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3rd year medicine > Endocrine Guidelines > Flashcards

Endocrine Guidelines Flashcards

1
Q

Fasting glucose threshold diabetes

A

<6 is normal >7 is diabetes

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2
Q

Random glucose threshold diabetes

A

>11.1 is diabetes

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3
Q

OGTT threshold diabetes

A

>11.1 is diabetes <7.8 is normal

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4
Q

HBa1C threshold diabetes

A

48+ is diabetes <42 is normal

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5
Q

how often should you self monitor for diabetes

A

4x per day

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6
Q

Daily glucose targets T1DM

A

4-7 5-7 when waking up

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7
Q

HTN in diabetic black person 1st line

A

ACEi and CCB

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8
Q

DKA diagnosis

A

pH <7.3 bicarb <15 ketones ++ or >3 glucose >11 or known diabetes

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9
Q

DKA management

A

Need fluids: 1 2 2 4 4 6 = litre NaCl 0.9% (with KCl after first hr)

Need potassium replacement = add 40mmol if 3.5-5.5, call senior if below that.

0.1U/kg/hr insulin. 5% Dextrose when blood glucose <15

DONT STOP LONG ACTING INSULIN, stop short acting insulin

worry about cerebral oedema in young patients on treatment for DKA - monitor neuro

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10
Q

T2DM first line

A

metformin + lifestyle

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11
Q

hba1c target with T2DM

A

48 (53 on gliclazide)

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12
Q

When do you add a second drug in T2DM

A

hba1c >58

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13
Q

when do you use GLP1

A

If triple therapy has not worked (i.e. it is fourth line) and BMI >35 with problem associated with obesity or BMI <35 but insulin would affect their work badly.

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14
Q

HHS management What do you check doing management

A
  1. Normalise the osmolality (gradually)
  2. Replace fluid and electrolyte losses
  3. Normalise blood glucose (gradually)

(will all occur with fluid)

Fluid loss = 10=20% (in litres) of body weight (kg)

Give fluid back (half in 12 hours, half in next 12 hours)

first line: 0.9% NaCl IV

Must check that osmolality is going down (2Na + urea + glucose) so plot it on graph:

  • glucose should fall by 4-6/hr
  • sodium should not fall by more than 10 in 24 hour

insulin should not be used unless significant ketonaemia or acidosis

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15
Q

Graves disease Mx

A

18 months of carbimazole or block and replace

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16
Q

TMG Mx

A

radioidine or lifetime carbimazole

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17
Q

Toxic adenoma Mx

A

Radioiodinde

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18
Q

Thyroid storm Mx

A

IV propranolol, Lugol’s iodine, anti-thyroid drugs (methimazole, propylthiouracil), dexamethasone

treatment of underlying cause

the five ‘Bs’

  • Block synthesis (antithyroid drug)
  • Block release (Lugol’s iodine)
  • Block T4 to T3 conversion (propylthiouracil, dexamethasone (steroid))
  • BB (propanolol)
  • Block enterohepatic circulation (cholestyramine)
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19
Q

When should you start at a lower dose with levothyroxine

A

Elderly or heart disease (start at 25 instead of 50 ug)

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20
Q

When do you check TFTs after starting Tx for hypothyroidism and what do you aim for

A

Normal TSH after 6-8w

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21
Q

Levothyroxine dose in pregnancy

A

Increase by 25-50microgram

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22
Q

levothyroxine dose alongside iron?

A

No, leave 2 hours in between as iron reduces levothyroxine absorption

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23
Q

Do you treat subclinical hypothyroidism

A

Depends If >80, no

If <80 + TSH >10, yes

If TSH only a bit raised (4-10), treat if <65

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24
Q

de quervains thyroiditis Mx

A

self limiting steroids may help hypothyroid phase

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25
Q

post-partum thyroiditis

A

propranolol in hyperthyroid phase

levothyroxine in hypothyroid phase

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26
Q

primary hyperPTH Mx

A

Parathyroidectomy

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27
Q

Can you ever not treat primary hyperPTH

A

Yes, if >50, Ca raised by <0.25, no end organ damage

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28
Q

Secondary hyperPTH

A

calcium and vit D supplementation

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29
Q

Tertiary hyperPTH - what about if just had a renal transplant

A

Excision of culprit gland Wait 12m after a renal transplant as many resolve

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30
Q

how to differentiate between pseudo and real cushings

A

Best = low dose dex suppression test Also used = insulin stress test

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31
Q

best test for cushings

A

overnight dex suppression test - give dex, and cortisol should be reduced the next morning. First do low dose then do high dose.

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32
Q

Addison’s best test

A

spank the adrenals with SYnACTHen to see if they work. measure cortisol before and 30 min after ACTH given.

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33
Q

Addisons ABG

A

hypoglycaemia, hyponatraemia, hyperkalaemia, metabolic acidosis

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34
Q

Mx of Addisons

A

hydrocortisone TDS with biggest dose in the morning + fludrocortisone

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35
Q

Addisons crisis management

A

IV hydrocortisone 100mg (big dose) only saline + dextrose if needed

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36
Q

prolactinoma 1st and 2nd/definitve

A

1st = bromocriptine/cabergoline 2nd = surgery

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37
Q

hypoglycaemia

A

depends on access - conscious = oral - unconscious no IV = IM glucagon - unconscious with IV = dextrose

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38
Q

diabetic foot - who gets followed up

A

anyone with anything more than a simple callous (so moderate or severe as opposed to mild)

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39
Q

hyponatraemia investigation: what do you do first

A

exclude pseudohypoNa (test lipid and protein) and exclude compensatory (test glucose)

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40
Q

Steps 1 to 3 for investigating hypoNa - addisons/diuretic - vomiting/diarrhoea - SIADH/hypothyroid - nephrotic syndrome, CCF, cirrhosis

A

Step 1 = depleted euvolaemic, overloaded Step 2 = urinary sodium >20 or <20 Step 3 = imagine the flow diagram and figure out what it is - addisons/diuretic = dehydrated + UNa >20 - vomiting/diarhoea = dehydrated + UNa <20 - SIADH/hypothyroid = euvolaemic + UNa >20 - failures = overloaded + UNa <20

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41
Q

Treatment of hypoNa - rate of Na correction - use of hypotonic saline?

A

normal saline 0.9% for F1 always - no more than 10mmol/24 hours - only in cerebral oedema under senior supervision

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42
Q

severe hypoCa management

A

10ml calcium glutinate 10% with ECG monitoring

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43
Q

hyperPTH : Ca, PO4, PTH, ALP

A

high Ca, low PO4, high PTH (or inappropriately normal), high ALP

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44
Q

malignancy with bone met: Ca, PO4, PTH, ALP

A

High Ca, high PO4, low PTH, high ALP

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45
Q

Mx of hypercalcaenia - first - ongoing helper management

A

3-4L per day of normal saline Bisphosphonates can be used too but these take 2-3 ays to work with maximal effect at 7d

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46
Q

recurrence of thyroid cancer

A

yearly check of thyroglobulin antibodies

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47
Q

HypoPTH: PTH, PO4, Ca hypoPTH vs pseudohypoPTH vs psuedopseudohypoPTH Best way to diagnose pseudohypoPTH

A

Low PTH, high PO4, low Ca

give PTH infusion:

hypoPTH = high PTH, high PO4, high Ca (as its usually due to PTH insufficiency so will correct if given PTH)

pseudo = high PTH, high PO4, low Ca (target cells insensitive to PTH therefore no production of calcium regarless of PTH infusion)

pseudopseudo = normal everything but physically looks like pseudo )low IQ, short 4/5th metacarpal, short BUT best way to diagnose pseudohypoPTH is by measuring urinary cAMP/PO4 after PTH infusion (stays same in pseudo as not responsive)

48
Q

Mx of true hypoPTH

A

alfacalcidol to boost the low calcium

49
Q

Conn’s syndrome (hyperaldosteronism) best Ix

A

aldosterone:renin will be HIGH

50
Q

ABG in Conn’s

A

high Na, low K, metabolic alkalosis

51
Q

Once Conn’s diagnosed, what test do you then do

A

Need to find out the cause: Do high resolution CT scan and adrenal vein sampling. helps distinguish between adenoma or hyperplasia

52
Q

Mx of Conn’s - adenoma - hyperplasia

A

surgery spironolactone

53
Q

Pheochromocytoma Ix

A

metanephrine/VMA in urine (NOT SERUM)

phaeochromocytoma is a tumour on adrenals releasing metanephrine and epinephrine

54
Q

Phaeo Mx

A

surgery, but give alpha (phenoxybenzamine) then beta blockage in meantime

55
Q

Acromegaly Ix FIRST BEST

A

first = Serum IGF1

Best (to confirm) = OGTT (to try and suppress axis. in acromegaly GH doesn’t suppress after glucose) - do if IGF-1 levels raised

acromegaly: excess GH released from anterior pituitary

56
Q

Acromegaly 1st line other Tx?

A

first line: surgery - trans-sphenoidal

medical Tx includes octreotide (somatostatin analogue) or dopamine agonist (cabergoline/bromocriptine) GH receptor antagonist (pegvisomant - prevents dimerisation of the receptor)

57
Q

Diabetes insipidus

Ix:

  • to confirm
  • to detect type
A

Check serum and urine osmolality to confirm:

  • high plasma osmolality, low urine osmolality = DI
  • a urine osmolality >700mOsm/kg excludes DI

Do desmopressin test to check which type:

  • desmopressin is analogue of vasopressin (ADH)
  • in cranial DI vasopressin not released therefore giving desmopressin would help things
  • in nephrogenic DI, vasopressin released from cranial but doesnt work on kidneys therefore giving desmopressin wont work
58
Q

Check for primary polydipsia as cause of polyuria (Ddx for diabetes insipidus)

A

Water deprivation test (urine conc will eventually go up in primary polydipsia)

59
Q

Neprhogenic vs cranial DI Mx

A

Cranial = desmopressin Nephrogenic = thiazides and low salt/protein diet§

60
Q

What do you do if metformin isn’t tolerated due to GI SEs

A

You try metformin MR before going to second line treatment

61
Q

Thyroid eye disease management

A

topical lubricants ORAL not injection steroids radiotherapy surgery

62
Q

bitemporal hemianopia (upper quadrant mainly affected)

moon face

striae

diagnosis

A

pituitary adenoma - ACTH secreting

= cushings disease

cushings disease over syndrome as bitemporal hemianopia due to pressure on optic chiasm from pituitary adenoma

63
Q

pituitary adenoma Ix

A

pituitary blood profile (GH, prolactin, ACTH, FH, LSH, TFTs)

formsl visual field testing

MRI brain with contrast

64
Q

pituitary adenoma Mx

A

hormonal therapy

surgery - determined by size of tumour in non-functioning pituitary adenoma - consider trans-sphenoidal surgery if progression in size noted

radiotherapy

65
Q

most common type of pituitary adenoma

A

prolactinoma - produce excess prolactin

features of excess prolactin

men: impotence (hard to get erection), loss of libido, galactorrhoea
women: ammenorrhoea, infertility, galactorrhoea, osteoporosis

66
Q

acromegaly features

A

excess growth hormone secondary to pituitary adenoma (most commonly)

coarse fascies

spade-like hands

increase in shoe size

large tongue

excessive sweating

bitemporal hemianopia - if caused by pituitary tumour

raised prolactin in 1/3 cases –> galactorrhoea

67
Q

what conditions are acromegaly associated with

A

HTN

diabetes

cardiomyopathy

colorectal cancer

68
Q

what does parathyroid hormone do

A

causes release of calcium from bone to blood

if hypoparathyroidism: low blood calcium

if hyperparathyroidism: high blood calcium

69
Q

main cause of primary hypoparathyroidism

A

thyroid surgery

70
Q

Mx of hypoparathyroidism

A

alfacalcidol

71
Q

main symptoms of hypoparathyroidism

A

symptoms mainly due to the low calcium:

muscle twitching, cramping, spasm

perioral paraesthesia

trousseau’s sign: carpal spasm if brachial artery occluded by BP cuff

Chvostek’s sign: tapping over parotid causes facial muscles to twitch

ECG: prolonged QT interval

72
Q

primary hyperparathyroidism - most common cause

A

solitary adenoma

73
Q

features of primary hyperparathyroidism

A

high calcium

bones, stones, abdominal groans and psychic moans:

bone pain/fracture

polydipsia, polyuria

peptic ulceration/ constipation/ pancreatitis

depression

HTN

74
Q

sign?

cause?

what other abnormalities would you see on investigations

A

pepperpot skull (like ground glass appearance) on Xray

=

hyperparathyroidism

Ix:

  • raised calcium, low phosphate

PTH may be raised or normal

technetium-MIBI subtraction scan

Xray - pepper pot skull (can also get it in other bones)

75
Q

features of hypopituitarism

A

loss of anterior or posterior pituitary hormones:

GH deficiency:

dwarfism in children

wrickled skin

Gonadotrophin deficiency:

delay in puberty

amenorrhoea, impotency, loss of libido

TSH deficiency:

  • secondary hypothyroidism - sensitivity to cold, dry skin, coarseness of hair

ACTH deficiency:

  • decreased skin pigmentation
  • poor apetite, nausea, vomiting, muscle weakness, loss of axillary and pubic hair in females

prolactin deficiency:

  • failure of lactation in post-partum patients

loss of posterior pituitary hormones:

  • ADH deficiency: polyuria, thirst
  • local effects in region of pituitary fossa (eg if neoplastic, infiltrative):

headache

visual field degects: superior bi-temporal quadrantanopia

progressing to bitemporal hemianopia

cerebrospinal fluid rhinorrhoea due to inferior extension of tumour

III, IV and VI nerve palsies due to lateral extension of tumour

76
Q

ix hypopituitism

A

base levels T4, T3, TSH, prolactin, gonadotrophins, testerone, cortisol, U+Es (dilutional hyponatraemia)

FBC (normochromic normocytic anaemia)

assessment of visual fields

skull radiology

CXR signs of primart tumour thats produced mets, sarcoidosis or TB

77
Q

primary vs secondary hypogonadism in males

A

primary hypogonadism: elevated gonadotropin levels and low testosterone levels

secondary hypogonadism: low to normal gonadotrophin levels and low testosterone levels

78
Q

hypogonadism ix males

A

morning basal testosterone (before 11am)

if >12:

repeat TT + LH, FSH, (to determine difference between gonadal disease and hypothalamic-pituitary disease)

+ PRL (prolactin) if TT<5.2 + low LH & FSH

if TT < 8 = confirmed testosterone deficiency

if high LH = primary TD

if low/ normal LH = secondary TD

for symptomatic TD also include:

  • haematocrit as part of FBC
  • PSA
79
Q

Mx for primary hypogonadism in males and secondary TD where ferility not desired in males

A

trial of Testosterone therapy (measure T levels at 3,6,12 months and then every 12 months

+ lifesytle modification

80
Q
A
81
Q

mx for secondary TD where ferility desired

A

AVOID T therapy (may reduce spermatogenesis)

instead use:

  • HCG
  • SERMs (e.g. clomifene)

Als

82
Q

features of hypogonadism in females

A

primary and secodnary result in:

oestrogen deficiency

abnormal menstrual cycle (anovulatory cycling then irregularity then ammenorrhoea)

Ix and Mx under ammenorhoea

83
Q

hypogonadotrophic hypogonadism Vs hypergonadotrophic hypogonadism

A

hypogonadotrophic hypogonadism:

decreased secretion of gonadotrophic hormones LH and FSH by anterior pituitary

causes:

  • hypopituitarism
  • selective gonadotrophic deficiency

hypergonadotrophic hypogonadism:

underlying unresponsiveness of gonads resulting in hypogonadism. get positive feedback to promote gonadotrophs to increase

84
Q

features of DKA

A

abdominal pain

polyuria, polydipsia, dehydration

Kussmaul respiration (deep hyperventilation)

Acetone-smelling breath (‘pear drops’ smell)

85
Q

HHS features

A

associated with T2DM

comes on over days whereas DKA comes on over hrs

General: fatigue, lethargy, nausea and vomiting

Neurological: altered level of consciousness, headaches, papilloedema, weakness

Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)

Cardiovascular: dehydration, hypotension, tachycardia

86
Q

HHS diagnosis

A
  1. Hypovolaemia
  2. Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
  3. Significantly raised serum osmolarity (> 320 mosmol/kg)
87
Q

thyroid storm features

A

fever > 38.5ºC

tachycardia

confusion and agitation

nausea and vomiting

hypertension

heart failure

abnormal liver function test - jaundice may be seen clinically

88
Q

thyroxicosis with tender goitre

+ raised ESR

diagnosis

A

subacute (De Quervain’s thyroiditis)

89
Q

phases of subacute (De quervains) thyroiditis

A

causes hyper then hypo- thyroidism

in phase 1: hyperthyroidism with painful goitre, raised ESR

phase 2: euthyroid

phase 3: hypothyroidism (weeks - months)

phase 4: thyroid structure and function back to normal

90
Q

Ix for subacute (De quervains) thyroiditis

A

thyroid scintigraphy: globally reduced uptake of iodine-131

91
Q

post partum thyroiditis

A

three stages:

  1. thyrotoxicosis
  2. hypothyroidisim
  3. normal thyroid function (high recurrence rate in future pregnancies)

anti TPO antibodies found in 90% patients

92
Q

dexamethasone suppression test

A

low dose dexamethosone: determines pseudo cushings from cushings

in normal/ pseudo: dexamethasone decreases ACTH which causes reduced production of cortisol

in cushings: cortisol remains same as another source (pituitrary, adrenal, ectopic)

high dose dexamethasone test to distinguish between pituitary, adrenal, ectopic

pituitary (cushings disease): cortisol low (high dose dex enough to reduce pituitary adenoma)

adrenal cushings syndrome (adrenal adenoma): high dose dex suppresses ACTH but cortisol still secreted from adenoma

ectopic (small cell lung cancer): cancer secretes ACTH (not reduced by high dose dex) and therefore cortisol still secreted

93
Q

features of diabetes insipidus

A

polyuria

polydipsia (due to the polyuria)

94
Q

drug known to cause diabetes insipidus

A

lithium

95
Q
A
96
Q

graves diseas antibodies

A

TSH receptor antibodies

97
Q

mx of concurrent illness with addisons disease

A

double the glucocorticoid (hydrocortisone) and keep the mineralocorticoid (fludrocortisone) the same

98
Q

management for galactorrhoea

A

bromocriptine

99
Q

mx for MODY (maturity onset diabetes of the young)

A

sulphonylureas e.g. gliclazide

100
Q

features of MODY

A

diabetes with strong family hx of early onset

usually presents <25yrs

ketosis is not a feature at presentation

patients with the most common form (MODY 3) are sensitive to sulphonylureas (gliclazide)

HNF-1 apha gene in 70% of cases

101
Q

endocrine parameters reduced in stress response

A

insulin

testosterone

oestrogen

therefore all decreased during surgery

102
Q

first line ix in primary hyperaldosteronism

A

aldosterone/renin ratio

  • will be elevated ratio in primary hyperaldosteronism
103
Q

myxoedemic coma mx

A

coma from hypothyroidism

mx: levothyroxine + hydrocortisone

the hydrocortisone is used to treat the presumes associated adrenal insufficiency

104
Q

renal replacement therapy for independent patients first line

A

peritoneal dialysis

however contraindicated in concurrent abdo conditions (e.g. chrons) therefore use haemodialysis instead

105
Q

when should people with CKD be put on an ACEi

A

ACEi are protective in CKD

give in high albumin:creatinine ratio

give if:

  • ACR > 3 + co-existant diabetes
  • ACR > 30 + co-existant HTN
  • ACR > 70
106
Q

which hormone should you monitor for recurrence of medullary thyroid cancer

A

serum calcitonin levels

  • secrete calcitonin
107
Q

primary hyperaldosteronism

features

ix

mx

A

HTN (treatment resistant) + hypokalaemia

first line ix: plasma aldosterone/ renin ratio = high

then high res CT abdo and adrenal vein sampling

mx:

adrenal adenoma (Conns syndrome): surgery

bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

108
Q

screening for ischaemia of diabetic foot disease

A

done by palpating for both dorsalis pedis pulse and posterial tibial artery pulse

109
Q

screening for neuropathy of diabetic foot disease

A

use a 10g monofilament on various parts of the sole of foot

110
Q

what is the first thing that should be initiated in a DKA

A

1L 0.9% NaCl IV over 1 hr

1,2,2,4,4,6

fluids first as patients are dehydrated

then 0.1units/kg/hr

long acting insulin continued, short acting insulin stopped

111
Q

thyrotoxicosis + tender goitre

A

subacute (de Quervain’s) thyroiditis

112
Q
A
113
Q

most common cause of addisons disease in industrialised nations

A

autoimmune adrenalitis

114
Q

most common cause of addisons disease worldwide

A

TB

  • look for TB risk factors
115
Q

how many units are there in 1 ml of insulin

A

100 units

3rd year medicine (31 decks)

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