, Vit D

High PTH

Treatments:

Cholecalciferol

Alfacalcidol (active D3) - for renal impairment, hypoparathyroidism

21
Q

Cushings syndrome

A

Excess cortisol secretion

Symptoms:

Moon face, buffalo hump, abdo striae, weight gain, hyperglycaemia

Causes:

Iatrogenic: excess steroids (leads to atrophy of adrenal glands due to decreased ACTH)

ACTH dependent:

Pituitary adenoma

Paraneoplastic ACTH secretion e.g. small cell carcinoma of lung

ACTH independent:

Adrenal adenoma

Adrenal carcinoma

Adrenal hyperplasia

Investigations

24 hour urinary free cortisol

Late night salivary cortisol (should be undetectable)

Dexemethasone test (supresses ACTH from pituitary tumour, but not ectopic ACTH (due to carcinoma)

Management:

Adrenalectomy

Ketoconazole

22
Q

Congenital adrenal hyperplasia

A

Autosomal recessive due to defect in steroidgenic genes

Lack of CYP21 (21 alpha hydroxylase)

Deficiency in cortisol, aldosterone

Increase in androgens

Females: ambigous genatalia

Males: Adrenal crisis

Treatment

Mineralcorticoid, glucocorticoid

23
Q

Adrenal cortex

A

Glomerulosa - Aldosterone

Fascularis - Cortisol

Reticularis - Androgens

Medulla: Chromaffin cells - Catecholamines

Aldosterone:

Mineralcorticoid

Stimulates Na2+ absorption (hence H2O)

Excretion K+, H+

Cortisol:

Stress leads to activation of hypothalamus secreting CRH - ACTH - cortisol

Stimulates gluconeogenesis, lipolysis, supresses insulin release, immune suppression

24
Q

Primary and seondary aldosteronism

A

Commonest secondary cause of HTN

Primary (suppressed renin):

Adrenal adenoma (Conn’s syndrome) or bilateral adrenal hyperplasia, adrenal carcinoma

Biochem:

Raised Na, decreased K+

ARR (aldosterone-renin ratio) increased

Increased aldosterone, decreased renin

Clinical features:

HTN, hypokalaemia, alkalosis

Treatment:

Stop B-blockers (causes increased ARR)

Saline suppression test: Give saline, aldosterone should not be high

MR antagonists: Spironolactone

Surgical - only if adrenal adenoma

Secondary aldosteronism (increaed renin)

HF, cirrhosis of liver, nephrotic syndrome, liqorice ingestion

High renin and aldosterone

25
Q

Adrenal insufficiency

A

Decreased aldosterone and cortisol

Primary:

Addison’s disease - primary adrenal insuffieciency, affects adrenal glands, leading to decreased aldosterone and cortisol

Causes: TB (most common cause worldwide), autoimmune, metastatic cancer (e.g. colonic carcinoma), adrenal haemorrhage, drugs (ketoconazole)

Symptoms:

Fatigue, anorexia, GI symptoms e.g nausea and vomiting, salt craving

Signs: Weight loss, hyperpigmentation (sun-exposed areas and mucosa), postural hypotension,

Biochemistry:

Anaemia, eosinophilia

Decreased Na, Increased K+

Hypoglycaemia

Decreased aldosterone, increased renin

Increased ACTH

Investigations

Short synacthen test: give ACTH, and see if levels increase

Adrenal autoantibodies

Treatment:

Hydrocortisone (good glucocorticoid activity and mineralcorticoid activity)

Fludrocortisone potent mineralcorticoid activity. Mild glucocorticoid activity)

SE: hyperglycaemia, immunodeficiency, Cushing’s, gastric irritation (need to take with food)

Other points: don’t stop abuptly, take high dose when ill, carry steroid card)

Secondary (Due to pituitary)

Panhypopituitarism - pituitary tumours, TB, sarcoidosis

Tertiary (hypothalamus)

  • Chronic high dose glucocorticoids
26
Q

Localisation of cortisol source (if high)

A

plasma ACTH (if low, then adrenal)

Dexamethasone suppression test

  • Pituitary tumours respond (cortisol will decrease), ectopic tumours don’t

CRH test

Pituitary tumours respond, ectopic tumours don’t

CT or MRI adrenal

27
Q

Ammenorrhoea

A

Primary

Rokitansky syndrome (no uterus)

Turners syndrome

Secondary (due to piuitary)

Kallmans

Ashermans syndrome

PCOS

Pregnancy, iatrogenic - OCP

28
Q

Hirsutism

A

Excess hair growth in male pattern due to increased androgens

Causes:

PCOS, congenital adrenal hypertrophy, androgen secreting tumour

29
Q

PCOS

A

Annovulation (ammenorrhoea) , and hyperandrogenism (hirsutism, ance)

Usually presents inn adolescence

Assoc. with metabolic syndromes e.g. TMD2

Pathophysiology

Gonadotropins

Increaesd LH, decresaed FSH

Androgens

Increased androgen production from theca cells under LH

Decreased SHBG (sex hormone binding globulin) which binds testosterone (only free testosterone is active)

Insulin resistance

Increased insulin secretion, which stimulates theca cells

Reduces SHBG production

Increases circulating androgens

Investigations

Testosterone

DHEAS

SHBG

LH/FSH

Treatment:

Metformin (only for those at high risk of developing diabetes)

COCP (suppresses ovarian production of androgens)

Corticosteroids (suppresses adrenal production of adrogens)

Spironolactone (MR anatagonist)

30
Q

Hypogonadism

A

Clinical syndrome of symptoms/signs and biochemistry of testosterone deficiency

Symptoms:

No pubertal growth spurt

Delayed growth

Decreased libido

Erectile problems

Investigations

Testosterone (early morning)

SHBG

LH/FSH - determine if primary or secondary

Primary hypogonadal hypogonadism

  • Decreased testosterone, N/increased LH/FSH

Normal prolactin

Increased oestrogen

Causes: Klinefelter’s, Leydig cell failure (due to chemo)

Klinefelter’s syndrome

XXY (karyotype 47)

Decreased testosterone, increased LH/FSH (but leydig cells dont work properly)

Clinical features:

Gynaecomastia

Delayed puberty

Azospermia

Treatment:

Androgen replacement therapy

Side effects: libido issues, mood issues

hcG, recombiant LH/FSH

Secondary hypogonadal hypogonadism

Low testosterone, low LH/FSH

Decreaed cortisol, IGF, TSH, increased Na+

Causes: Kallman’s syndrome, Pituitary tumour, Cerebellar ataxia

Kallman’s syndrome

Failure of migration of GnRH cells to hypothalamus from olfactory placode

Aplasia of olfactory lobes - anosmia

Symptoms:

Slow growth, micro penis, cryptorchidism, assoc. with deafness

Famlial:

KAL 1 - X linked rec

KAL 2 - AD

KAL 3 - AR

31
Q

Thyrotoxicosis vs. hyperthyroidism

A

Thyrotoxicosis: Excess T4 and/or T3 thyroid hormones in body

Hyperpthyroidism: overactive thyroid gland due to thyrotoxicosis

32
Q

Eye signs specific to Grave’s opthalmopathy

A

Redness, grittiness

Periorbital oedema

Opthalmoplegia (weakness of eye muscles)

Proptosis /exopthalmos (bulging of eye anteirorly)

Lid retraction

33
Q

Treatment Grave’s eye disease

A

Artificial tears

Eyelid tape

Steroids

34
Q

Myxodema

A

Severe hypothyroidism where there is an accumulation of mucopolysaccharides of dermis leading to thickened skin

Signs:

Expressionless face

Pale skin

Cerebellar ataxia

Pericardial effusion

Myxoedema coma - reduced conciousness and hypothermia. Reduced BP, hyponatraemia

Treated with IV fluid, slow rewarming, IV T3

35
Q

Non diabetes related hypoglycaemia

A

Hypoglycaemia: <4 in diabetics, non diabetics: <3

Whipple’s trad:

Low blood glucose

Symptoms of low blood glucose (sweating, palpitations, headache, confusion)

Relief of symptoms after glucose

<4.6 - inhibtion of insulin

<3.8 - release counter-regulatory hormones e.g. glucagon - leads to symptoms e.g. sweating, palpitations

<2.5 - impaired congitive function - confusion

< 2 - EEG changes

<1.5: coma

36
Q

Investigations of hypoglycaemia

A

Glucose

Insulin

C peptide

B-hydroxybutyrate (low in insulinoma)

72 hours fast

Imaging - CT

Arterial Ca2+ stimulation: Differentiated between insulinoma and diffuse disease (Ca2+ causes insulin release from insulinoma)

37
Q

Causes of spontaenous hypoglycaemia

A

Insulinoma

Islet cell disorder, not insulinoma- nesidioblastoma

Non islet cell tumour

Drugs - lithium, trimethoprim

Endocrine - hypopituitarism

Sepsis

Anorexia

In ill people:

Drugs

Critical illness

Hormone deficiency

Healthy people:

Increased endogenous insulin e.g. insulioma

Accidental

38
Q

DKA

A

Characterised by hyperglycaemia, metabolic acidosis, ketonaemia/ketonuria

Symptoms: polyuria, polydipsia, Kassmaul’s breathing, weight loss, abdo pain

Pathophys:

  • Insulin deficiency
  • increase in couter-regulatory hormones e.g. glucagon
  • increase lipolysos, free fatty acid release
  • FFAs are substrates for ketone production in liver
  • Ketones (B-hyroxybutyrate) excreted by kidneys but eventually cant compensate - acidosis
  • Gluconeogenesis occurs - hypergylcaemia - osmotic diuresis - dehydration - acidosis

Causes

New onset diabetes

Stopping insulin

Infection

MI

Pregnancy

Steroids

Substance abuse

Treatment:

IV fluids (NaCl)

IV insulin

Pottasium

39
Q

Hyperglycaemic hyperosmolar state

A

Severe hyperglycaemia (>30 glucose), hyperosmolality and hypovolaemic without ketoacidosis

May lead to coma

Causes:

Infection, poor compliance, drugs

Treatment:

IV fluids (NaCl), insulin, LMWH ( as pt increased risk of co-agulation), foot protection

40
Q

Autoimmune polyendocrine sydnrome type 2

A

Triad of Addison’s, TMD1, autoimmune thyroiditis

HLA DR3/4

Assoc. with coeliac, alopecia, pernicious anaemia, myasthenia gravis

(HLA DR4 assoc. with RA)

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