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Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

The anterior pituitary gland releases:

A

Thyroid Stimulating Hormone (TSH)
Adrenocorticotropic Hormone (ACTH)
Follicle Stimulating Hormone (FSH) and Luteinising Hormone (LH)
Growth Hormone (GH)
Prolactin

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2
Q

The posterior pituitary gland releases:

A

Oxytocin
Antidiuretic Hormone (ADH)

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3
Q

The thyroid axis

A

hypothalamus releases thyrotropin-releasing hormone –> Ant pit releases thyroid stimulating hormone –> thyroid releases triiodothyronine (T3) and thyroxine (T4)

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4
Q

The Adrenal Axis

A

Hypothalamus releases corticotropin release hormone –> ant pit releases adrenocorticotrophic hormone –> adrenal gland releases cortisol

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5
Q

Cortisol actions

A

Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness

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6
Q

The growth hormone axis

A

Hypothalamus releases growth hormone releasing hormone –> ant pit releases growth hormone –> liver releases insulin-like growth factor 1

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7
Q

Renin-Angiotensin System

A
  1. Renin convert angiotensinogen (released by the liver) into angiotensin I.
  2. Angiotensin I converts to angiotensin II in the lungs with the help of angiotensin-converting enzyme (ACE).
  3. Angiotensin II acts on blood vessels to cause vasoconstriction. This results in an increase in blood pressure. Angiotensin II also stimulates the release of aldosterone from the adrenal glands.
  4. This causes sodium reabsorption, potassium and hydrogen secretion, water follows sodium by osmosis to increase bp
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8
Q

Diabetes Random plasma glucose and 2 hour plasma glucose

A

Confirms diagnosis in the presence of symptoms of
1. polyuria
2. polydipsia
3. and unexplained weight loss
result ≥11 mmol/L (≥200 mg/dL).

A blood sugar level less than 140 mg/dL (7.8 mmol/L) is normal.

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9
Q

Diabetes HbA1c

A

≥48 mmol/mol (≥6.5%)

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10
Q

Diabetes Fasting plasma glucose

A

Result ≥6.9 mmol/L (≥126 mg/dL)

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11
Q

C-peptide level in T1D

A

< 0.2 nmol/L is suggestive
its levels reflect insulin production. Low or undetectable C-peptide level indicates absence of insulin secretion from pancreatic beta cells

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12
Q

diabetes autoimmune markers

A

Anti glutamic acid decarboxylase [GAD]-65 ( anti -Gad is to an an enzyme found within beta cells of the pancreas,and is most commonly identified.)
insulin, islet cells,
islet antigens (IA2 and IA2-beta),
and the zinc transporter ZnT8
tyrosine phosphatase 2

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13
Q

Diagnosis DKA

A

ketonaemia 3 mmol /l and over or significant ketonuria (more than 2 + on standard urine sticks)
blood glucose over 11 mmol /l or known diabetes mellitus
venous bicarbonate (HCO3 ) ) below 15 mmol /l (<18 for children) and /or venous pH less than 7.3

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14
Q

Treatment DKA

A

Fluid
Insulin fixed ( corrects hyperglycaemia and acidosis)
Glucose (GKI- glucose insulin and potassium)
Potassium ( monitor)
Infection-treat trigger
Chart fluid balance
Ketone monitoring

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15
Q

Hypoglycaemia treatment if conscious

A

Eat quick acting sugar 15- 20g CHO eg glucojucie,glucogel, 2-3 jelly babies, 200ml of full fat milk,dextrose /lucozade tablets, a small can/100ml of Coca-Cola, sweets or fruit juice/ 110ml lucozade.
AVOID chocolate
Follow with longer acting carb like digestive biscuits/toast to keep levels up

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16
Q

Hypoglycaemia treatment if unconscious

A

Glucose (Dextrose) iv- 100ml 20% (20g in 100ml) glucose , or 200ml 10% glucose ( same thing) . Follow with lower rate infusion . Works with everyone, less side effects than glucagon.
1mg/kg glucagon IM if no IV access

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17
Q

Type 2 diabetes treatment

A

1.Metformin
2. SU or pioglitazone or DDP4 (or SGLT2 if CVD present)
3. Triple therapy
4.GLP1 agonist / insulin

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18
Q

Diagnosis HHS

A

marked hyperglycaemia, raised serum osmolarity, and mild/absent ketonaemia.
Laboratory glucose: > 30.0 mmol/L
Serum osmolarity: > 320 mOsm/kg
Ketones:
Urine: 1+, trace, negative OR
Blood: < 3 mmol/L

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19
Q

hyperthyroidism causes

A

graves disease
toxic multi nodular goitre
amiodarone
subacute thyroiditis ( de quervains starts hyperthyroid then goes hypo)
postpartum thyroiditis ( starts hyper then goes hypo)

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20
Q

hypothyroidism causes

A

hashimotos thyroiditis
iodine deficiency
lithium

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21
Q

Grave’s disease

A

body produces antibodies to the receptor for thyroid-stimulating hormone that mimic TSH and chronically stimulate the TSH receptors on the thyroid causing excess production of thyroid hormone from thyroid gland

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22
Q

myxoedema coma

A

emergency. thyroid hormone levels become very low, causing symptoms such as confusion, hypothermia and drowsiness.

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23
Q

Management of myxoedema coma

A

ITU/HDU care as required
IV T3/T4
50-100mg IV hydrocortisone
Mechanical ventilation and oxygen - if hypoventilation
IV fluid - to correct hypovolaemia
Correct hypothermia
Correct hypoglycaemia
Treat any heart failure

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24
Q

Management of thyrotoxic storm

A

Symptom control:
IV propanolol
IV digoxin if propanolol fails or is contraindicated (e.g. asthma, low BP)
Reduce thyroid activity:
Propylthiouracil through NG - preferred because it inhibits peripheral thyroxine conversion
Lugol’s iodine 4/6 hours later
Methimazole/carbimazole is considered second-line
IV hydrocortisone to reduce thyroid inflammation

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25
Q

Actions of parathyroid hormone

A
  • Bones release Ca
  • Kidneys reabsorb Ca
  • Kidneys release calcitriol (via D) which tells GIT to increase Ca absorption
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26
Q

Primary hyperparathyroidism

A

One parathyroid gland (or more) produces excess PTH independently of calcium level
This may be asymptomatic or can lead to hypercalcaemia
Makes kidneys hold onto calcium and get rid of phosphate.

PTH and Ca high, phosphate low

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27
Q

Secondary hyperparathyroidism

A

there is increased secretion of PTH in response to low calcium because of kidney, liver, or bowel disease

PTH high Calcium low/normal, phosphate low if vitamin d deficiency high if CKD

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28
Q

Tertiary parathyroidism

A

There is autonomous secretion of PTH, usually because of chronic kidney disease (CKD).

PTH and Calcium high
Phosphate low or high

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29
Q

Pseudohypoparathyroidism

A

rare genetic condition resulting in failure of target organs to respond to normal levels of parathyroid hormone
Shortened 4th/5th metacarpal
Low Ca
High phosphate
High PTH
Normal/high ALP

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30
Q

Treatment hypercalcaemia

A
  1. Aggressive IV Fluids
  2. Bisphosphonates - Inhibits osteoclast activity reducing calcium release
  3. Calcitonin
  4. Glucocorticoids - In lymphoma, other granulomatous diseases or 25OHD poisoning
  5. Calcimimetics -Licensed for hypercalcaemia due to primary hyperparathyroidism, parathyroid carcinoma or renal failure
  6. Parathyroidectomy -considered in acute presentation of primary hyperparathyroidism if severe hypercalcaemia and poor response to other measures
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31
Q

Definition of Addison’s Disease

A

The adrenal glands have been damaged/destroyed, resulting in a reduction in the secretion of cortisol and aldosterone. This is also called Primary Adrenal Insufficiency

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32
Q

Definition of Secondary Adrenal Insufficiency

A

is a result of inadequate ACTH stimulating the adrenal glands, resulting in low cortisol release.
This is the result of loss or damage to the pituitary gland

33
Q

Definition of Tertiary Adrenal Insufficiency

A

is the result of inadequate CRH release by the hypothalamus. This is usually the result of patients being on long term oral steroids (for more than 3 weeks) causing suppression of the hypothalamus. When the exogenous steroids are suddenly withdrawn the hypothalamus does not “wake up” fast enough and endogenous steroids are not adequately produced

34
Q

Electrolyte abnormalities in addisonian crisis

A

hyponatraemia, hyperkalaemia and hypoglycaemia

35
Q

Addison disease features

A

lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia

36
Q

Test of choice for adrenal insufficiency.

A

Short synacthen test (ACTH stimulation test).
A failure of cortisol to rise (less than double the baseline) indicates primary adrenal insufficiency (Addison’s disease).

37
Q

Treatment of adrenal insufficiency

A

Treatment of adrenal insufficiency is with replacement steroids titrated to signs, symptoms and electrolytes. Hydrocortisone is a glucocorticoid hormone and is used to replace cortisol. Fludrocortisone is a mineralocorticoid hormone and is used to replace aldosterone if aldosterone is also insufficient.

38
Q

Management of Addisonian Crisis

A
  • Intensive monitoring if unwell
  • Fluid resuscitation if hypotensive. 1-3L of 0.9% Saline in first 12-24 hrs
    Parenteral steroids (i.e. IV hydrocortisone 100mg stat then 100mg every 6 hours, accounts for mineralocorticoid too bc of conversion)
  • Correct hypoglycaemia with iv dextrose
  • Careful monitoring of electrolytes and fluid balance
  • Consider fludrocortisone if there is adrenal disease
39
Q

Waterhouse- Friderichsen’s syndrome

A

is caused by a severe bacterial infection which results in disseminated intravascular coagulation and subsequent adrenal haemorrhage and failure,

non-specific infection which progresses into a macular, petechial and subsequently purpuric rash along with septic shock.

40
Q

Cushing’s syndrome

A

used to refer to the signs and symptoms that develop after prolonged abnormal elevation of cortisol.

41
Q

Causes of Cushing’s Syndrome

A

Exogenous steroids
Cushing’s Disease
Adrenal Adenoma
Paraneoplastic Cushing’s eg Small Cell Lung Cancer

42
Q

Cushing’s Disease

A

used to refer to the specific condition where a pituitary adenoma (tumour) secretes excessive ACTH. Cushing’s Disease causes a Cushing’s syndrome,

43
Q

Cushing’s Syndrome clinical features

A

Round in the middle with thin limbs:
- Round “moon” face
- Central Obesity, fluid retention
- Abdominal striae ( purple because of it exposing underlying dermis which is vascular)
- Buffalo Hump (fat pad on upper back)
- Proximal limb muscle wasting (proximal myopathy)
High levels of stress hormone:
- Hypertension
- Cardiac hypertrophy
- Hyperglycaemia (Type 2 Diabetes) and polyuria and polydipsia due to new onset diabetes mellitus.
- Depression
- Insomnia
Extra effects:
- Osteoporosis
- Easy bruising and poor skin healing

44
Q

Dexamethasone test

A

Test of choice to diagnose Cushing disease
It should suppress cortisol. When cortisol is not suppressed it indicates cushing disease

45
Q

High dose Dexamethasone Suppression Test helps determine causes

A

In Cushing’s Disease (pituitary adenoma) the pituitary still shows some response to negative feedback and 8mg of dexamethasone is enough to suppress cortisol.

Failure to suppress cortisol in:
- Adrenal adenoma/carcinoma
- Corticosteroid use
- Ectopic acth production

46
Q

Other Ix for Cushing disease

A

24-hour urinary free cortisol
FBC (raised white cells) and electrolytes (potassium may be low if aldosterone is also secreted by an adrenal adenoma)
MRI brain for pituitary adenoma
Chest CT for small cell lung cancer
Abdominal CT for adrenal tumours
Glucose is high

47
Q

Cushing disease Tx

A

surgically remove the tumour
if not possible, remove both adrenal glands and give the patient replacement steroid hormones for life

48
Q

Graves’ disease typical antibodies

A

thyroid stimulating hormone receptor antibodies

49
Q

autoimmune hypothyroidism antibodies

A

antibodies to thyroid peroxidase (TPO) and thyroglobulin (Tg)

50
Q

Aldosterone actions

A

Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts

51
Q

Primary Hyperaldosteronism (Conn’s Syndrome)

A

Adrenal glands produce too much aldosterone
Could be from Benign adrenal adenoma,Bilateral adrenal hyperplasia,Familial hyperaldosteronism

52
Q

Secondary Hyperaldosteronism

A

Excessive renin stimulating the adrenal glands to produce more aldosterone. Serum renin will be high.Blood pressure in the kidneys is disproportionately lower than the blood pressure in the rest of the body
Could be from Renal artery stenosis, Renal artery obstruction, Heart failure

53
Q

Hyperaldosteronism Ix

A

check renin and aldosterone levels and calculate a renin / aldosterone ratio

Blood pressure (hypertension)
Serum electrolytes (hypokalaemia)
Blood gas analysis (alkalosis)

CT / MRI to look for an adrenal tumour
Renal doppler ultrasound, CT angiogram or MRA for renal artery stenosis or obstruction

54
Q

Hyperaldosteronism Mx

A

Aldosterone antagonists eg Spironolactone, Eplerenone
Definitive management
Treat the underlying cause
- Surgical removal of adenoma
- Percutaneous renal artery angioplasty via the femoral artery to treat in renal artery stenosis

55
Q

Syndrome of Inappropriate Anti-Diuretic Hormone

A

Anti-diuretic hormone (ADH) is produced in the hypothalamus and secreted by the posterior pituitary gland. In SIADH here is inappropriately large amounts of ADH leading to excessive water reabsorption

56
Q

Causes of SIADH

A

Post-operative from major surgery
Infection
Head injury ( intracranial bleed/stroke)
Medications (thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDSs,)
Malignancy, particularly small cell lung cancer
Meningitis

57
Q

SIADH Ix

A

Clinical examination will show euvolaemia.
U+Es will show a hyponatraemia.
Urine sodium and osmolality will be high.
Lower plasma osmolality (more water going into blood)

58
Q

SIADH Mx

A

Fluid restriction - to correct the hyponatraemia without meds
Tolvaptan. “Vaptans” are ADH receptor blockers
Demeclocycline is a tetracycline antibiotic that inhibits ADH ( rarely used now)

59
Q

Pituitary apoplexy ( acute pituitary failure) features

A

Sudden onset
Retro orbital pain
vomiting
Compression of the cavernous sinus (contains cranial nerves) and horners may develop, ocular palsy can develop ( 3,4 6 all in cavernous sinus)
Low sodium and hypotensive

60
Q

Phaeochromocytoma

A

tumour of the chromaffin cells in the adrenal medulla that secretes unregulated and excessive amounts of adrenaline.

61
Q

Phaeochromocytoma clinical features

A

Episodic headache is from episodic hypertension,
sweating
tachycardia

62
Q

Pheochromocytoma Ix

A

24 hour urine catecholamines/metanephrines

CT

63
Q

Pheochromocytoma Mx

A
  1. Alpha blockers (i.e. phenoxybenzamine) (to control blood pressure and prevent a hypertensive crisis)
  2. Beta blockers once established on alpha blockers eg labetalol
  3. Adrenalectomy to remove tumour is the definitive management, Medical treatment prior to this is 4- 6 weeks
64
Q

Signs and symptoms of hyperprolactinaemia

A

in women
- amenorrhoea
- infertility (is why after pregnancy is like a natural contraception)
- galactorrhoea
- osteoporosis

in men
- Impotence,Erectile dysfunction
- loss of libido
- galactorrhoea

65
Q

Hyperprolactinaemia Mx

A

Dopamine inhibits prolactin release so Dopamine agonists are useful if not contraindicated
(e.g. cabergoline first line, bromocriptine second )
also used to reduce the tumour size
surgery is performed for patients who cannot tolerate or fail to respond to medical therapy

66
Q

Acromegaly

A

clinical manifestation of excessive growth hormone (GH). most common cause is pituitary adenoma

67
Q

Features of acromegaly

A

Space Occupying Lesion
- Headaches
- Visual field defect (“bitemporal hemianopia”)
Overgrowth of tissues
- Prominent forehead and brow (“frontal bossing”)
- Large nose
- Large tongue (“macroglossia”)
Large protruding jaw (”prognathism”)
- Early Arthritis
- carpal tunnel
Raised GH
- Development of new skin tags
- Profuse sweating

68
Q

Acromegaly Ix

A

Insulin-like Growth Factor 1 (IGF-1)
Oral glucose tolerance test whilst measuring growth hormone
(high glucose normally suppresses growth hormone) In a positive test, there is failure of the normal suppression of GH

69
Q

Acromegaly Mx

A

Trans-sphenoidal surgical removal of the pituitary tumour
- patients who are younger or who have pressure symptoms

Repeat hormonal testing should be undertaken 6 weeks after surgery ( IGF1 and random growth hormone ) and if surgery has not been completely curative, then adjuvant treatment should be offered. External irradiation is used in older patients

70
Q

Medications used to block growth hormone

A

1.Somatostatin analogues to block GH release (e.g. ocreotide)
2. Dopamine agonists to block GH release (e.g. bromocriptine)
Pegvisomant (GH antagonist given subcutaneously and daily) used if everything else has failed, expensive

71
Q

Diabetes insipidus

A

a lack of antidiuretic hormone (ADH) or a lack of response to ADH.

72
Q

Nephrogenic Diabetes Insipidus

A

collecting ducts of the kidneys do not respond to ADH.
Can be caused by lithium, kidney disease, hypo and hyperCa

73
Q

Cranial Diabetes Insipidus

A

Hypothalamus does not produce ADH for the pituitary gland to secrete.
Usually due to form of brain injury

74
Q

water deprivation test/desmopressin (synthetic ADH) stimulation test

A

urine osmolality is measured and synthetic ADH (desmopressin) is administered. 8 hours later urine osmolality is measured again.
cranial - end result high osmolality
nephrogemic - end result low osmolality

75
Q

Klinefelter’s syndrome

A

XXY
Klein means small
small testes, infertility, gynaecomastia, above average height and a lack of secondary sexual characteristics

76
Q

Kallmann’s syndrome

A

lack of smell (anosmia) in a boy with delayed puberty
hypogonadism, cryptorchidism
normal or above-average height

77
Q

MEN 1

A

para-pit-pan (parathyroid adenoma, pituitary adenoma, pancreatic neoplasia)

78
Q

MEN 2

A

T-A-P (thyroid medullary carcinoma, adrenal pheochromocytoma, parathyroid adenoma)

79
Q

Horner’s syndrome is also associated with

A

lung cancer, diabetes mellitus, CVS disease, demyelination, trauma, carotid aneurysm, carotid dissection ,skull base tumours

Medicine (72 decks)

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