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AA Y4 Finals cards NE > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what HbA1c level is classed as pre-diabetes?

A

42-47mmol/l

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2
Q

what HbA1c level is suggestive of diabetes?

A

> 48mmol/l

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3
Q

in a T2DM patient taking metformin, what is the target range for HbA1c?

what should HbA1c raise to before you add in a second drug?

A

you can titrate up metformin and encourage lifestyle changes up to an HbA1c of 48mmol/l

HbA1c should rise to 58mmol/l before you add in a second drug

ie- metformin target range is up to 58mmol/l

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4
Q

in T2DM, what is the initial target weight loss in an overweight person?

A

5-10% loss

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5
Q

what dietary advice should be given to someone with T2DM?

A
  • high fibre, low glycemic source of carbs
  • ## low fat dairy products and oily fish
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6
Q

how often should HbA1c levels be checked?

A

every 3-6 months till stable, then 6 monthly once stable

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7
Q

at what HbA1c level should metformin be started?

A

metformin should be started if the HbA1c rises to 48mmol/l despite lifestyle interventions

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8
Q

name the 4 drugs that can be started in combination with metformin in T2DM?

A
  • sulphonylureas
  • gliptin
  • pioglitazone
  • SGLT-2 inhibitor
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9
Q

when should a 3rd drug be added in T2DM management?

A

if the HbA1c rises to, or remains above, 58mmol/l

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10
Q

name the 3 ways in which metformin works?

A
  1. increases insulin sensitivity
  2. reduces gluconeogenesis in the liver
  3. may reduce absorption of carbs from GIT
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11
Q

what is the most common side effect of metformin?

A

GI upset

nausea, anorexia and diarrhoea intolerable in 20%

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12
Q

which biochemical profile can result from metformin?

A

lactic acidosis

occurs in patients with severe liver failure or renal failure

this is why metformin must be stopped in patients with eGFR <30

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13
Q

why should metformin be stopped following a recent MI?

A

the recent tissue hypoxia puts the patient at increased risk of lactic acidosis

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14
Q

if a patient has an eGFR < 30, what is the 1st line medication for T2DM?

A

sulphonylurea

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15
Q

what type of metformin should be considered in patients who develop intolerable side effects?

A

modified release metformin

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16
Q

name 2 side effects of sulphonylureas?

A
  • weight gain - not a good one to start if Px already obese

- hypoglycemia - they can’t be used by HGV drivers

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17
Q

which type of diabetes medication can cause recurrent UTIs?

A

SGLT 2-inhibitors

excess glucose is peed out

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18
Q

in which conditions is pioglitazone (TZDs) contraindicated?

A
  • heart failure - it causes fluid retention, so can exacerbate HF
  • bladder cancer
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19
Q

name 4 risks of taking TZDs (thiazolidinediones)?

A
  1. fluid retention
  2. weight gain
  3. liver impairment
  4. increased risk of fractures
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20
Q

which diabetes medication is good in heart failure?

A

SGLT-2 inhibitors

they also cause weight loss

TZDs are contraindicated in HF due to fluid retention

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21
Q

what is the initial Ix of choice for phaeochromocytoma?

A

urinary metanephrines

if they come back raised, then CT chest, abdomen and pelvis would be done

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22
Q

what are hyponatremia and hyperkalemia in a patient with lethargy highly suggestive of?

A

Addison’s disease

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23
Q

what is the definitive investigation for Addison’s disease?

A

ACTH stimulation test

short synthACTHen test

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24
Q

what is the one thing patients with MEN 1 and 2 have in common on their presentation?

A

primary hyperparathyroidism

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25
Q

which form of MEN presents with a pheochromocytoma?

how does this present?

A

MEN II

pheochromocytoma will cause raised metenephrines, adrenal mass on CT and hypertension

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26
Q

which form of MEN puts patients at greatest risk of medullary thyroid cancer?

A

MEN 2

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27
Q

what is the most common Ix to confirm Cushing’s syndrome?

what is the finding in patients with cushing’s?

A

overnight dexamethasone suppression test

patients with cushing’s do not have their morning cortisol spike supressed

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28
Q

what would be the cortisol and ACTH readings in a high dose dexa suppression in a patient with an ectopic cause for ACTH release, such as small cell lung cancer?

A

neither cortisol or ACTH would be suppressed

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29
Q

compare the cortisol and ACTH findings in high dose dexa suppression in Cushing’s syndrome vs cushing’s disease?

A

Cushing’s syndrome: ACTH suppressed, cortisol not suppressed

cushing’s disease: ACTH and cortisol suppressed

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30
Q

describe the sick day rules for diabetic drugs?

A

insulin must continue to be taken at a normal dose

if patient is on metformin, it should be stopped due to risk of lactic acidosis

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31
Q

where does the underlying mechanism for secondary adrenal insufficiency occur?

A

the pituitary

the mechanism is hypopituitarism - there is a lack of cortisol production 2ndary to a lack of ACTH

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32
Q

what is the easiest way to differentiate between primary and secondary adrenal failure?

A

if there is skin pigmentation or not…

skin pigmentation = primary adrenal failure

no skin pigmentation= secondary adrenal failure

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33
Q

name one T1DM specific antibody?

A

anti GAD

its presence can be used to distinguish T1 from T2 DM

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34
Q

which antibody is found in patients with graves disease?

A

anti-TSH receptor antibodies

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35
Q

PTH is released in response to what?

A

low serum calcium

PTH increases osteoclastic activity, causing reabsorption of calcium from the bone into blood

this increases serum calcium

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36
Q

name the 3 effects of PTH?

A
  1. increases osteoclastic activity
  2. reduces calcium excretion from kidneys
  3. increased conversion of vit D into calcitriol, which promotes calcium absorption from food

all 3 help raise the level of serum calcium

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37
Q

what is the overall effect of increased renin

A

it causes vasoconstriction, which increases blood pressure

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38
Q

what is aldosterone?

how does it act on the kidneys?

A

it is a mineralocorticoid steroid

  • increases Na reabsorption
  • increases K secretion
  • increases H+ secretion

water follows the Na that is reabsorbed, leading to increased intravascular vol and increased BP

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39
Q

name the 2 roles of angiotensin II?

A
  1. acts on blood vessels to cause vasoconstriction

2. stimulates release of aldosterone from adrenal glands

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40
Q

what is the difference between cushing’s disease and syndrome?

A

cushings syndrome is a set clinical picture that occurs due to prolonged elevation of cortisol

cushing’s disease: when the elevation of cortisol is directly due to a pituitary adenoma secreting excess ACTH

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41
Q

name the 4 causes of cushing’s syndrome?

A
  • exogenous steroids
  • cushings disease - pituitary adenoma
  • adrenal adenoma
  • paraneoplastic - ACTH release from small cell lung cancer
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42
Q

compare low and high dose dexamethasone suppression tests done in Cushing’s syndrome?

A

low dose test is done 1st: it identifies if cushings syndrome is present. an abnormal response suggesting cushings is if the morning cortisol has not been suppressed by low dose dexa

high dose is done 2nd: it identifies the underlying cause of the cushings. it is only done if low dose test is abnormal (ie- high cortisol)

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43
Q

what cause would high ACTH and high cortisol following a high dose dexa test be suggestive of?

A

paraneoplastic cushings

the ACTH is being released from the small cell lung cancer, so is independent to the pituitary

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44
Q

what cause would low ACTH and high cortisol following a high dose dexa test be suggestive of?

A

adrenal adenoma

the adrenal adenoma is releasing cortisol independent from the pituitary. therefore, the dexa will suppress the ACTH from the pituitary, but ACTH will continue to be released from the adenoma

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45
Q

what cause would low ACTH and low cortisol following a high dose dexa test be suggestive of?

A

cushing’s disease

ie - a pituitary adenoma

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46
Q

compare which imaging techniques are best for each cause of cushing’s?

A

pituitary adenoma: MRI brain

small cell lung cancer: CT chest

adrenal tumour: CT abdomen

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47
Q

how are all 3 causes of cushing’s best managed?

A

surgical removal

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48
Q

what is primary adrenal insufficiency also known as?

A

Addison’s disease

the most common cause of primary adrenal insufficiency is autoimmune

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49
Q

compare the defective site in primary, secondary and tertiary adrenal insufficiency?

A

primary: damage to the adrenal glands impairing cortisol release
secondary: damage to pituitary impairing release of ACTH
tertiary: inadequate CRH release by the hypothalamus

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50
Q

what is the most common cause of tertiary adrenal insufficiency?

A

patients being on long term (>3weeks) steroids suppress the hypothalamus

when the steroids are withdrawn, the hypothalamus does not wake up fast enough and endogenous steroids are not produced fast enough

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51
Q

name 5 symptoms of adrenal insufficiency?

A 
fatigue
nausea 
cramps 
abdominal pain 
reduced libido
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52
Q

why do patients with primary adrenal insufficiency get bronzed skin and hyperpigmentation in the skin creases?

A

the ACTH is unregulated to try and stimulate the adrenal glands (non-functioning) to produce cortisol

increased ACTH stimulates melanocytes, which produce melanin

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53
Q

sometimes, what is the only presenting feature of adrenal insufficiency?

hint: its a biochemical marker…

A

hyponatremia

aldosterone is released from the adrenal glands as well as cortisol

if the gland is defective, aldosterone won’t be produced

there is reduced reabsorption of Na, which causes hyponatremia

can also cause hyperkalaemia as less K+ is being excreted

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54
Q

what is the Ix of choice to diagnose adrenal insufficiency?

A

short synthACTHen test

synthACTHen is synthetic ACTH

synthACTHen will stimulate healthy adrenal glands to produce cortisol, so can differentiate between primary and secondary adrenal insufficiency

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55
Q

compare ACTH levels in primary and secondary adrenal failure?

A

primary: ACTH levels are high, trying to stimulate the non functioning adrenal glands
secondary: ACTH levels are low, as the problem is in the pituitary

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56
Q

name the antibodies present in AI adrenal insufficiency?

A

adrenal cortex antibodies

21-hydroxylase antibodies

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57
Q

in a short synthacthen test, by how much must the cortisol rise by to discount primary adrenal insufficiency (Addison’s disease)?

A

cortisol must rise to at least double the baseline

if it fails to rise to double the baseline, then primary adrenal insufficiency is diagnosed

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58
Q

compare the steroids that are given to treat adrenal insufficiency?

A

hydrocortisone: replaces cortisol
fludrocortisone: replaces aldosterone if it is also insufficient

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59
Q

how are doses of steroids to treat adrenal insufficiency altered in cases of acute illness?

A

steroid doses are doubled during acute illness

this is different from diabetic meds during acute illness, which are kept the same. metformin is stopped due to risk of lactic acidosis

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60
Q

describe the presentation of addisonian crisis?

A

reduced consciousness
hypotension
hypoglycaemia, hyponatremia, hyperkalemia

it can be the 1st presentation of Addison’s or can be triggered by infection, trauma or other acute illness in someone with addison’s

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61
Q

how is addisonian crisis managed?

A

do not wait for Ix’s

  • intensive monitoring
  • parenteral steroids (IV hydrocortisone 100mg stat then 100mg every 6 hours)
  • IV fluid resuscitation
  • correct hypoglycaemia and monitor electrolytes
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62
Q

when is the one time in hyperthyroidism when TSH is high?

A

when the hyperthyroidism is due to a pituitary adenoma that secretes TSH

in all other cases of hyperthyroidism, the TSH is low due to the negative feedback exerted by the high T3 and T4

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63
Q

compare the TSH and T3/4 levels in primary and secondary hypothyroidism?

A

primary hypothyroidism: high TSH, low T3/4

secondary hypothyroidism: low TSH, low T3/4

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64
Q

what 2 antibodies are present in Grave’s disease?

A

anti TPO antibodies - antibodies against the thyroid gland

TSH receptor antibodies - mimic TSH and stimulate T3/4 release - they are the cause of graves disease

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65
Q

in what condition is there diffuse high uptake of radioactive iodine in the thyroid?

A

grave’s disease

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66
Q

in what condition is there patchy uptake of radioactive iodine in the thyroid?

A

toxic multinodular goitre

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67
Q

in what condition is there cold areas (abnormally low uptake) of radioactive iodine in the thyroid?

A

thyroid cancer

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68
Q

presence of which antibody is pathognomic for grave’s disease?

A

TSH receptor antibodies

mimic TSH and stimulate the TSH receptors on the thyroid

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69
Q

what is the cause of exopthalmos in grave’s disease?

A

inflammation, swelling and hypertrophy of the tissue behind the eyeball

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70
Q

what is pretibial myxoedema a reaction of?

A

a reaction to the TSH receptor antibodies

a specific finding in grave’s disease

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71
Q

describe the presentation of de quervain’s thyroiditis?

A

viral infection with neck pain, fever, dysphagia and tenderness

+symtoms of hyperthyroidism

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72
Q

how is de quervein’s thyroiditis treated?

A

self limiting

NSAIDs for pain and inflammation

BBs for symptomatic relief of hyperthyroidism

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73
Q

what is the 1st line drug used for hyperthyroidism?

describe how it can be used once patient has normal thyroid levels?

A

carbimazole

“titration block” - dose is carefully titrated to maintain normal levels

“block and replace”- the dose is sufficient to block all production and patient takes levothyroxine titrated to effect

complete remission usually achieved in 18 months and can stop taking carbimazole

74
Q

which BB is used to manage the adrenaline related symptoms of hyperthyroidism?

A

propranolol

non-selective BB

75
Q

name the 2 antibodies seen in hashitmoto’s?

A

anti TPO

anti thyroglobulin

76
Q

how should patients with pheochromocytoma be medically managed prior to surgery?

A

alpha blocker then a beta blocker

ie - phenoxybenzamine given before propranolol

77
Q

which 2 drugs used to treat other conditions can cause hypothyroidism?

A

lithium - can cause goitre and hypothyroidism

amiodarone - usually causes hypothyroidism but can also cause thyrotoxicosis

78
Q

compare the sites of pathologies in primary and secondary hypothyroidism?

A

primary = thyroid gland (high TSH, low T3/4)

secondary= pituitary gland (low TSH and T3/4)

79
Q

what hormone is responsible for glycogenolysis and gluconeogenesis?

A

glucagon

80
Q

what causes osmotic diuresis in T1DM?

A

high glucose content in blood

glucose begins to be filtered into the kidneys and urine

water follows glucose, resulting in polyuria and severe dehydration

81
Q

what affect does insulin have on potassium?

A

it moves potassium into the cells

when Tx with insulin beings in hypoglycaemia, K+ can move very fast into cells, causing a severe hypokalaemia which can predispose to arrhythmias

82
Q

what are the 3 most dangerous aspects of DKA?

how does this influence Tx of DKA?

A

dehydration

potassium imbalance

acidosis

the priority is fluid resuscitation and insulin infusion

83
Q

compare the BGLs seen in fasting and OGTT that would be suggestive of a diagnosis of diabetes?

A

fasting BGL: >7.1mmol/l

OGTT: >11.1mmol/l

84
Q

compare the HbA1c Tx targets for new T2DMs with those who have moved beyond metformin Tx alone?

A

new T2DMs: 48mmol/l

diabetics who are on additional medication to treat: 53mmol/l

85
Q

what is the most common cause of tertiary hyperparathyroidism?

A

longstanding CKD

86
Q

when is metformin considered in T1DM?

A

only when BMI > 25

87
Q

compare the diagnostic criteria for a patient with and without symptoms of diabetes?

A

asymptomatic: 2 raised fasting or OGTT results
symptomatic: 1 raised fasting or OGTT result

88
Q

what HbA1c range should a patient with diabetes on treatment aim to keep within?

A

HbA1c = 48-53

regardless if its lifestyle only or with metformin

89
Q

name 2 benefits of taking SGLT2 medications for diabetes?

eg- dapagilflozin

A
  • pee out glucose and calories, so lose weight

- it is cardio protective

90
Q

name 2 contraindications to using sulfonylureas?

eg- glicazide

A
  • patient overweight

- patient is an HGV driver - cannot take due to risk of hypoglycaemia

91
Q

what medication should all diabetics over 40 y/o be started on, regardless of their lipid profile?

A

a statin

diabetes is a risk factor for atherosclerosis

this can put patients at risk of:
stroke, MI, ischemic heart disease and PAD

92
Q

what is the main cause of death in diabetic patients?

A

MI

93
Q

what is the most common type of neuropathy seen in diabetics?

A

peripheral polyneuropathy

glove and stocking distribution of sensory disturbance

94
Q

compare how a hypoglycaemic attack should be managed in a conscious patient, depending on if they are co-operative and capable or not?

A

cooperative and capable: 15-20g of rapid acting glucose via tablets

uncooperative and incapable: 1.5/ 2 tubes of glucogel

95
Q

how should an unconscious patient with BGL < 4mmol/l be treated?

A

ABCDE
stop any IV insulin
call for help
start IV glucose over 10 minutes - 75mls 20% glucose

recheck BM after 10 mins and repeat if necessary
check for ketones

96
Q

why is kussmaul’s breathing present in DKA?

A

there is a metabolic acidosis, so the deep sighing breathing is an effort to offload CO2 to reduce acidosis

97
Q

why is there not elevated ketones in HHS?

A

there is still some residual insulin left in HHS

it can move some glucose into the cells, so they are not totally depleted of energy, so they dont need ketones to produce energy

98
Q

how is HHS managed?

A
  1. fluids- 0.9% NaCl 1st line - aim to replace 50% of lost fluids in the 1st 12 hours
  2. start on insulin sliding scale
  3. monitor U&Es, glucose and events like stroke
99
Q

how is a lactic acidosis managed?

A

fluid resuscitation

bicarbonate infusion

100
Q

how does stress affect the release of TSH and TRH?

A

stress reduces the release of TSH and TRH

101
Q

comment on the potency and activeness of T3 and T4

A

T3 is more potent

both T3 and T4 are biologically active when they are free and unbound

102
Q

describe what is seen on an iodine uptake scan in de quervain’s thyroiditis?

A

reduced uptake

103
Q

when is propylthiouracil favoured over carbimazole in hyperthyroidism?

A

1st trimester of pregancy

carbimazole is used in the 2nd and 3rd trimester

104
Q

name 2 risks associated with carbimazole?

A

agranulocytosis and jaundice

105
Q

what is the 2nd line option to treat hyperthyroidism if medication doesnt work?

A

radio-ablation - using radioactive iodine

106
Q

how is thyroid storm managed?

A
  • fluids
  • control HR: BB or digoxin
  • hydrocortisone - prevents conversion of T4 –> T3
  • carbimazole
107
Q

what cancer is Hashimoto’s thyroiditis a risk for?

A

B cell non-hodgkins lymphoma

108
Q

what is the most common cause of hypothyroidism?

describe what is felt on examination?

A

atrophic thyroiditis

associated with atrophy so no goitre is felt

109
Q

compare the doses of levothyroxine given in young people and elderly people?

A

young: 50-100mcg

elderly or known IHD: 25-50mcg

110
Q

how is myxoedema coma treated?

A

IV thyroid replacement
IV fluid
IV corticosteroids
electrolyte imbalance correction

111
Q

what is by far the most common type of thyroid cancer?

who does it typically affect?

A

papillary thyroid cancer

affects younger patients (20-30)

112
Q

describe the histological features of papillary thyroid cancer?

how does it spread?

A

orphan Annie nuclei

calcified psammoma bodies

lymphatic spread

113
Q

what is the 2nd most common form of thyroid cancer, present in >50 y/os?

A

follicular

it is spread haematologically, papillary is spread lymphatically

114
Q

which thyroid cancer is seen in MEN 2 syndromes?

what does it secrete paraenoplastically?

A

medullary thyroid cancer

associated with abnormal secretion of calcitonin and hypercalcaemia

115
Q

which thyroid cancer is fast growing, invasive and has a poor prognosis?

A

anaplastic

7% 5 year survival - poor prognosis

116
Q

which thyroid cancer is almost always associated with an underlying AI thyroid disease?

A

lymphoma

usually Hashimoto’s thyroiditis

117
Q

what is the gold standard diagnosis for suspected thyroid cancer?

A

US guided FNA

118
Q

deficiency in which nutrient causes osteomalacia/rickets?

what are some causes of this deficiency?

A

vit D deficiency

due to:

  • poor diet
  • lack of sunlight
  • malabsorption: coeliac disease
119
Q

how is renal bone disease a cause of osteomalacia?

A

reduced kidney excretion causes hyperphosphaemia and hypocalcemia

there is also reduced vit D being activated to calcitriol

this drives secondary hyperthyroidism

120
Q

which class of drugs can cause osteomalacia?

A

anti convulsants

121
Q

what is the main finding on bloods that allows osteomalacia to be differentiated from osteoporosis?

A

osteoporosis: normal blood test values
osteopenia: hypocalcemia

122
Q

name the 1st and 2nd most common causes of hyperparathyroidism?

A
  1. solitary parathyroid gland adenoma (80%)

2. hyperplasia of all 4 parathyroid glands (20%)

123
Q

other than hypertension, name the other 2 features of hyperparathyroidism that cause symptoms?

A
  1. increased bone reabsorption: causing bone pain, fractures and osteoporosis
  2. hypercalemia: stones, bones, moans, psychiatric undertones
124
Q

name the 4 diagnostic features needed to diagnose hyperparathyroidism?

A
  • hypercalcemia, high PTH
  • normal U&Es
  • high urine calcium
  • not on lithium or thiazide
125
Q

what is the difference between primary and secondary parathyroidism?

A

primary: parathyroid tumour secreting excess PTH

secondary and tertiary: increased PTH being secreted in response to pre-existing hypocalcemia

126
Q

compare the differences between secondary and tertiary parathyroidism?

A

secondary: a physiological response to low calcium, with an increase in PTH that is proportional to deficit
tertiary: hyperplastic changes in the parathyroid glands in response to prolonged hypocalemia

127
Q

compare the biochemical profile of secondary and tertiary hyperparathyroidism?

A

secondary: low Ca, high PTH, high PO4
tertiary: high Ca, very high PTH, normal/rasied PO4

128
Q

which type of lung cancer can secrete parathyroid released protein?

which type of lung cancer secretes ACTH?

A

parathyroid related protein: sqaumous cell lung cancer

ACTH secreting: small cell lung cancer

129
Q

which type of lung cancer can cause hypercalcemia but a low PTH?

how does it do this?

A

squamous cell lung cancer

it releases parathyroid related protein, which results in increased serum calcium

PTH is low due to negative feedback

130
Q

describe the presentation of hypocalcemia?

in which thyroid dysfunction is it seen?

A

numbness, muscle cramps, spasms, wheeze, anxiety

it is seen in hypoparathyroidism

131
Q

which genetic condition presents with low IQ, obesity and short stature with a low Ca but high PTH?

A

pseudo-hypoparathyroidism

due to peripheral resistance to PTH

132
Q

what is the commonest cause of hypercalcemia?

A

primary hyperparathyroidism

133
Q

what electrolyte imbalance can dehydration cause?

A

hypercalcemia

134
Q

what 2 diagnostic investigations must be done for hypercalcaemia?

A

bloods: do PTH
urine: 24 hour urinary calcium

135
Q

in the context of hypercalcemia, what would isolated raised albumin and urea suggest the cause is?

A

dehydration

136
Q

is the alk phos level high or low in:

bone mets, sarcoidosis, thyrotoxicosis, myeloma, vit D excess?

A

high alk phos: bone mets, sarcoidosis, thyrotoxicosis

low alk phos: myeloma, vit D excess

137
Q

how is acute hypercalcemia managed?

A

rehydration

IV biphosvohonates

steroids can be used to reduce gut reabsorption of Ca

loop diuretics - can prevent Ca reabsorption in kidneys

138
Q

name 3 causes of hypocalcemia with normal or decreased PO4?

A
  • osteomalacia
  • acute pancreatitis
  • overhydration
139
Q

name 4 causes of hypocalcemia associated with increased PO4?

A

hypoparathyroidism

vit D deficiency

CKD

low magnesium

140
Q

what is seen on ECG in hypocalcemia?

A

prolonged QT interval

141
Q

compare how acute severe and chronic, mild hypocalcemia managed?

A

acute severe: IV calcium gluconate

chronic, mild: calcium and vit D supplements

142
Q

which MEN syndrome presents with parathyroid hyperplasia and a phaeochromocytoma?

A

MEN 2a

143
Q

which MEN syndrome presents with parathyroid, pituitary and pancreas secreting tumours?

A

MEN 1

parathyroid

pituitary: prolactinoma or GH secreting tumour
pancreas: gastrinoma, insulinoma, glucogonoma

144
Q

what is the target hormone for GH secreted from the ant pit?

A

IGF1- insulin like growth factor 1

145
Q

what test is done to measure GH and ACTH reserves?

how does this test work?

A

insulin stress test

involves giving IV insulin, which causes hypoglycaemia and is a natural stimulator of GH and ACTH/cortisol release

146
Q

how does Sheehan syndrome commonly present?

A

as a failure to produce breast milk

due to pituitary ischemia and haemorrhage following PPH

147
Q

what is a natural stimulator of GH and ACTH/cortisol release?

A

hypoglycaemia

following an insulin stress test, both GH and ACTH/cortisol should rise

148
Q

what type of tumour are almost all pituitary tumours?

A

benign adenomas

prolactinoma is most common

149
Q

if you suspected a prolacinoma, what investigations would you do?

A

test all hormones: ACTH, GH, TSH, GnRH, prolactin

imaging: MRI

150
Q

all pituitary tumours are treated by trans sphenoidal surgery except prolactinoma.

how is a prolactinoma treated?

A

dopamine agonists: cabergoline, bromocriptine

dopamine exerts negative feedback on prolactin release

151
Q

what is the most common cause of a lower quadrant visual field defect?

A

craniopharyngioma

causes superior chiasmal compression

presents in 5-15 y/o then 60-70 y/os

152
Q

name the 2 classes of drugs that can cause a hyperprolactineamia?

A

anti-emetics (dopamine antagonists): metoclopramide, domperidone

anti-psychotics: typical and atypical

both reduce levels of dopamine, which is needed to suppress release of prolactin

153
Q

why are males more likely to experience pressure symptoms from a prolactinoma than women?

A

they have less prominent galactorrhea and are more likely to present later, so disease process will be more advanced

154
Q

what test must always be done in a patient with galactorrhea?

A

pregnancy test

155
Q

what do GH secreting tumours causing acromegaly commonly develop as part of?

A

MEN 1

parathyroid
pituitary!
pancreas

156
Q

how does acromegaly cause diabetes?

A

GH is an insulin antagonist

this will lead to impaired glucose tolerance

157
Q

what test is gold standard when diagnosing acromegaly?

A

OGTT

normally, GH is inhibited with high levels of glucose, but in acromegaly, the GH levels remain high

158
Q

trans sphenoidal surgery is 1st line for acromegaly.

what is 2nd line Pharma treatment if surgery unsuccessful? how does this work?

A

somatostatin analogue: octerotide, sandosatin

somatostatin is the precursor of GH

increased levels of somatostatin will provide negative feedback and reduce GH levels

159
Q

how long do somatostatin analogues take to work in acromegaly?

A

they relieve headache almost immediately but take uo to a year to shrink tumour

160
Q

describe the 2 causes of diabetes insipidus?

A

central: impaired secretion of ADH
nephrogenic: impaired response of kidneys to ADH

ADH concentrates urine as it causes water to be absorbed

161
Q

what is the gold standard test for diabetes insipidus?

what result suggests DI?

A

water deprivation test

indicates if the body is able to concentrate urine

osmolality > 600

162
Q

compare the serum and urine osmolality in DI?

A

serum osmolality: blood doesn’t have enough water, so HIGH PLASMA osmolality

urine osmolality: urine has tonnes of water, so LOW URINE osmolality

163
Q

compare how central and nephrogenic DI are treated?

A

central: desmopressin (synthetic ADH)
nephrogenic: thiazide diuretics

164
Q

which 2 conditions is a MALT lymphoma associated with?

A

Hashimoto’s thyroiditis

H.Pylori

165
Q

how many units are in 1ml of insulin?

A

100 units

166
Q

what is the common venous blood gas in cushing’s syndrome?

A

hypokalaemic metabolic alkalosis

excessive cortisol causes excess aldosterone, which increases acid and potassium secretion from kidney

167
Q

what is the role of aldosterone?

A

keeps Na

excretes K+ and H+

excess aldosterone causes hypokalaemic metabolic alkalosis

168
Q

what is the 1st line test for acromegaly?

A

serum IGF-1

OGTT is used to confirm diagnosis if IGF-1 levels are raised

169
Q

what is the 1st line Ix for suspected primary hyperaldosteronism?

A

plasma aldosterone:renin ratio

an elevated ratio suggests aldosterone is inappropriately raised, indicative of primary hyperaldosteronims

170
Q

how is bilateral adrenocortical hyperplasia treated?

A

aldosterone antagonist

eg- spironolactone

171
Q

what is conn’s syndrome?

A

it is an adrenal adenoma causing primary hyperaldosteronism

it used to be thought of as the most common cause of primary hyperaldosteronism but is 2nd to bilateral ideopathic adrenal hyperplasia now

172
Q

what is the initial management of DKA?

A

IV fluids

after giving fluids, then think about giving IV insulin

173
Q

how should the steroids used in Addison’s disease be altered if there is a intercurrent illness?

A

double the glucocorticoids, keep the fludrocortisone the same

174
Q

hypokalaemia + hypertension = ?

A

primary hypoaldosteronism

175
Q

compare LH and FSH levels in a male with Kallmann syndrome and Klinefelter syndrome?

A

Kallmann: LH/FSH levels are low/normal

Kleinfelter’s: LH and FSH increased

both have low testosterone

176
Q

what is the HbA1c target in a patient taking a sulfonylurea?

A

53mmol/l

the target is 53 (rather than 48) in any drug that may cause hypoglycaemia

177
Q

in DKA, what should the IV insulin infusion be started at?

A

0.1 unit/kg/hour

178
Q

compare the IV insulin infusion rate for DKA and HHS?

A

DKA: 0.1 unit/kg/hour

HHS: 0.05 unit/kg/hour

179
Q

what can give a falsely high HbA1c level due to the increased lifespan of RBCs?

A

splenectomy

conversely, sickle cell anaemia, G6PD deficiency and hereditary spherocytosis cause lower than expected levels of HbA1c

180
Q

what is the key parameter to monitor in patients with HHS?

A

serum osmolality

AA Y4 Finals cards NE (40 decks)

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