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Y3 Medicine > Endocrinology and Diabetes > Flashcards

Endocrinology and Diabetes Flashcards

1
Q

Give one drug which can cause hyperthyroidism other than levothyroxine

A

Amiodarone

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2
Q

A patient with graves has a thyroidectomy, why may they still develop thyroid eye disease?

A

Autoantibodies still present, thyroid eye disease is due to autoantibodies rather than thyroid hormone

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3
Q

How is thyroid eye disease treated? (vaguely)

A

Steroids

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4
Q

Suggest 2 investigations to find the cause of hyperthyroidism?

A
  • thyroid auto- antibodies
  • technetium uptake scan
  • USS
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5
Q

Describe how the appearance of a technetium uptake scan would differ between graves, a single toxic nodule and a multi nodular goitre

A

Graves= Same absorbtion distribution as normal thyroid but darker as more uptake
Single toxic nodule= one dense area, not thyroid shaped
Multi-nodular goitre= many dense areas, with outline of thyroid seen

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6
Q

When should a patient on carbimazole stop taking their medication and why?

A

If they get an infection, because it can cause bone marrow surpression and decrease WBCC

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7
Q

Describe Na+ and osmolality changes to blood and urine in SIADH?

A

High Na+ conc in urine (as retaining water) and high urine osmolality (>100)
Low Na+ conc in blood (<135 mmol/l) with low serum osmolality (<280)

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8
Q

Other than SIADH, what else could cause hyponatuaemia with high urine Na+?

A

Adrenal insufficiency- less mineralcoritcoid production= less reuptake of Na+ in collecting duct

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9
Q

What is pituitary apoplexy?

A

Bleeding into or impaired blood supply to the pituitary gland

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10
Q

How does pituitary apoplexy present?

A

Headache with cavernous sinus signs (4th, 6th, 3rd nerve palsys), also hypopituitaryism

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11
Q

How is pituitary apoplexy treated? (Vaguely)

A

If optic chiasm involvement (bitemporal hemianopia) then usually needs surgery.
If not just need to medically replace hormones and wait for recovery.

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12
Q

Which causes a higher prolactin, prolactinoma or tumour stopping dopamine effect by compression stalk?

A

Prolactinoma (v high prolactin, treat with dopamine agonists)
Pituitary stalk tumour (lower prolactin, treat with surgical removal)

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13
Q

How can diabetes be diagnosed? (3 ways)

A
  1. random blood glucose test over 11.1 with symptoms
  2. fasting glucose >7, if theyre asymptomatic you need two >7
  3. Hba1c> 6.5%
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14
Q

Give 5 symptoms of diabetes mellitus?

A
  • tiredness
  • frequent UTIs
  • Weightloss (T1 only)
  • Polyurea
  • Polydipsia
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15
Q

Describe the presentation of decompensated ketoacidosis?

A
  • onset over 24 hrs
  • PMH T1 diabetes, recent precipitating factor
  • polyurea and poly dipsia
  • N+ V
  • Altered mental state
  • weakness
  • lethargy
  • hyperventilation
  • pear drop smell on breath
  • dehydrated and volume deplete on examination
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16
Q

What may precipitate DKA? (4)

A
  • Infection.
  • Discontinuation of insulin (unintentional or deliberate).
  • Inadequate insulin.
  • Cardiovascular disease - eg, stroke or myocardial infarction.
  • Drug treatments - eg, steroids, thiazides or sodium-glucose co-transporter 2 (SGLT2) inhibitors.
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17
Q

How should DKA be investigated? (group into diagnosis, finding cause and assessment of severity/ complications)

A
  • To diagnose: Blood glucose, blood ketones, urine dip for ketones, ABG showing low bicarbonate (metabolic acidosis)
  • To asses severity: U&E- for dehydration and hyperkalaemia, also urea and creatine raised if AKI, 12 lead ECG, CT/ MRI of head, anion gap raised
  • to find cause: blood cultures, urine dip, CXR to look for infection
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18
Q

Describe and explain serum osmolality, K+ and Na+ changes in DKA?

A
  • K+ usually high due to acidosis meaning H+ going into cells and K+ coming out, however may be low due to osmotic diuresis
  • Osmolality is low due to glucose and ketones causing osmotic diuresis, which is also why Na+ conc seems high or normal. Can be low as body compensates by letting sodium go
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19
Q

Describe the management of DKA in detail

A
  • Fixed rate IV infusion of insulin dose of 0.1 units/ Kg bodywieght every hour
  • IV fluids to rehydrate: 1st bag= 1L normal saline over an hour, then 1L normal saline with K= over 2 hrs, then same then 1L NS w/ K+ over 4 hrs then same again, then 1L NS w/ k+ over 6 hrs. Reason for this is the insulin will cause cells to uptake K+ and cause hypokalaemia.
  • Monitor closely (every hour) and if targets in HCO3- increases and ketone decreases are not met then increase the insulin
  • When blood glucose is over 14mmol/l add 5% dextrose solution infusion to prevent hypo, continue until eating and drinking normally
  • treat complications
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20
Q

When does hyperosmolar hyperglycaemic state/ syndrome (HSS) occur?

A

It occurs in T2 diabetes when blood glucose levels are allowed to be very high for a sustained period of time, causing an osmotic diuresis and so loss of water meaning high serum osmolality. There is no ketoacidosis as there is still a basal level of insulin they respond to sufficient to prevent ketoacidosis but too low to prevent hyperglycemia.

21
Q

What could cause HHS?

A
  • infections
  • inability to take medications
  • hypo/hyperthermia
  • MI
  • Medications
  • undiagnosed/ first presentation of diabetes
  • Many others
22
Q

How is HSS present?

A

With severe dehydration, fast deterioration, focal or global neurological dysfunction, often PMH of diabetes, N+V, lethargy, seizures

23
Q

How is HHS treated?

A
  • Fluid resus: 0.9% normal saline, can use hypotonic (0.45%) if serum osmolality not going down, however this is rare. You dont want osmolality to decrease too fast (>10mmol/l/hr)
  • Fixed rate iv infusion of insulin- 0.05 units per kg per hr ONLY if high ketones
  • monitor closely (blood biochemistry as well as neuro function)
24
Q

Describe 3 early and 3 late signs of hypoglycaemia

A 
early= hungry, sweats, tremor, palpitations, shaking 
late= confused, headache, drowsy, slurred speech, coma
25
Q

Describe treatment of hypoglycaemia if theyre conscious and orientated

A

Oral glucose (dextrose tablets, 150-200ml fruit juice/ original lucozade/ glucojuice) with complex carbs later (bread etc)

26
Q

Describe treatment of severe hypoglycaemia (unconscious or unable to swallow)

A
  • Iv dextrose (120-200ml 20% solution)

- or IM glucagon often given in community

27
Q

What is involved in a synacthen test? What does it assess?

A

You give synthetic ACTH, which should stimulate the adrenals to produce cortisol over about 30-60 mins.
It tests primary adrenal failure- the cortisol will not increase significantly in addisons.

28
Q

What is involved in an insulin tolerance test? What does it test for?

A

You give 0.1 units/ kg insulin to induce a hypo (glucose <2).
The cortisol should the rise to >600. If it doesnt you may have problem with adrenals (primary adrenal failure) or hypopituitarism (failure to produce ACTH). It is used when the synacthen test is inconclusive as more sensitive at detecting adrenal insufficiency

29
Q

What is involved in a glucose tolerance test? What does it test for?

A

Give a bolus of glucose, which should surpress growth hormone production. Tests for acromegaly

30
Q

What are the clinical features of acromegaly?

A
  • usually occurs between ages 30-50
  • growth of hands and feet
  • prognathism
  • frontal bossing
  • spade like hands
  • coarse fatures
  • headache
  • sweating
  • carpal tunnel
  • cardiomegaly
  • hepatosplenomegaly
  • macroglossia
  • colonic polyps
  • diabetes and its complications
31
Q

How should acromegaly be investigated? (6)

A
  • check visual feilds
  • urine dip (high glucose)
  • BP- often HTN
  • TSH and T4, prolactin, FSH, LH, GH, IGF1 for pituitary failure
  • glucose tolerance test (positive if failure of normal suppression of GH to less than <2)
  • MRI pituitary fossa
32
Q

How is acromegaly treated?

A
  • Surgery: transpehnoidal removal of lesions
  • radiotherapy
  • Medical: somatostatin analogues (octreotide) or GH receptor blockers (pegvisomant, bromocriptine, cabergoline))
33
Q

Describe the clinical features of cushings syndrome?

A
  • plethoric
  • moon face
  • thinning of skin
  • easy bruising
  • buffalo hump
  • central obesity
  • abdo striae
  • HTN and DM
34
Q

How could you initially screen someone you suspect has cushings? (4 options)

A
  • 24 hr urinary cortisol x3
  • ACTH (only at specialist centres)
  • Midnight cortisol (should be lowest, difficult inpractice)
  • Low dose dexamethasone surpression test (best screening test)
35
Q

What is the low dose dexamethasone surpression test good for?

A
  • give 0.5mg dexamethasone qds for 48 hrs
  • cortisol should go down to <30, if >30 (doesnt surpress) then true cushings
  • psuedocushings can be causes by alcohol or depression
36
Q

What could cause cushings? (4)

A
  • ACTH secreting pituitary tumour
  • Ectopic ACTH (small cell carcinoma)
  • adrenal tumour
  • steroids
37
Q

How can you diffentiate between an adrenal tumour causing cushings and ectopic ACTH secretion or a pituitary tumour causing cushings?

A

If adrenal tumour- ACTH will be low

If ectopic ACTH or pituitary cause- ACTH will be high

38
Q

How can you differentiate between ectopic ACTH and pituitary cushings?

A
  • Pituitary cushings will surpress on high dose dexamethasone surpression test- ectopic ACTH will now
  • MRI pituitary fossa may show a lesion
39
Q

Give 3 physical effects of non functional pituitaty tumours?

A
  • visual field disturbances (tunnel vision most commonly)
  • headache
  • hyperprolactinaemia
  • hypopituitarism
40
Q

how can you differentiate between prolactinomas and non functioning adenoma causing hyperprolactinaemia?

A

prolactinomas will cause prolactin to be >5000

41
Q

How are prolactinomas and nonfunctioning adenomas causing hyperprolactinaemia managed?

A

prolactinomas= dopamine agonist (inhibits prolactin release)

non functioning adenoma= cut it out

42
Q

Describe the clinical features of an addisonians/ hypoadrenal crises?

A
  • vomiting
  • drowsy
  • weight loss
  • tanned skin
  • low BP
  • high HR
  • Low blood glucose
  • hyponaturaemia
  • hyperkalaemia
43
Q

How should a hypoadrenal crises be managed?

A
  • aggressive fluid resus
  • hydrocortisone 100mg IV every 6 hrs
  • urine catheter to monitor output
  • treat sepsis (usual cause)// fine cause
  • Give glucose
44
Q

How can addisons be biochemically confirmed?

A
  • low 9am cortisol (should be at its highest)
  • ACTH level (high if adrenal cause)
  • renin
  • synacthen test
45
Q

How should addisons be managed?

A
  • hydrocortisone
  • fludocortisone
  • education
  • emergency HC injection kit
  • endocrine follow ups
46
Q

Describe the diagnosis criteria for DKA and HHS

A

DKA: acidaemia (ph<7.3 or hco3 <15) and hyperglycaemia (>11.1) and ketonuria (++) or ketonaemia (>3)
HHS: hyperglycaemia >30, no acidosis, no ketosis, serum osmolality >320

47
Q

how can serum osmolality be calculated

A

2x (Na + glucose + urea)

48
Q

How well do thyroid function tests corellate with symptoms?

A

Generally very well- if someone is experiencing symptom changes but with normal T3/T4 and TSH, think about other causes, dont change thyroxine/ carbimazole doses

49
Q

What is more sensitive to treatment changes TSH or T3/4?

A

T3/4 is much more sensitive so more reliable in early stages of treatment to tirate dose
TSH may be a better indicator of adherance as will change less when someone remembers to take meds leading up to a test

Y3 Medicine (9 decks)

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