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Phase 4 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What do alpha cells in the Islets of Langerhans secrete?and what is the function of that hormone?

A

Glucagon - breaks down glycogen into glucose

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2
Q

What do beta cells in the Islets of Langerhans secrete?

and what is the function of that hormone?

A

Insulin - increases glucose uptake and stores as glycogen in tissues

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3
Q

What happens with hormones in a post-prandial state (just after eating a meal)

A

Insulin production is increased to reduce blood glucose levels. In the liver- it stores glucose as glycogen and inhibits gluconeogeneis - so glucose isn’t produced.

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4
Q

What happens with hormones in a fasting state?

A

Insulin production is low and glucagon production is increased to release glucose from glycogen and lipolysis- breakdown of fatty acids to produce glucose

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5
Q

Give 4 causes of diabetes

A 
Type 1 diabetes
Type 2 diabetes
Gestational diabetes
MODY- maturity onset diabetes of the young- AD, diagnosed young, high genetic association 
Acromegaly 
Cushing's 
Steroids
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6
Q

What is the pathophysiology of type 1 diabetes

A

Autoimmune destruction of beta cells leading to insulin deficiency. This causes glucose production with no conversion to glycogen.

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7
Q

What are the symptoms of T1DM?

A

Polyuria (increased urinary glucose), polydipsia, weight loss, fatigue, hunger

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8
Q

What initial investigations are done for T1DM?

A 
Random plasma glucose >11mmol
Fasting plasma glucose >7 (on 2 occasions) 
2 hour OGTT >11 
HbA1c (for monitoring)- >48mmol
may do urine dipstick for ketones
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9
Q

What is the first line treatment for T1DM?

A

Insulin

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10
Q

What is the first line insulin regime for T1DM?

A

Basal-bolus regime.
Long acting OD/BD + rapid acting before each meal
eg. lantus/levermir + novorapid
need to know how much carb eating to give correct bolus

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11
Q

What is second line insulin regime for T1DM?

A

Mixed insulin regime- mixed (containing rapid + short) + intermediate BD eg. Humulin I

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12
Q

What is the third line insulin regime for T1DM?

A

continuous insulin infusion

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13
Q

What are the monitoring requirements for both T1 and T2 DM?

A

HbA1c 3 monthly - target =48mmol
Eye and foot screening yearly
eGFR and urinary albumin: creatinine ratio yearly

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14
Q

What is the pathophysiology of T2DM?

A

Insulin resistance. so get decreased conversion of glucose to glycogen –> hyperglycaemia

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15
Q

What are the risk factors for T2DM

A

Central obesity, FMH, ethnic group eg. asians, lack of exercise, HTN

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16
Q

Initial investigations for T2DM?

A 
Random plasma glucose >11
Fasting glucose >7
OGTT >11
HbA1c >48mmol (pre=diabetes: 42-47) 
U&Es (renal failure), lipids, LFTs (NAFLD)
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17
Q

What is first line treatment for T2DM?

A

Control RF- stop smoking, lose weight, exercise, statins, control BP

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18
Q

What is first line drug treatment for T2DM?

A

Metformin. SE: abdo pain/diarrhoea, lactic acidosis,

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19
Q

When would you start a second drug (in addition to metformin) in T2DM?

A

If the HbA1c > 58 despite the max dose of metformin

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20
Q

What second line drugs would be used in addition to metformin in T2DM?

A

Sulfonylureas - gliclazide SE: hypoglycaemia, weight gain
SGLT-2 inhibitors- gliflozins SE: UTI, genital thrush
Thiazolidinediones eg. pioglitozone- SE: weight gain, heart failure
DPP-4 inhibitors eg. sitagliptin. SE: few- GI discomfort
GLP-1 agonists eg. -tides SE: weight loss,

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21
Q

What is the associated dermatological condition with T2DM and why?

A

Acanthosis nigracans- dark hyper pigmented patches in folds of skin eg. groin, armpit, neck

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22
Q

What are the only 2 drugs allowed to treat diabetes in pregnancy?

A

Insulin and metformin. Discontinue all others.

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23
Q

What is the pathophysiology of DKA?

A

In absence of insulin to break down glucose- use free fatty acids are a source of energy which are broken down to ketones
The high levels of glucose cause lots of glucose to be excreted in kidney and water follows–> dehydrated

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24
Q

What is the triad of DKA?

A

Hyperglycaemia >11mmol or known DM
Ketones 2+ urinary, >3mmol blood
Acidosis ph<7.3 or bicarb <15

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25
Q

What are the signs and symptoms of DKA?

A

Polyuria, polydipsia, N&V, abdo pain. Signs= ketotic breath, Kussmaul breathing (deep laboured breathing to blow off CO2)

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26
Q

What investigations would you do for DKA?

A

Urine dip for ketones, blood ketones, blood glucose, FBC , U&E, CRP, ABG/VBG, infection screen- MSU, CXR?

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27
Q

What is the treatment for DKA?

A
  1. 1L 0.9% Normal Saline
  2. Fixed rate insulin at 0.1ml/kg/hour (prescribe 50 units Actrapid in 50ml saline). If glucose <14= add 5% dextrose.
    Electrolytes: K 3.5-5.5= add 40mmol
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28
Q

A patient with known T2DM presents with significant dehydration (low BP, dry skin & mouth), leg cramps and weakness along with polyuria and polydipsia. Thinking of the likely diagnosis- what is the best initial investigation?

A

Blood glucose

Will be >30 if hyperosmolar hyperglycaemic state

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29
Q

What are some causes of HHS?

A

Infection, stroke, MI, hypo/hyperthermia

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30
Q

What is the pathophysiology of HHS?

A

Marked hyperglycaemia means the kidneys are unable to reabsorb it all so it spills out into the urine causing an osmotic diuresis- become dehydrated.

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31
Q

What are the investigations to with a patient presenting with HHS?

A 
Blood glucose
Ketones- absent 
Serum osmolality >320 
Bloods- FBC, U&amp;E- dehydration, LFTs, CRP, ABG/VBG- no acidosis 
Infection screen- CXR, urine sample
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32
Q

What is the treatment for HHS?

A

IV 1L 0.9% normal saline
Only give insulin if ketones raised or if glucose isnt dropping with saline alone.
Add 40mmol KCl if K 3.5-5.5

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33
Q

Patient is admitted with sweating, hunger, tachycardia, feeling drowsy. You manage to elicit from the history that he has taken excess of his diabetic medication. What initial investigation would you like to do?

A

Blood glucose. He is likely hypoglycaemic (blood glucose <3.9)

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34
Q

This patient has a decreased GCS, how would you treat his hypoglycaemia

A

IV glucose STAT (if no IV access= IM glucagon)

Then 1L 10% glucose 4-8 hourly and monitor glucose every 30 mins , keep it above 5

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35
Q

This patient has a normal GCS, how would you treat his hypogylcaemia?

A

15g quick acting carb eg. lucozade or 1 glycogel oral
If it is still low after 3 of these= IM glucagon or IV glucose
Once recovered: long acting carb= toast

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36
Q

What are the causes of hypoglycaemia?

A

Excess insulin/anti-diabetic drug in diabetic
Accidental dose in non-diabetic
Alcohol
Hypoglycaemia unawareness- lose the sympathetic drive after long time
Renal impairment

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37
Q

Describe the HPA (hypothalamus –> pituitary –> adrenal) axis

A

Hypothalamus –> CRH–> ACTH–> cortisol (negatively feedbacks)

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38
Q

What hormones do the adrenal cortex release from each zone? And from the medulla?

A

Cortex:
Zona glomerulosa: aldosterone
Zona fasiculata: cortisol
Zona reticularis: androgens

Medulla:
Adrenaline and noradrenaline

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39
Q

What are the causes of Cushing’s syndrome?

A

Exogenous- Oral steroids (ACTH independent- low )
Endogenous:
Cushing’s disease- Pituitary adenoma - ACTH dependent
Ectopic ACTH production (SCLC)- ACTH dependent
Adrenal adenoma- ACTH independent

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40
Q

Patient presents with moon face, scapular fat pad and. central obesity. Additionally- he struggles to stand up from the chair using his arms and legs. What condition does he have? And what other symptoms might he present with?

A 
Cushing's syndrome. 
Other Symptoms include: 
Easy brushing, striae on skin 
He has proximal myopathy (protein breakdown by cortisol)
Acne, hirsutism 
Recurrent infections
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41
Q

What ophthalmic/neuro sign would be found if pituitary adenoma was the cause of Cushing’s?

A

Bitemporal hemianopia

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42
Q

What is the first test done to diagnose Cushing’s?

A

24h urinary free cortisol

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43
Q

What is the diagnostic test for Cushing’s disease?

A

Dexamethasone suppression test. In Cushing’s disease and endogenous cause: cortisol will stay high (ACTH is driving production)

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44
Q

What would be found on 9am plasma ACTH if the patient had Cushing’s disease (pit adenoma) and ectopic ACTH or if he had adrenal adenoma

A

Cushing’s disease: 9am plasma ACTH will be high

Adrenal adenoma: low ACTH

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45
Q

What test would be used to would you differentiate between Cushing’s disease (pit adenoma) or ectopic ACTH secretion as the cause of Cushing’s syndrome

A

High dose dexamethasone
Cushing’s disease: serum cortisol will drop
ectopic ACRH: it will stay high

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46
Q

How would you image and treat Cushing’s disease?

A

Pit adenoma: MRI pituitary. Tx: surgical removal

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47
Q

How would you treat steroid induced Cushing’s syndrome?

A

Gradual decrease and stop steroids

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48
Q

What imaging and treatment would be done for ectopic ACTH production as cause?

A

CT chest, abdo, pelvis- looking for cancer (usually lung). Tx cancer.

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49
Q

A young person presents with intermittent headaches, sweating, palpitations. On taking the BP - it is 170/120. What is the likely diagnosis and its cause?

A

Phaechromacytoma.

Benign tumour of adrenal medulla - secreting adrenaline and noradrenaline

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50
Q

What is the first line investigation for phaechromacytoma?

A

24 hour plasma and urinary metanephrines. If this is +ve= CT abdo & pelvis

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51
Q

What is the treatment for phaechromacytoma?

A 
Beta blockers (propranolol) then alpha blockers (phenoxybenzamine) 
Then surgical resection of the tumour
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52
Q

What is the pathophysiology of Addison’s disease?

A

Destruction of the adrenal cortex –> aldosterone and cortisol deficiency

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53
Q

What are the signs and symptoms of Addison’s disease?

A

Derm: Hyperpigmentation- mouth and palmar creases (excess ACTH)
MSK: Muscle weakness (proximal myopathy) , fatigue
GI: vomiting, abdo pain
Neuro: postural hypotension

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54
Q

What would be the electrolyte derangement in Addison’s disease? What would be the aldosterone and renin level change?

A

Decreased Na, raised Potassium (no aldosterone)

Decreased aldosterone, raised renin

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55
Q

What would be the initial test for diagnosis Addison’s disease?

A

9am cortisol- will be low

56
Q

What would the short synacthen test show for Addison’s disease?

A

SST- no rise in cortisol (adrenal cortex is destroyed)

57
Q

What test would be done to differentiate Addison’s (primary) from secondary adrenal insufficiency
What sign will not be presented in secondary?

A

Plasma ACTH
Addison’s: plasma ACTH will be high (no cortisol giving negative feedback)
Secondary (pit gland adenoma/apoplexy/): ACTH will be low and cortisol will be low
Since ACTH is low= no hyperpigmentation

58
Q

How do you treat Addison’s disease? How does that differ from secondary AI?

A

PO hydrocortisone daily + PO fludrocortisone

Secondary: no fludrocortisone (just decreased ACTH and cortisol)

59
Q

What is important to tell patients about their steroid treatment in Addison’s disease?

A

When unwell- double the dose, IM if vomiting

60
Q

How do you treat an adrenal crises? (shock, vomiting, hyperkalaemia, hyponatraemia)

A

100mg IV/IM hydrocortisone + 1L normal saline until eating and drinking. Treat the precipitant eg, infection;.

61
Q

A patient is presenting in clinic. He is describing headaches, muscle cramps and weakness and constipation along with his heart feeling ‘funny’. His BP is 140/100 on examination. What is the likely electrolyte abnormality on U&Es underlying this presentation?

A

This is primary hyperaldosteronism. Aldosterone causes Na and water retention (causing HTN) and excretes K
Hypernatraemia and hypokalaemia - producing the signs

62
Q

What is the most likely cause of primary hyperaldosteronism?

A

Conn’s syndrome- aldosterone producing adenoma

63
Q

Apart from U&Es, what other 2 investigations may you do in primary hyperaldosteronism?

A

Measure aldosterone: renin ratio= raised aldosterone, low renin (high ratio)
CT/MRI adrenals

64
Q

How do you treat Primary hyperaldosteronism in general? How do you treat Conn’s?

A

Spironolactone- K sparing diuretic and aldosterone antagonist.
Conn’s: adrenalectomy

65
Q

What is the pathophysiology behind CAH?

A

Defect in the 21-hydroxylase enzyme needed to make mineralocorticoids (aldosterone) and glucocorticoids (cortisol). increased production of androgens- testosterone.

66
Q

What are the symptoms of CAH?

A

Due to decreased aldosterone (salt losing): vomiting, dehydration, collapse, dizziness
Due to decreased cortisol: hypoglycaemia
Due to increased androgens: virilisation of external genitalia, acne, hirsutism, precocious puberty, amenorrhea when older

67
Q

What electrolyte derangement on U&Es would be found in a patient with CAH?

A

Hyperkalaemia and hyponatraemia (no aldosterone)

68
Q

What is the treatment for CAH?

A

Hydrocortisone and fludrocortisone (if salt wasting form)

May need surgery in girls- vaginoplasty

69
Q

What is carcinoid syndrome?

A

Paraneoplastic syndrome secondary to carcinoid tumour - serotonin production–> flushing, diarrhoea & com, abdo pain . Tx: octreotide - somatostatin analogue- decreases serotonin production.

70
Q

What is the mechanism of vitamin D production (broadly eg. kidney, liver)

A

Vitamin D is absorbed from sunlight and converted to 25-hydroxyvitamin D in the liver (from cholecalciferol/vitamin D3). It is then converted to it’s active form: 1,25 dihydroxyvitamin D in the kidney (driven by PTH)

71
Q

When is PTH secreted and what are its actions on bone, kidney and GI?

A

PTH is secreted in response to low Calcium levels in the blood
Bone: causes resorption of bone leading to increased Ca levels
Kidney: causes increased reabsorption of Ca and increased excretion of phosphate. As well as increased production of active vitamin D. (process driven by PTH)
GI: increased calcium resorption (due to increased production of active vitamin D)

72
Q

What are 4 causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Malignancy- bone metastases (multiple myeloma, prostate), tumour PTH secretion (lung, lymphoma)
  • Tertiary hyperparathyroidism
  • Sarcoidosis
  • Thiazide diuretics
  • Vitamin D intoxication
  • Lithium
  • Thyrotoxicosis
73
Q

A patient with a background of prostate cancer presents with abdominal pain and confusion. He is limping on his left leg and says it’s very difficult to weight bear there. He also says he’s been urinating more frequently than normal. What is the likely diagnosis and underlying cause?

A 
Hypercalcaemia due to bony metastases
Symptoms include: 
Bones- bone pain leading to fractures
Stones- renal stones
Groans- abdominal pain, constipation
Moans- confusion, depression
Thrones- polyuria, polydipsia
74
Q

What may show up on ECG if the patient had hypercalcaemia?

A

Shortened QT interval

75
Q

What initial investigations would you want to do if a patient presented with hypercalcaemia?

A

U&Es, FBC, PTH, Vitamin D levels, creatinine, Calcium, phosphate, bone profile , TFTs

76
Q

What investigation would help you differentiate the causes of hypercalcaemia?

A

Hyperparathyroidism= PTH raised, Calcium high, phosphate low
Malignancy: Calcium raised, PTH low (DEXA scan shows lytic lesions)

77
Q

How do you treat hypercalcaemia?

A

IV fluids- 1L 0.9% normal saline
IV bisphophonates- aldendronate
2nd line: glucocorticoids- increased GI excretion of Ca

78
Q

What is the most common cause of primary hyperparathyroidism?

A

Solitary adenoma of the pituitary gland

Other: gland hyperplasia

79
Q

What are the symptoms of primary hyperparathyroidism?

A

Bones, stones, groans, moans, thrones

80
Q

What initial investigations would you do for primary hyperparathyroidism? How would the results differ from secondary hyperparathyroidism and tertiary hyperparathyroidism ?

A

FBC, U&E, PTH, calcium, phosphate, bone profile, creatinine
Primary: PTH raised, Ca raised, phosphate low
Skull X ray- ‘salt and pepper skull’- sub-periosteal erosions
Secondary: PTH raised, Ca low, phosphate raised (kidneys can’t reabsorb Ca/excrete phosphate)
Tertiary: parathyroid autonomous- PTH v v raised, Ca raised eventually, phosphate high (kidneys can’t excrete phosphate)

81
Q

How do you treat primary hyperparathyroidism?

A

Surgery to remove pituitary adenoma
Bisphosphonates eg. aldendronate
Cinacalet- calcimimetic- for those who dont want/unfit for surgery

82
Q

What are the causes of secondary hyperparathyroidism? (2) and the pathophysiology of this?

A

CKD- the kidney can’t produce active vitamin D (1,25 dihydroxyvitamin D) so can’t absorb calcium from the gut –> serum Ca decreases–> PTH production rises
Vitamin D deficiency - same process

83
Q

What are the symptoms of secondary hyperparathyroidism?

A

Bony pain, joint pain

CKD sx- haematuria, proteinuria

84
Q

How do you treat secondary hyperparathyroidism?

A

Treat the cause - vitamin D supplements, calcium supplements.
CKD= phosphate binders, restrict dietary phosphate (kidneys can’t excrete phosphate so it builds up)

85
Q

Tertiary hyperparathyroidism develops in patients with what co-morbidity?

A

CKD

eventually PTH secretion becomes autonomous

86
Q

What are the symptoms of tertiary hyperparathyroidism?

A

Stones, groans, moans, bones, thrones

CKD symptoms- haematuria, proteinuria

87
Q

How do you treat tertiary hyperparathyroidism?

A

Cinacalet

Parathryoidectomy

88
Q

A patient on the ward has started developing spasms in his arms and has had a few seizures. He was recently treated for oesophageal cancer and had radiotherapy to his neck. What is the likely cause of the current symptoms?

A

Hypocalcaemia

89
Q

What are the signs and symptoms of hypocalcaemia?

A

Muscle spasms and tetany - Chovstek’s sign (inflate BP cuff and hand curls) and Trousseau’s signs (tap over facial nerve and spasms)
Seizures
Paraesthesia of toes and fingers
Increased muscle tone and reflexes

90
Q

What would you find on ECG in hypocalcaemia?

A

prolonged QT which can lead to tosades de points

91
Q

What are the causes of hypocalcaemia?

A

Low PTH- hypoparathyroidism (due to destruction of parathyroid gland- surgery, radiation to neck), congenital syndromes eg. Di-George
Secondary hyperparathyroidism picture:
- Vitamin D deficiency (Vitamin D needed to absorb calcium in the gut)- low Ca, raised PTH in response
-Renal failure- kidney can’t absorb Ca (low Ca, raised PTH in response)

92
Q

What investigations would you do for a patient with hypocalcaemia?

A

PTH- rises in vitamin D deficiency to compensate (secondary hyperparathyroidism), will be low if destruction to gland is cause
Calcium, phosphate, U&Es, FBC, bone profile, Vitamin D, Magnesium (needed for PTH)

93
Q

How would you treat hypocalcaemia?

A

Calcium gluconate- PO/IV depending on severity 10mls 10% bolus then infusion
Vitamin D supplements if needed

94
Q

How does hypoparathyroidism cause hypocalacaemia?

A

Decreased PTH- decreased absorption of Ca in the gut and decrease resorption from the bones, decreased reabsorption in the kidney –> low Ca

95
Q

What are the symptoms of hypoparathyroidism?

A 
Sx and signs of hypocalcaemia
muscle spasms and tetany- chovstek's and trousseau's sign
seizures
paraesthesia
increased tone and reflexes
prolonged QT on ECG
96
Q

What are the causes of hypoparathyroidism?

A

primary causes: autoimmune destruction, congenital syndromes e.g DiGeorge
secondary causes: Surgery to neck, radiotherapy to the neck, Mg deficiency (need Mg to use PTH)

97
Q

What would you see on initial tests in hypoparathyroidism? How would this differ from pseudohypoparathyrodism and pseudo pseudohypoparathryroidism?

A

hypoparathyroidism: PTH low, Ca low, phosphate raised (less excretion)
pseudohypoparathyrodism: resistance to PTH. PTH normal/high, Ca low (resistance), phosphate high (no effect of PTH). Sx: short metacarpals, short stature, round face
pseudopseudohypoparathryroidism: PTH normal, ca normal, phosphate normal.

98
Q

How do you treat hypoparathyroidism?

A

Calcium supplements, vitamin D supplements (calcitriol), recombinant PTH analogue
Replace Mg first if low

99
Q

What are the classic fractures associated with osteoporosis?

A

Colles (distal radius), hip, vertebra

100
Q

Name 5 risk factors for osteoporosis

A

Age - post-menopausal
Female
Low BMI/anorexic eg. athletes
Reduced mobility and activity- reduced loading
Inflammatory disease eg. RA, SLE
Smoking and alcohol
Drugs: Long term steroids , anti-oestrogen
FMH of osteoporosis
Endocrine disorders- hyperthyroidism, primary hyperparathryodism (lots of PTH causing calcium resorption), Cushing’s- cortisol drives osteoclasts

101
Q

What two scores are used in osteoporosis?

A

DEXA - T score =

102
Q

What are the treatments for osteoporosis ?

A
  1. lifestyle changes- exercise, lose weight, vitamin D and ca supplements, stop smoking, decrease alcohol consumption
  2. Bisphosphonates eg. alendronate
    HRT - oestrogen - for use in menopausal women to reduce bone resorption
    Denosumab- monoclonal antibody to slow down osteoclasts
    Teriparatide- increases osteoblast activity. Analogue of PTH.
103
Q

What hormones does the anterior pituitary produce?

A

cortisol (from ACTH), growth hormone (from GHRH and releases IGF-1), TSH (from TRH), FSH & LH (from GnRH), prolactin (release inhibited by dopamine)

104
Q

What hormones does the posterior pituitary store?

A

ADH and oxytocin

105
Q

What causes hyperprolactinaemia?

A

Prolactinoma- prolactin secreting pituitary adenoma
Dopamine antagonists eg. antipsychotics, antidepressants (stop dopamine production which usually inhibits prolactin)
Compression of pituitary stalk- non-secretory pituitary adenoma
Breastfeeding

106
Q

What symptoms/signs may you see in a patient with hyperprolactinaemia?

A

Women: infertility, amenorrhea, decreased libido (aised prolactin inhibits GnRH), galactorrhea
Men: erectile dysfunction, decreased facial hair, gynaecomastia, galactorrhea
If big adenoma: bitemporal hemianopia , headaches

107
Q

What investigations would you do in a patient with hyperprolactinaemia?

A 
Prolactin 
Pregnancy test- rule it out as a cause
FBC, U&amp;E, TFTs 
Check all other hormones (may get hypopituitarism if big tumour)- cortisol, FSH &amp; LH, TFTs, IGF-1
MRI pituitary !
108
Q

How do you treat a prolactinoma?

A
  1. dopamine agonists eg. cabergoline/bromocriptine

2. if sx fail to respond= surgical removal of adenoma

109
Q

A patient with a known pituitary adenoma presents to A&E with an short onset very severe headache. She also has neck stiffness and decreasing GCS. On visual field examination you find she has a bitemporal hemianopia. She is very unwell. Thinking of the diagnosis, what tests would you do?

A

FBC, U&E, clotting, LFTS, cortisol, TFTs, may do FSH/LH
MRI pituitary !
This is a pituitary apoplexy

110
Q

What is a pituitary apoplexy?

A

Infarction of the tumour within a pituitary gland usually secondary to HTN, head trauma, major surgery, anticoagulants but can be spontaneous

111
Q

What signs/symptoms would you see in a patient with a pituitary apoplexy?

A

Usually a known tumour
Severe, sudden onset headache, nausea and vomiting
Meningism - neck stiffness, decreasing GCS , photophobia
Bitemporal hemianopia, palsy of 3,4,6

112
Q

How do you treat a pituitary apoplexy?

A

IV saline & Hydrocortisone (replace lost cortisol) 100mg IV
Treat the cause eg. cabergoline for a prolactinoma

113
Q

What is Sheehan’s syndrome?

A

Post-partum pituitary necrosis leading to hypopituitarism

A rare type of pituitary apoplexy

114
Q

What symptoms might a patient with Sheehan’s have?

A 
Hypopituitarism 
Decreased FSH, LH = amenorrhea
Decreased prolactin= agalactorrhea
Decreased TSH= weight gain, cosntipation, cold intolerance 
Decreased cortisol and ACTH
115
Q

How do you treat Sheehan’s syndrome?

A

Replace the deficient hormones for life

116
Q

What is the cause of acromegaly?

A

Excess GH secretion from a pituitary tumour causing excess IGF-1 production from the liver which acts on the skeletal tissues

117
Q

What symptoms and signs may a patient with acromegaly present with?

A 
Large hands- 'spade like' 
Large jaw 
Thick lips and wide nose
Macroglossia
Sweating
Gigantism- if it occurs before the growth plates fuse
Bitemporal hemianopia 
Obstructive sleep apnoea- snoring 
Headaches
'Rings and shoes becoming tight'
118
Q

What are the complications that a patient with acromegaly can develop

A 
Insulin resistant diabetes (GH increases blood glucose levels and opposes insulin)
Cardiomyopathy
Hypertension
Carpal tunnel 
Colorectal cancer
Stroke
Arthritis
119
Q

What investigations would you do to diagnose acromegaly?

A

GH- not very reliable
1. IGF-1 - raised
2. OGTT - GH raised- not suppressed by glucose as it usually would be
Pituitary MRI

120
Q

How do you treat acromegaly?

A
  1. Surgical removal of pituitary tumour
  2. Somatostatin analogues eg. octreotide (decreases GH release)
    Radiotherapy- alongside medical treatment - but can cause hypopituitarism
121
Q

What are the two types of diabetes insipidus?

A

Cranial: not enough ADH production
Nephrogenic: kidneys do not respond to ADH

122
Q

What are the causes of diabetes insipidus?

A

Cranial: tumour (posterior pituitary), infection- encephalitis, meningitis, trauma
Nephrogenic: CKD, congenital, uncontrolled diabetes, lithium

123
Q

What are the symptoms of diabetes insipidus?

A

Lack of ADH –> lack of water reabsorption:
Polyuria
Polydipsia
Hypernatraemia - dehydrated

124
Q

What initial investigations would you do for diabetes insipidus? (2)

A

FBC, U&Es- hyperNa, serum calcium, creatinine

Serum and urine osmolality- serum osmolality raised, urine osmolality low

125
Q

What is the diagnostic test for diabetes insipidus?

A

Water deprivation test: there will no change in osmolality= continue to have dilute urine

126
Q

What test is used to differentiate between cranial and nephrogenic diabetes insipidus?

A

Desmopressin test- synthetic ADH
Cranial : urine osmolality rises (high)- ADH reabsorbs water so urine is concentrated
Nephrogenic: urine osmolality stays low- kidneys don’t respond to the ADH

127
Q

How do you treat diabetes insipidus- cranial and nephrogenic ?

A

Cranial: MRI pituitary & do surgery if tumour present. Give desmopressin.
Nephrogenic: treat cause, avoid precipitating drugs

128
Q

What are the signs and symptoms of hypernatraemia?

A

Dehydration- dry mucuous membranes, poor urine output, delayed CRT
Lethargy, weakness, thirst, confusion

129
Q

How do you treat hypernatraemia?

A

Give water orally if possible

IV 5% glucose 1L slowly - monitor urine output

130
Q

What are the signs/symptoms of hyponatraemia?

A 
Nausea and vomiting 
Headache
Confusion
Seizures
Decreasing GCS
131
Q

What are the causes of hyponatraemia? (hypovol, euvol, hypervol)

A

hypovolaemia: low urinary Na: diarrhoea and vomiting, pancreatitis, burns, marathon running. high urinary na: diuretics, renal failure, Addison’s disease
euvolaemic: SIADH
hypervolaemia: too much IV fluid, nephrotic syndrome, heart failure, liver cirrhosis
Drugs- diuretics, NSAIDs

132
Q

How do you treat hyponatraemia?

A

Stop hypertonic saline, and drugs
hypovolaemia: if low GCS/seizures: hypertonic saline 3% and then change to 0.9% normal saline. If no neuro sx: 0.9% normal saline - raise Na slowly.
Hypervol: fluid restrict
Treat any underlying cause eg. AI - hydrocortisone

133
Q

What happens in SIADH?

A

Excess ADH production leading to hyponatraemia. Euvolemic though because RAAS system switches off aldosterone production causing kidneys to excrete Na (and water) instead of reabsorbing- balances out.

134
Q

What are some causes of SIADH?

A 
Malignancy- ectopic ADH production from SCLC
Meningitis, encephalitis, head injury 
Stroke
Pneumonoa
Drugs- SSRIs, opiates, carbamazepine
135
Q

What would the urinary Na be in SIADH?

A

Raised

136
Q

What would the plasma and serum osmolality be in SIADH?

A

Plasma osmolality will be low

Urine osmolality will be raised

137
Q

How do you treat SIADH?

A

Fluid restriction to <1L a day- bring Na up slowly

Vaptans (ADH receptor antagonists) or demecocyline (ADH blocker)

Phase 4 (15 decks)

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