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FINALS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

 what are the symptoms of hypercalcaemia?

A

confusion hallucinations stupor fatigue and easy tiring constipation muscle weakness (from slow muscle contractions) slow or absent reflexes

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2
Q

what feature in a patient’s history may give signs of chronic hypercalcaemia?

A

a history of kidney stones

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3
Q

what is the most classic sign of hypercalcaemia?

A

Slow or absent reflexes

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4
Q

how does hypercalcaemia slow muscle contractions and reflexes

A

sodium channels are stabilised by calcium channels if there is excess calcium in the action potential is harder to reach meaning that neurons are less excitable

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5
Q

what metabolic state does hypercalcaemia predispose to?

A

metabolic acidosis

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6
Q

what features would you find on ECG of hypercalcaemia?

A

bradycardia AV block shortened QT interval

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7
Q

how do you diagnose hypercalcaemia?

A

serum calcium levels > 10.5

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8
Q

what are common causes of hypercalcaemia?

A

THe CHIMPANZEES

Thyrotoxicosis
Excess Vitamin D + A

C onsumption of calcium
H ydration (dehydration) // hyperparathyroid
I mmobilisation
M yeloma (+leukaemias)
P arathyroid cancer/ademoma
A drenal insufficiency
N eoplasm (Breast and lung + mets prostate)
(thia) Z ide diuretics
E thanol
Excess PTH
S arcoidosis
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9
Q

what is the management of hypercalcaemia?

A

increase urinary excretion by using loop diuretics (frusemide) and increasing fluids + bisphosphonates to prevent bone resorption by inhibiting osteoclastsadj. glucocorticoids (beclamethosone) -> prevent bone resorption

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10
Q

what little rhyme can help you remember the symptoms of hypercalcaemia?

A

stones bones abdominal moans , thrones and psychic groans

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11
Q

what are common causes of hypocalcaemia?

A

HPV x2

hypoparathyroidism 
vitamin D deficiency
hypo magnesium 
hyperventilation
Phosphate infusions
pancreatitis
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12
Q

what are the uncommon causes of hypocalcaemia?

A

renal failure burns and sepsis

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13
Q

w patient adjusted calcium comes back at <3mmol, are they likely to be symptomatic?

A

no

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14
Q

what is the management of the patient who presents with serum calcium of 3-3.5

A

prompt treatment with fluids and bisphosphonates

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15
Q

what is the management of a patient who presents the serum calcium of >3.5

A

urgent correction

fluids + diuretics (loop)

consider glucocorticoids

Bisphosphonates

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16
Q

what is pseudo-hypocalcaemia?

A

hypocalcaemia caused by hypo albuminemia as there is less bound calcium but ionised Calcium is the same

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17
Q

what are the symptoms of hypocalcaemia?

A

muscle cramps abdominal pain. Oral tingling seizures in extreme cases tetany with involuntary muscle contractions tachycardia brisk reflexes and abnormal ones paraesthesia numbness and tingling as well as poor memory and slowed thinking

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18
Q

what is the effect of hypocalcaemia on action potential?

A

causes neuronal Destability allowing for easier depolarisation

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19
Q

what abnormal reflexes can be seen in hypocalcaemia?

A

Chavatekes and Trousseuds

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20
Q

what ECG changes can hypocalcaemia cause

A

arrhythmias such as atrial fibrillation prolonged ST segment and prolonged QT interval

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21
Q

describe primary hyperparathyroidism

A

and endocrine disorder in which there is autonomous overproduction of parathyroid hormone resulting in deranged calcium homeostasis

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22
Q

what are the usual causes of primary hyperparathyroidism

A

parathyroid adenoma - can also be caused by radiation and lithium therapy

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23
Q

does hyperparathyroidism always cause high calcium?

A

now can also be normal cosmic despite high PTH

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24
Q

as well as the normal symptoms for hypercalcaemia what else can be present in hyperparathyroidism?

A

bone pain easy fractures and a history of osteoporosis/osteopenia

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25
Q

what bloods should you perform in primary hyperparathyroidism

A

serum calcium ( norm/+) serum intact PTH (+) serum vitamin D levels norm/low) phostphate (-)

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26
Q

after bloods lead you to suspect hyperparathyroidism what further investigations should you perform?

A

head CT for underlying adenoma and DEXAscan for bone density

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27
Q

what is the management of primary hyperparathyroidism?

A

parathyroidectomy with adjuncts of: bisphosphonates vitamin D supplements and Cinacalet (helps reduce serum calcium)

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28
Q

what all the common causes of secondary hyperparathyroidism?

A

chronic kidney disease malabsorption syndromes low vitamin D and drugs

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29
Q

how does chronic kidney disease caused secondary hyperparathyroidism?

A

diminishes parathyroid hormone effect on kidneys mean there is less calcium absorption

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30
Q

how do malabsorption syndromes lead to secondary hyperparathyroidism?

A

less calcium absorption in the GI tract means that there will be access parathyroid hormone produced

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31
Q

what things can increase the metabolic requirement of calcium?

A

bisphosphonate and growing

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32
Q

what drugs increase calcium loss?

A

loop diuretics

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33
Q

how do you diagnose secondary hyperparathyroidism?

A

low serum calcium (+) serum intact parathyroid hormone (+) phasphate (+) vitamin D + finding any underlying cause such as doing coeliac testing, U+E, imaging of parathyroid gland

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34
Q

what can help manage secondary hyperparathyroidism?

A

dietary phosphate restriction and a phosphate binder

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35
Q

what are examples of phosphate binders?

A

calcium acetate or Sevelamer

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36
Q

what are the causes of low vitamin D?

A

using SPF avoiding the sun inadequate dietary intake obesity drugs and malabsorption

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37
Q

what drugs cause low vitamin D?

A

glucocorticoids antiepileptics HAART rifampicin

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38
Q

what does low vitamin D cause in children?

A

Ricketts

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39
Q

what x-ray findings would you see for Ricketts

A

widening of endo- epithelial plates of long bones and ragged poor mineralisation

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40
Q

what does low vitamin D causing adults?

A

can cause osteopenia osteomalacia and osteoporosis however usually it is asymptomatic with some lethargy and possibly proximal muscle weakness

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41
Q

what bloods would you need to perform for vitamin D deficiency?

A

vitamin D (-) alkaline phosphate (+ in rickets or psteomalacia ) serum calcium (- long standing low vD)

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42
Q

how do you manage vitamin D deficiency?

A

ergocalciferol sensible UV exposure calcium – calcium carbonate

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43
Q

the patient presents with some lethargy and proximal muscle weakness, you perform a blood test and noticed that vitamin D is low alkaline phosphate is raised and serum calcium is low what does this mean

A

there is vitamin D deficiency which has been a long-standing causing osteomalacia

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44
Q

what does a raised alkaline phosphate mean in context of low vitamin D?

A

Ricketts or osteomalacia

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45
Q

what does a low serum calcium mean in context of low vitamin D

A

long standing low vitamin D

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46
Q

what are the causes of hypoparathyroidism?

A

post surgical genetic autoimmune

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47
Q

what is meant by postsurgical hypoparathyroidism?

A

is one of: accidental removal of parathyroid glands vascular compromise transient and hungry bone syndrome

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48
Q

why does transient postsurgical hypoparathyroidism occur?

A

in hypercalcaemia due to hyperparathyroidism tissues have suppressed and once hyperparathyroidism is corrected and the core is removed it takes a while for the parathyroid tissues to return to normal function

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49
Q

what is hungry bone syndrome?

A

hypocalcaemia and hypophosphataemia occurring after thyroidectomy or parathyroidectomy

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50
Q

a patient presents with muscle cramps abdominal pain and tingling of the skin they have brisk reflexes so you perform a full blood screen on them you find serum calcium (-) albumin (norm) parathyroid hormone (-) magnesium (slightly +) vitamin D (-) phosphurus (+) - what is the most likely diagnosis?

A

hypoparathyroidism

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51
Q

described their blood test results that you would find on hyperparathyroidism

A

calcium (-) albumin (norm) PTH (- or norm) Magnesium (inhibits PTH secretion) vitamin D (-) creatine and phosphurus (+)

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52
Q

what is the management of hypoparathyroidism?

A

PO/ IV calcium + vitamin D- if not a enough add recombinant PTH - if you notice that calcium is being lost in the urine add thiazide diuretic

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53
Q

what other causes of hypomagnesaemia?

A

loop and thiazide diuretics long-term PPI use dietary and malabsorption syndromes acutely occurs after an MRI occurs in acute pancreatitis

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54
Q

how does hypomagnesaemia affect potassium and calcium?

A

potassium: potassium efflux is increased as it is normally inhibited by magnesium calcium: low magnesium causes high calcium as calcium release is normally inhibited by magnesium however low magnesium can also cause hypo para which would cause low calcium

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55
Q

how do you treat hypomagnesaemia

A

loading dose plus IV infusion of magnesium - make sure to check renal function and stop magnesium inclusion if you notice bradycardia or hypotension

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56
Q

what diseases are associated with posterior pituitary?

A

lack of vasopressin (cranial diabetes insipidus) resistance to action of vasopressin (nephrogenic diabetes insipidus) too much vasopressin (SIA DH)

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57
Q

if you notice hyponatraemia what is one of the first steps you should do

A

note serum osmolality and thenthe hydration status as it can indicate the cause of hyponatraemia

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58
Q

what are the three types of hypotonic hyponatraemia

A

hypovolaemic hypovolaemic ebovulaemic

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59
Q

what are the causes of hypovolaemic hyponatraemia?

A

GI fluid loss mineralocorticoid deficiency and dehydration

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60
Q

what are the causes of hypovolaemic hyponatraemia?

A

AKI/CKD CHF cirrhosis nephrotic syndrome

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61
Q

what are the causes of evovulaemic hyponatremia?

A

SEI ADH high fluid low so you or electrolytes which can occur in marathon running for example medications and adrenal insufficiency beer diets

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62
Q

what medications can cause Evovolumia hyponatremia?

A

thiazide like diuretics combination diuretics loop diuretics and ACE inhibitors anticonvulsants hormonal analogues such as desmopressin and oxytocin hypnotics such as temazepam recreational drugs such as ecstasy SSRI MAOI

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63
Q

describes the homeostasis of plasma osmolality?

A

osmolality gets too low thirst is suppressed and vasopressin is suppressed this dilutes your in increasing osmolality there is then negative feedback on the posterior pituitary

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64
Q

describe the renin angiotensin aldosterone system

A

when blood pressure is too low, or salt (NaCl) or circulating vol decreases the perfusion to the juxtoglomerlular apparatus decreases / this causes an increase on the production of renin by the kidneys/ renin converts angiotensinagen to angiotensin I/ ace is secreted by the surface of the pulmonary and renal endothelium which then converts angiotensin I –> angiotensin II / angiotensin II increases sympathetic activity increases tubular salt reabsorption and potassium excretion as well as water retention it causes the adrenal gland cortex to secrete furthera ldosterone which further propagate this / it causes arteriolar vasoconstriction causing an increase in blood pressure and an increase in the pituitary glands of posterior lobe antidiuretic hormone secretion causing water absorption from the collecting duct of the kidney all of this causes water and salt retention effective circulation volume increase and increases the perfusion of the juxta glomeruli apparatus which then causes negative feedback on the kidneys

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65
Q

what is the presentation of hyponatraemia?

A

mild cognitive symptoms: confusion headache and balance low in urine output, hypovolaemia and hyponatraemia dizziness fatigue nausea and profuse sweating hyponatraemia predisposes to seizures

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66
Q

what is a consequence of hyponatraemia occurring rapidly less than 48 hours

A

causes cerebral oedema

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67
Q

what is the presentation of cerebral oedema caused by hyponatraemia?

A

altered mental status seizures coma

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68
Q

what is the immediate management of cerebral oedema caused by hyponatraemia?

A

medical emergency requiring hypertonic 3% saline

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69
Q

after assessing volume status what is the next step in finding the cause of hyponatremia

A

checking urine sodium and urine osmolality

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70
Q

if a patient is hypervolaemic in the urine sodium is less than 20 what is the likely cause

A

heart failure cirrhosis or nephrotic syndrome

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71
Q

if the patient is hypervolaemic and the urine sodium is over 20 is the most likely cause?

A

chronic renal failure

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72
Q

the patient is Euvovolumic and the osmolality is high what is the most likely cause?

A

SIADH + drugs

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73
Q

the patient is Euvovolumic and the osmolality is variable what is the most likely cause?

A

prolonged exercise or high fluid intake

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74
Q

the patient is Euvovolumic and the osmolality is high what is the most likely cause?

A

primary polydipsia or potomania

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75
Q

the patient is hypovolumic and urine sodium is less than 20 what is most likely cause

A

non-renal sodium losses

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76
Q

the patient is hypovolumic and urine sodium is less than 20 what is most likely cause

A

renal sodium losses

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77
Q

for a patient to be evolaemic what should the urine sodium be like

A

over 20

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78
Q

if there is hyponatraemia and serum osmolality is high what the most likely causes

A

hyperglycaemia and hypertonic fluid administration

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79
Q

if there is hyponatraemia and serum osmolality is normal what is the most likely cause

A

pseudo-hyponatraemia is the most common cause of isotonic hyponatraemia

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80
Q

describes the steps of the investigation of hyponatraemia?

A
  1. serum sodium
  2. serum osmolality IF HYPOtonic
  3. volume status
  4. Urine sodium to assess cause
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81
Q

Apart from assessing serum osmolality and urine sodium what other tests should be performed in a person with hyponatraemia? And why?

A

glucose test – hypoglycaemia associated with low sodium thyroid function test – hypothyroidism needs to be excluded in order to diagnose NSAID H serum cortisol – excludes adrenal insufficiency serum lipids – high lipids means pseudo-hyponatraemia

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82
Q

What is the first step of management of acute hyponatraemia?

A

IV hypertonic saline line over 20 minutes regularly check sodium and repeat IV infusions of 3% hypotonia say line over 20 minutes until there is a 5mm/L increase in sodium

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83
Q

after you have managed to get sodium to increase by 5mmol/l what is the next step in the management of hyponatraemia?

A

stop infusion and start an IV line of not .9% say line on minimum volume find and manage the underlying cause

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84
Q

at what rate should sodium levels increase during the first 24-hour is after initial stabilisation? And what about after the first 24 hours?

A

increased to 10mmol/l and then an increase of 8mmol/lUNTIL 130mmol/l

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85
Q

how often should you check sodium whilst the stabilising hyponatraemia?

A

initially check after every IV infusion once initial stabilisation has occurred checked every six , 12 hours and then daily

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86
Q

what are the risks associated of to too rapid an increase in sodium in the management of hyponatraemia?

A

predisposes to central pontine myelinosis and cerebral oedema (causing osmotic demylination)

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87
Q

what is central pontine myelinosis

A

brain damage caused by pseudo-bulbar and pons demyelination in the cortico spinal and cortico bulbar tracts

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88
Q

what is the presentation of central pontine myelinosis

A

spastic quadriplegic confusion horizontal gaze paralysis mutism this is called locked in syndrome occurring over 48 – 72 hours

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89
Q

apart from medical management causing central pontine myelinosis what else can cause this?

A

beer potomania the rapid and consecutive drinking of bacon drop sodium very low leading to locked-in syndrome

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90
Q

what is SIADH?

A

syndrome of inappropriate antidiuretic hormone - too much antidiuretic hormone is secreted this impairs urinary excretion leading to fluid retention

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91
Q

where does antidiuretic hormone target in the kidneys?

A

the distal convoluted tubule and the collecting ducts is where there is the actual antidiuretic hormone causing fluid retention

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92
Q

what type of hyponatraemia does SIADH cause?

A

evolumic hypotonic hyponatraemia

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93
Q

what is another name for antidiuretic hormone

A

vasopressin

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94
Q

what are causes of SIADH?

A

malignancy including SCLC GI pulmonary infections CNS disorders such as infections MS GBS drugs such as SSRI amitriptyline amiodarone carbamazepine

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95
Q

if you suspect SIA DH what blood test must you perform in order to get the diagnosis?

A

after finding out the type of hyponatraemia by using serum osmolality and urine sodium check diode function and serum cortisol as SIA DH is a diagnosis of exclusion

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96
Q

how do you manage S IAD H

A

treat hyponatraemia with acute treatment and chronic management

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97
Q

what is a chronic management of hyponatraemia

A

loop diuretics if caused by chronic heart failure own erotic syndrome Spironolactone caused by cirrhosis vasopressin receptor agonists are usually used second line

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98
Q

what is the definition of hyprenatraemia

A

serum sodium concentration of over 145 mmol /l

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99
Q

what other three types of causes of hypernatraemia

A

free water loss deficit in water losses sodium losses

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100
Q

what is the most common cause of hypernatraemia

A

dehydration

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101
Q

what is meant by free water loss causes of hypernatreamia

A

GI losses insensible losses and sweat renal concentrating defects osmotic diuresis diabetes insipidus

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102
Q

what is meant by deficit in water losses causes of hypernatraemia?

A

inability to drink water impaired thirst mechanism from brain tumours general lack of drinking

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103
Q

what is meant by sodium losses causes of hypernatraemia

A

hypertonic fluids excess sodium ingestion mineralocorticoid excess in Cushing’s or primary aldosteronism

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104
Q

in severe hypernatremia what is a consequence of its

A

acute cerebral shrinking

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105
Q

what is the presentation of hypernatremia

A

feelings of thirst weakness nausea and loss of appetite if more severe muscle twitching confusion + intracranial haemorrhage

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106
Q

which individuals most at risk of developing hypernatremia

A

patient of older age especially if living in a care home as they tend to get hypovolaemic

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107
Q

what investigation should you perform in hypernatremia?

A

U+E -? Renal impairment urine osmolality serum osmolality urine electrolytes and outputs

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108
Q

if urineosmolality is High Street higher than plasma osmolality what is the most likely aetiology

A

pure volume depletion from GI or insensible losses

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109
Q

if urine osmolality is the same as plasma osmolality what is the most likely cause

A

renal concentration defects such as renal failure osmotic diuresis or use of diuretics

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110
Q

what is the management of hypernatremia

A

give IV fluids loop diuretics if caused by yet eugenic causes or mineralocorticoid excess this is usually the case if the patient is hyper volumic

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111
Q

what is diabetes insipidus

A

metabolic disorder characterised by the inability to concentrate urine

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112
Q

what is the classic triad associated with diabetes insipidus

A

inapropiately dilute urine polyuria polydipsia

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113
Q

what are the two types of diabetes insipidus

A

central and nephrogenic

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114
Q

describe central diabetes insipidus

A

has an absolute or relative deficiency of AVP causing a reduced permeability of ducks within the nephron towards the reducing water resorption and increasing water loss

115
Q

what are some causes of central diabetes insipidus

A

pituitary surgery can be transient or long lasting crania for NGO ma post traumatic head injury due to lesions CNS infections vascular compromise – subarachnoid haemorrhage phenytoin or congenital/genetic mutations

116
Q

describe nephrogenic diabetes insipidus

A

renal and sensitivity or resistance to AVP reducing the permeability of ducts within the nephron to water reducing water resorption and increasing water loss

117
Q

what are some causes of nephrogenic diabetes insipidus

A

lithium gentamicin rifampicin systemic disease electrolyte abnormalities kidney disease obstruction

118
Q

what is an important measurement in the investigations of diabetes insipidus

A

measuring urine volume diabetes in separatists is unlikely if your volume is less than 3 L

119
Q

what is the electrolyte abnormality of diabetes insipidus

A

hypernatremia - any other electrolyte abnormalities suggests a different diagnosis

120
Q

describe the findings of urine and serum osmolality in a patient with diabetes insipidus

A

serum osmolality is raised and urine is low

121
Q

deviations and diabetes insipidus always have to be hypernatraemia

A

now sodium levels can be normal if they are managing to appropriately rehydrate

122
Q

what is a diagnostic test for diabetes insipidus

A

water deprivation test

123
Q

describe the results of the water deprivation test in diabetes insipidus

A

by starving a patient of water the normal physiological response is to keep the plasma osmolality equal but increase your in osmolality in diabetes insipidus the urine osmolality will remain on concentrated i.e. low

124
Q

how do you differentiate between central and nephrogenic diabetes insipidus

A

desmopressin challenge test

125
Q

describe a desmopressin challenge test and its results

A

by giving desmopressin you can differentiate between central and nephrotic because in central the euro and osmolality will increase as a VP will increase however in nephrogenic urine osmolality will stay the same as the kidneys remain insensitive to AVP

126
Q

after correcting hyponatraemia with fluids what is the management of diabetes insipidus?

A

Central: give desmopressin peripheral: sodium restriction and thiazide diuretics treat any underlying causes

127
Q

what are the types of adrenal insufficiency?

A

primary - adrenal cortex failure secondary pituitary or hypothalamus tertiary chronic glucocorticoid administration

128
Q

what other symptoms of adrenal insufficiency

A

fatigue lack of energy weight loss tan on skin postural hypotension cramps in legs

129
Q

what feature of adrenal insufficiency would you find primarily in primary adrenal insufficiency

A

skin pigmentation especially on palms scores and mucosa

130
Q

when would you find alabaster pale skin pigmentation in the context of adrenal insufficiency

A

if secondary: pituitary or hypothalamus

131
Q

how does adrenal insufficiency cause postural hypotension

A

mineralocorticoid or glucocorticoid deficiency causes this

132
Q

why is primary adrenal cortex failure dangerous

A

involves all the steering production reducing it so blood pressure and U+E are not properly regulated

133
Q

what features of an adrenal crisis

A

abdominal pain abdominal tenderness guarding and vomiting fever confusion somnolence delirium coma

134
Q

what electrolyte abnormalities might be present in adrenal insufficiency

A

hyponatraemia hyperkalaemia possibly hypercalcaemia

135
Q

Howard ran in and out this year own levels change in adrenal insufficiency caused by cortex failure

A

increase in running decreasing out the steering

136
Q

what is a diagnostic test for adrenal insufficiency

A

morning cortisol - if less than 350 adrenal insufficiency is probable greater than 430 is unlikely to be an adrenal crisis

137
Q

after you note that morning cortisol is low what further diagnostic test should be performed in the context of adrenal insufficiency

A

ACTH stimulation test a.k.a. short synactin test

138
Q

describes ACTH stimulation test

A

ACTH is injected and the amount of cortisol produced is measured in primary there is no response (the adrenal cortex itself cannot make the cortisol) in secondary if it is not too severe there will be an increase in cortisol as pathology is in the tutorial hypothalamus

139
Q

what is the management of adrenal insufficiency

A

ongoing glucocorticoid and mineralocorticoid replacement

androgen replacement therapy if decreased libido

140
Q

what is an adrenal crisis

A

extremely low value of cortisol bare mind in the context of physiological stress a value of less than 500 nmol/l is diagnostic

141
Q

what is the treatment of adrenal crisis

A

IN hydrocortisone 100 mg followed by 200 mg infusion over 24 hours plus IV .9% saline

142
Q

what patient education regarding adrenal crises should be given to patients with adrenal insufficiency

A

the six-day rule if unwell double the dose of PO glucocorticoids parenteral administration during prolonged vomiting or diarrhoea and give an emergency hydrocortisone kit

143
Q

described Cushing’s syndrome

A

the clinical manifestation of pathological hypercorticonsim from any cause.

144
Q

what all causes of Cushing’s

A

pituitary adenoma, adrenal adenoma exogenus causes alcoholism physiological stress pregnancy and malnutrition

145
Q

what is the physical presentation of Cushing’s?

A

a.k.a. facial plethora acne thinning hair main face increased facial hair easy bruising weight gain purple striae pendulous abdomen slow wound healing swelling of feet/legs a.k.a. peripheral oedema in arms and legs with weak bones supra-clavicular fullness a.k.a. buffalo hump

146
Q

what are the signs of Cushing’s

A

hypertension poor short-term memory. Even see poor concentration menstrual irregularity glucose intolerance headaches insomnia prepare an infection and depression

147
Q

how does Cushing’s tend to present in children

A

may have pubertal abnormalities

148
Q

how do you diagnose Cushing’s?

A

serum and urine cortisol will be elevated first-line diagnostic test is late night library cortisol

149
Q

if cortisol is increased what is the next investigation which you should perform and you suspect cushings?

A

dexamethasone suppression test

150
Q

describe the dexamethasone suppression test

A

1 mg of dexamethasone overnight and early morning cortisol is measured. In people without Cushing’s cortisol should be below as dexamethasone suppresses ACTH however in individuals with cuttings cortisol will remain high

151
Q

A patient presents with

increased fat on your chest and tummy, but slim arms and legs
a build-up of fat on the back of your neck and shoulders, known as a “buffalo hump”
a red, puffy, rounded face

you run serum cortisol and it comes back +++

whats your next Ix?

A

pituitary MRI or adrenal CT to check for pituitary or adrenal adenoma

152
Q

describe the HPA axis

A

hypothalamus secretes corticotropin releasing hormone which stimulates the anterior pituitary to release adrenocorticotropic hormone which stimulates the adrenal cortex to produce cortisol which has negative feedback on the hypothalamus’s production of CRH and the pituitary production of ACTH

153
Q

what is the management of Cushing’s syndrome?

A

if endogenous surgery for the tumour medical therapy can be used to surgery is not yet advised or contraindicated and is used in the interim period between diagnosis and surgery - somatostatin analogues are used (pasireotide)

154
Q

what is supposed surgical management of a patient who underwent surgery for Cushing’s disease?

A

steroids given for about a week after surgery then if total pituitary removal has occurred give levothyroxine testosterone if male oestradiol and medroxyprogesterone for female consider giving somatotropin and desmopressin necessary

155
Q

what is a prolactinoma

A

one of the most common types of pituitary adenoma, accounting for 40% of all pituitary adenomas is more common in females

156
Q

what features of prolactinoma typical for females

A

amenorrhoea and galactorrhea

157
Q

what features of a prolactinoma typical for males

A

erectile dysfunction hypogonadism and gynaecomastia

158
Q

what are the classic symptoms of a pituitary adenoma/prolactinoma

A

visual disturbances by temporal hernia nuclear osteoporosis headaches and loss of libido + sex organ fueatures

159
Q

here is more likely to present between postmenopausal and premenopausal women with a prolactinoma and why

A

premenopausal women are more likely to present earlier because they will experience early symptoms of a prolactinoma which on menstrual irregularities everyone else will present later when this starts to become compression of the optic hires and causing visual disturbances

160
Q

what investigations are diagnostic for a prolactinoma

A

serum prolactin (+++) pituitary MRI

161
Q

what is a management or prolactinoma

A

dopamine agonist —> surgery and radiotherapy ( presurgery you can add a COC key to control symptoms of a prolactinoma in premenopausal females)

162
Q

What is PCOS

A

defects in the HP PA access causes hyper- androgynous them through ovaries and adrenal glands causing a variety of symptoms including infertility

163
Q

what are the symptoms of PCOS

A

hertuism acne infertility regular menses weight gain hypertension

164
Q

what blood tests should be performed in ?pcos

A

serum prolactin(norm or +) serum testosterone (++) FSH (norm or - )and LH (+) fasting glucose (norm or +) fasting lipids(+)

165
Q

what blood test should be performed in PCOS to exclude differentials? And what are those differentials?

A

Serum 17 hydroxy progesterone – excludes adrenal hyperplasia where it would be elevated serum TSH – excludes thyroid dysfunction

166
Q

what is the management approach to PCOS?

A

manage the symptoms of PCOS such as infertility irregular periods acne hirtuism

167
Q

after finding blood results which are indicative of PCOS what further investigation would you perform

A

pelvic ultrasound scan: polycystic ovaries in 75% of patients

168
Q

what is the diagnostic criteria for PCOS

A

two out of three features of: irregular periods features of hyper androgenism (+/- lanb confirmation) ovarian cysts on ultrasound

169
Q

how would you manage infertility in an individual with PCOS

A

encourage weight loss if there is a high BMI –> clomiphene (+adj Metformin +/- dexamethasone +/- spironolactone) –> gonadotropins –> IVF

170
Q

how would you manage dysmenorrhoea in PCOS

A

cyclic progestin (then USS to measure endometrial thickness if normal roceed otherwise biospy for?endomerial cancer) –> COCP/ IUS/ POP —> metformin

171
Q

how you manage acne in PCOS

A

COCP –> top Abx –> top retinoids etc (Mx for acne vulgaris)

172
Q

how do you manage hyperandrogenism in PCOS

A

COCO —> antiandrogen —> combination therapy –> GnRH + COCP (adj. metfirmin all way through can be added)

173
Q

how does clomiphene work

A

helps release more FSH and LH thus inducing ovulation

174
Q

how does Spironolactone work in terms of PCOS management

A

has antiandrogen properties

175
Q

how does metformin work in terms of PCOS

A

reduces insulin levels and helps weight loss reducing testosterone levels and also helps stimulate monthly periods

176
Q

what drugs can cause weight gain

A

diabetic therapies: insulin metformin psychiatric: TCA SSRI lithium atypical and typical antipsychotics mood stabilisers plus carbamazepine and gabapentin / corticosteroids/ hormonal contraception / NSAIDs antihistamines especially diphenhydramine beta-blockers ACE inhibitors ARB calcium channel blockers

177
Q

what drugs can cause hertuism

A

anabolic steroids metoclopramide Meath although part progestins phenothiazines testosterone

178
Q

what is the difference between hirtuism and hypertrichosis

A

the excessive growth of hairs on androgen -dependent areas is heirtuism generalised overgrowth of her everywhere is hypertrichosis

179
Q

what drugs can cause hypertrichosis

A

cyclosporine hydrocortisone minoxidil penicillamine phenytoin streptomycin

180
Q

what value of hyperkalaemia is considered severe

A

> 6

181
Q

what other symptoms of hyperkalaemia

A

muscle weakness fatigue and arrhythmias which can be fatal

182
Q

what other ECG changes which you would see on hyperkalaemia

A

loss of P wave tall peaked T waves widen to QRS

183
Q

what are the causes of hyperkalaemia

A

excessive potassium intake ineffective potassium renal excretion from renal impairment hormonal causes intracellular potassium release medications pseudo-hyperkalaemia

184
Q

what are the causes of pseudo- hyperkalaemia

A

haemolysis during venipuncture thrombocytosis leucocytosis polycythaemia

185
Q

what other medications which cause hyperkalaemia?

A

ACE inhibitors Spironolactone NSAID cyclosporinetracolimus trimethoprim heparin

186
Q

what are the hormonal causes of hyperkalaemia

A

Addison’s congenital adrenal hyperplasia of the steering deficiency

187
Q

how do you treat hyperkalaemia

A

insulin and Ivy glucose unless there are severe arrhythmias then add calcium gluconate (doesn’t change potassium but stabilise the heart)

188
Q

how do ACE inhibitors cause hyperkalaemia

A

lowers aldosterone leading to decreased potassium excretion

189
Q

how does congenital adrenal hyperplasia or aldosterone deficiency cause hyperkalaemia

A

leads to loss of aldosterone causing decreased potassium excretion

190
Q

how does the spironolactone cause hyperkalaemia

A

it is a potassium sparing diuretic

191
Q

how does Hartmann’s solution because hyperkalaemia

A

contains potassium

192
Q

what all causes of hypokalaemia

A

increased other steering diuretics hypomagnesaemia renal tubular acidosis metabolic alkalosis decrease oral intake vomiting or diarrhoea fistulas insulin alkalosis

193
Q

how does insulin cause of hypokalaemia

A

drives potassium into cells

194
Q

what is hypothyroidism

A

a clinical state resulting in the under production of thyroid hormones T4 and T3

195
Q

describe secondary hypothyroidism

A

failure of the anterior pituitary to release TSH

196
Q

what are causes of hypothyroidism

A

autoimmune – Hashimoto’s (most common) thyroidectomy radiotherapy radioactive iodine therapy (using graves or nodular goitre) infiltrative disease such as sarcoidosis drugs

197
Q

what drugs cause hypothyroidism

A

lithium amiodarone + others not v common

198
Q

describes the thyroid hormone axis

A

the hypothalamus produces TR H which stimulates the pituitary gland to release TSH which causes the thyroid gland to produce T4 and T3 any teeth for produced is converted in the peripheral tissues to T3 high levels of T4 and T3 was negative feedback on both hypothalamus and pituitary

199
Q

describes the process of making thyroxine from thyroid follicles

A

a sodium iodine co-transporter transports sodium and iodine from the blood into the thyroid follicle the endoplasmic reticulum causes thyroglobulin secretion which then through XO psychosis is transported out of the thyroid follicular cell iodine moves through the thyroid follicular cell and through a pendrin transporter is transported out of the thyroid follicular cell into the follicle colloid where it is oxidised and joins with the thyroglobulin which has been released after this conjugation it moves from the follicle colloid back into the thyroid follicular cell to endocytosis through proto-losses it is cleaved into two molecules one of which is thyroxine this is then transported out through a transporter into the blood

200
Q

what are some transient causes of hypothyroidism

A

subacute granulomatous thyroiditis postpartum lymphatic thyroiditis

201
Q

what are the symptoms of hypothyroidism

A

weakness lethargy cold sensitivity constipation weight gain depression menstrual irregularity myalgia trial course gain eyelid oedema facial thickening thick tongue because her deep voice bradycardia delayed relaxation of tendon reflexes and rarely a goitre

202
Q

how do you investigate hypothyroidism

A

measure serum TSH and T4 also measure antithyroid peroxide antibodies (autoimmune cause such as Hashimoto’s)

203
Q

why is doing a U+E important in hypothyroidism

A

can cause hyponatraemia

204
Q

what is the management of hypothyroidism

A

levothyroxine unless it is a subclinical value or there is a history of coronary artery disease then gave low dose levothyroxine

205
Q

what is a myoxedemic coma?

A

a rare but life-threatening disorder caused by decompensated hypothyroidism

206
Q

what usually triggers a myoxedemic coma?

A

infection especially lung and urinary stroke surgery trauma drugs

207
Q

what are the symptoms of myoxedemic coma?

A

weakness hypothermia facial Tonga and lower leg oedema hypotension reduced consciousness hypercapnia progressing to hypocapnia and myoxedema

208
Q

what test should you always perform in myoxedemic coma?

A

thyroid function blood glucose and U+E for hyponatraemia

209
Q

what is the management of myoxedemic coma?

A

IV fluids and eelectrolyte correction IV thyroid hormone and cortisol mad blood glucose and hypothermia - hyponatraemia merged with hypertonic saline

210
Q

what is the most common cause of hyperthyroidism

A

graves disease

211
Q

what is Graves’ disease

A

and autoimmune condition attacking thyroid gland where TSH receptor antibodies because of overproduction of iodine and thus thyroid hormone

212
Q

what are causes of hyperthyroidism

A

graves toxic multi-nodular goitre iodine amiodarone

213
Q

how do toxic multi-nodular goitres cause hyperthyroidism

A

rogue nodules produces excess T3 and T4 or there is an adenoma secreting T3 and T4 this is known as a toxic adenoma

214
Q

how does excess iodine intake cause hyperthyroidism

A

used in thyroid synthesis (can be found in radio contrast agents)

215
Q

how does amiodarone cause hyperthyroidism

A

destruction of the thyroid cells and thyroiditis causing leakage of thyroid hormone

216
Q

what is the presentation of hyperthyroidism

A

weight loss tachycardia anxiety tremor heat intolerance sweating diarrhoea protruding eyes menstrual disturbances palpitations hair loss

217
Q

on examination what features may you find in tacky cardiac

A

enlarged thyroid gland or goitre lid lag incomplete eye movements due to orbitopathy

218
Q

if on examination you find a diffuse goitre what does this indicate

A

Graves’ disease

219
Q

what blood tests should you perform for hyperthyroidism

A

TSH (-) T3 T4 (+) TSH receptor antibodies (Graves)

220
Q

after finding increased levels of T3 T4 and decreased levels of TSH on a blood test what further investigations should you do

A

check for antibodies then also do a radioactive I dine or technetium scan or a thyroid ultrasound scan

221
Q

what would radioactive iodide or technetium scan show in hyperthyroidism

A

increased generalised uptake of radioactive iodine quartet nation shows grades if however uptake is in multiple focal spots it shows multi-nodular goitre focal spot shows adenoma thyroiditis or leakage would show uptake outside of the thyroid

222
Q

what is the management of hyperthyroidism

A

start symptomatic therapy of propranolol ( can use radioactive iodinebut this is used in pregnancy )ongoing management with carbimazole , surgery is used if there is relapse after trial of carbimazole

223
Q

what is the principle of management with carbimazole in

A

either titrate the dose up until you reach satisfactory T3 T4 or completely block the production of T3 T4 (this is done in Graves’ disease and then replace with thyroid hormone) after a course of treatment stop and sometimes it goes back to normal

224
Q

what drug is required in a thyroid storm?

A

propylthiuracil

225
Q

how would you treat orbitopathy/ thyroid disease

A

methylprednisolone

226
Q

describe thyroid disease

A

condition in which the eye muscles eyelids to glance in fatty tissues behind eyes become inflamed

227
Q

describe pre-tibial myexodema

A

skin manifestation of graves due to infiltrative deposition caused by the autoimmune nature of the disease

228
Q

what is acropathy

A

a dermopathy associated with Graves’ disease it is characterised by soft tissue swelling of the hands and clubbing of the fingers

229
Q

what are side effects of thionamides

A

are generally well tolerated but commonly cause a rash and less commonly cause arthralgia hepatitis neuritis thrombocytopenia and vasculitis symptoms usually occur within the first few months but resolved after stopping the drug

230
Q

what is thyrotoxicosis

A

extreme hyperthyroidism

231
Q

what is the management of thyrotoxicosis

A

high dose propylthiouracil I the hydrocortisone, esmolol Iv or immidiate relese propranolol + lugol solution

232
Q

what is lugol solution

A

iodine/potassium iodide used to avoid exacerbations

233
Q

how can cholestryramine help in thyrotoxicosis

A

helps reduce enterohepatic circulation of TSH and reduces thyroid hormone secretion

234
Q

what is acromegaly

A

a rare chronic disease caused by excessive secretion of growth hormone usually due to pituitary somatotropin adenoma

235
Q

what usually causes acromegaly

A

pituitary tumour

236
Q

what is the presentation of acromegaly

A

profuse sweating acral growth coarsening of facial features and a history of carpal tunnel syndrome, arthralgia, glucose intolerance or diabetes, amenorrhoea hypertension and sleep apnoea may be present

237
Q

what is the picture below show

A

acromegaly

238
Q

describes theHPG axis

A

hypothalamus produces GHRH this stimulates the pituitary to produce growth hormone HRH the hypothalamus is also stimulated by Ghrelin produced by the stomach in response to stress amino acids or hypoglycaemia. GH produced by the pituitary goes to the muscles adipose tissue producing free fatty acid growth plates and liver the growth plate and liver produce IGF one which causes cell differentiation and proliferation and also causes negative feedback on the pituitary and hypothalamus growth hormone also produces negative feedback on the hypothalamus and somatostatin also produces negative feedback on the hypothalamus

239
Q

described the blood tests required in acromegaly

A

measure IGF -! (++) be aware that other states like adolescents also increase this GH (++) OGTT can be raised if the growth hormone levels are normal on blood test an abnormal GTT can be partially diagnostic

240
Q

after performing blood tests for acromegaly what is the next step in the diagnosis

A

pituitary MRI or CT finding the underlying cause

241
Q

what is the management of acromegaly

A

surgical but somatostatin analogues can be used to reduce hypothalamic GHRH ( they are GHR agonists) dopamine agonists can be used as adjuncts to increase IGF responsiveness

242
Q

how does anabolic steroid use affect the HPT - gonad axis

A

testosterone is responsible for adrenergic and anabolic functions it causes negative feedback on the axis and suppresses GNR HLH and FSH, anabolic steroids

243
Q

what are male features of anabolic steroid use

A

testicular atrophy decreased sperm count and motility impotence acne and oily skin irreversible gynaecomastia high voice

244
Q

what are the female features of anabolic steroid use

A

acne and oily skin menstrual abnormalities changes in libido hirtuism male pattern baldness deep voice clitoral hypertrophy

245
Q

what are endocrine myopathies

A

hormonal imbalances causing atrophy and muscle weakness mainly causing proximal myopathy

246
Q

what are symptoms of endocrine myopathies

A

muscle stiffness cramps slowed reflexes and in severe cases muscle breakdown

247
Q

what are the most common causes of endocrine myopathies

A

hyper and hypothyroidism and parathyroid disorder

248
Q

how does hyperthyroidism cause proximal myopathies

A

thyroxine in excess is toxic to neuromuscular junctions

249
Q

how does hypothyroidism cause proximal myopathies

A

not well understood - to do with thyroxines role in metabolic cellular function leading to abnormal gluconeogenesis and insulin resistance leading to muscle atrophy

250
Q

how does parathyroid disorder cause proximal myopathies

A

causes hypercalceamia + hypomagnesemia which leads to proximal myopathy

251
Q

what are carcinoid syndromes

A

XS seratonin and other vasopeptides are released from carcinoid tumoir

252
Q

where do most carcinoid tumours occur

A

midgut neuroendocrine tumours

253
Q

what does the picture below show

A

facial flusching associated with carcinoid tumours

254
Q

what is the common presentation of carcinoid tumours

A

facial flushing diahhorea which is v long standing (years) plus… tachycardia abdominal cramipng and signs of RSHF

255
Q

what does RSHF mean in the context of carconoid tumours

A

that cardinoid heard disease is occuring

256
Q

how do you diagnose carcinoid syndrome

A

imaging and biopsy + urinary 5 hydroxyindoleacelic acid (++) - an indicative factor

257
Q

What is Conns disease?

A

aka Primary aldosteronism. A common and specifically treatable cause of hypertension

258
Q

What is the pathophysiology of primary aldosteronism?

A

XS aldosterone means there is XS sodium (+ Cl-, K+ excretion and H2O is retained in tubule so XS urine) reabsorbtion leading to hypertension and decreased RAAS activation

259
Q

What metabolic abnormalities does Conns disease cause?

A

hypernatremia, hypokalemia (metabolic acodosis!!)

260
Q

What is the presentation of Conns disease?

A

Hypertension and strong family history of hypertension Nocturia and polyuria + symptoms of hypernatremia - irritability difficulty concentrating, anxiety depression, feelings of thirst, –> muscle twitching and confusion

261
Q

what is the diagnostic investigation of Conns disease?

A

aldosterone/renin ratio with confirmation using fludrocortisone suppression test

262
Q

describe the fludrocortisone suppression test?

A

fludroCortisone administered over four days then upright plasma aldosterone is measured if there is failure to suppress the steering and plasma cortisol is lower at 10 AM then it is at 7 AM with correction in potassium then it is a positive diagnosis for conns disease

263
Q

why does plasma cortisol have to be lower at 10am than 7 AM to be a positive diagnosis for conns disease?

A

because acute ACTH rise from another pathology prevents aldosterone suppression (so wouldn’t be 1ry hyperaldosteronism)

264
Q

after a positive fludrocortisone test what is the next step in the investigation for Conns?

A

Adrenal CT - aldosterone producing tumour / genetic testing - familial PA

265
Q

what is the management of conns?

A

spironolactone - aldosterone antagonist + surgery if applicable

266
Q

what drugs cause hirtuism?

A

anabolic steroids / testosterone/ glucocorticoids / cyclosporin/ phenytoin

267
Q

What is pituitary apoplexy

A

infarction or haemorrhage into a pituitary tumour which causes extremely low levels of ACTH and cortisol

268
Q

what is the biggest risk of pituitary apoplexy

A

acth and cortisol can cause circulatory collapse

269
Q

what is the presentational pituitary apoplexy

A

the presentation is similar to a subarachnoid haemorrhage

270
Q

what structures would surround the pituitary gland and could get compromised in pituitary apoplexy

A

optic nerves lateral to the pituitary and the chiasm is superior

271
Q

what is the investigation is required for pituitary apoplexy

A

pituitary screen and CT head may be needed as Px is similar to SAH

272
Q

what is tested in a pituitary screen

A

LH FSH TSH T4 T3 cortisol prolactin ACTH- if possible

273
Q

what is the first line management of pituitary apoplexy

A

IM/Ivy hydrocortisone for adrenal failure which occurs in apoplexy

274
Q

what is a pheocytochroma?

A

tumour arising from the catecholamine producing chromaffin cells of the adrenal medulla

275
Q

what do chromaffin cells of the adrenal medulla produce

A

adrenaline and noradrenaline and rarely dopamine

276
Q

who is a typical patient which gets a pheocytochroma?

A

young adults/teenagers

277
Q

What is a presentation of a pheocytochroma?

A

headaches palpitations diaphoresis hypertension very high which is sustained and paroxysmal

278
Q

what is a consequence of pheocytochroma?

A

hypertensive retinopathy

279
Q

what is a first line management for suspected pheocytochroma?

A

ASAP alpha blockers - phentolamine until BP is stabalised

280
Q

what is contraindicated in the acute management of pheocytochroma?

A

beta-blockers in the acute phase of the management of pheocytochroma beta-blockers or worsen the hypertension

281
Q

what is the ongoing management of pheocytochroma?

A

alpha blocker and beta-blocker hydration and a high salt diet ( can give adjacent calcium channel blocker) definitive management is with surgery

282
Q

how would you diagnose a pheocytochroma?

A

24-hour urine collections of catecholamines genetic testing required to rule out SD HB MRI/CT

283
Q

in an acute presentation of pheocytochroma what test should you do?

A

serum free metanephins and normetanephins (both +++) +/- CT

FINALS (24 decks)

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