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FINALS- random flashcards per system > endocrine > Flashcards

endocrine Flashcards

1
Q

management of hyperkalaemia

A

calcium gluconate

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2
Q

management of a pituitary adenoma

A

trans-sphenoidal surgery

dopamine agonists- cabergoline

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3
Q

causes of primary, secondary and tertiary hyperparathyroidism

A

primary- pituitary tumour

secondary- poor absorption of vitamin D (ckd/ digestive problem) or low vitamin D

tertiatry- excess PTH due to hyperplasia of the parathyroid gland from secondary hyperparathyroidism

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4
Q

functions of PTH

A

vitamin D uptake
enhances vitamin D
increase osteoclast activity
increased calcium absorption in gut

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5
Q

calcium levels in primary, secondary and tertiary hyperparathyroidism

A

primary- high

secondary- low/ normal

tertiary- high

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6
Q

symptoms of hypercalcaemia

A

bone pain
renal stones
abdo groans- n&v, constipation
psychiatric moans- depression, fatigue, psychosis

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7
Q

management of hypercalcaemia

A

correct dehydration

bisphosphonates

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8
Q

what is cushings

A

excess cortisol

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9
Q

difference between cushings disease and syndrome

A

syndrome- excess cortisol

disease- excess cortisol due to a pituitary tumour secreting acth

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10
Q

causes of cushings syndrome

A

excess exogenous steroids
paraneoplastic tumour (usually a Small cell lung cancer secreting ACTH)
adrenal adenoma

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11
Q

presentation of cushings

A

moon face
central obesity
abdominal striae
buffalo hump
proximal limb muscle wasting

hypertension
T2DM
depression

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12
Q

diagnosis and management of cushings

A

Dx- oral dexamethasone suppression test, 24 hour urinary free cortisol test

tx- underlying cause

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13
Q

what is a normal anion gap and how to calculate it

A

normal is 10-18 mmol/L

calculate by positive ions subtract negative ions

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14
Q

side effects of metformin

A
  • gi problems- nausea, diarrhoea
  • lactic acidosis
  • poor vitamin B12 absorption
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15
Q

cushings disease- metabolic findings

A

hypokalaemic metabolic alkalosis

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16
Q

what are the functions of aldosterone?

A

raise BP- increase Na reabsoprtion, increase potassium and hydrogen secretion

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17
Q

what is primary hyperaldosteronism?

A

adrenal glands producing too much aldosterone

serum renin is low- As excess aldosterone increased BP (due to sodium reabsorption)

causes- bilateral adrenal hyperplasia (most common), adrenal adenoma (Conn’s), familial hyperaldosteronism

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18
Q

what is secondary hyperaldosteronism?

A

excess renin stimulates more aldosterone

high serum renin and high aldosterone

causes- renal artery stenosis, renal artery obstruction, HF

this is because the decreased blood flow to the kidney results in a decreased BP in the kidney, so therefore renin is secreted to raise blood pressure

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19
Q

features of hyperaldosteronism

A

hypertension
hypokalaemia
alkalosis

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20
Q

investigations in hyperaldosteronism

A

aldosterone/ renin ratio

high aldosterone, low renin= primary

high aldosterone, high renin= secondary

BP, serum electrolytes, ABG

CT/ MRI to check for tumour

21
Q

treatment of hyperaldosteronism

A

aldosterone antagonists- spironolactone/ eplerenone

surgical removal of adenoma

22
Q

phaeochromocytoma- presentation

A

HTN, headaches, palpitations, sweating, anxiety

23
Q

what is a phaeochromocytoma?

A

catecholamine secreting tumour (adrenaline)

24
Q

what are phaeochromocytoma’s commonly associated with?

A

MEN 2, neurofibromatosis,

25
Q

investigations to confirm a diagnosis of a phaeochromocytoma

A

24 hour urine catecholamines
Plasma free metanephrines (metanephrines are the breakdown product of catecholamines, so last longer in the blood, hence less variability, hence this is a more accurate measurement than plasma free catecholamines)

26
Q

management of a phaeochromocytoma

A

surgery is definitive

alpha blockers (1st line)- phenoxybenzamine

beta blockers (labetalol)

27
Q

diabetes- most appropriate second line management (after metformin) if the patient has CVD/ high risk of CVD

A

SGLT2 inhibitor- dapagloflozin

28
Q

thyrotoxicosis + tender goitre= ?

A

subacute (De Quervain’s) thyroiditis

29
Q

contraindications to metformin

A
  • chronic kidney disease: NICE recommend that the dose should be reviewed if the creatinine is > 130 µmol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 µmol/l (or eGFR < 30 ml/min)

metformin may cause lactic acidosis if taken during a period where there is tissue hypoxia. Examples include a recent myocardial infarction, sepsis, acute kidney injury and severe dehydration

iodine-containing x-ray contrast media: examples include peripheral arterial angiography, coronary angiography, intravenous pyelography (IVP); there is an increasing risk of provoking renal impairment due to contrast

nephropathy; metformin should be discontinued on the day of the procedure and for 48 hours thereafter

alcohol abuse is a relative contraindication

30
Q

Diabetes management: Biguanide’s
- examples of drugs in class
- action
- side effects

A

metformin

increase peripheral insulin sensitivity, decrease gluconeogenesis in the liver

SE’s- diarrhoea, abdo pain, lactic acidosis

notes:
- DOES NOT CAUSE HYPOGLYCAEMIA
- if SE’s- can use modified release

31
Q

Diabetes management: Thiazolidinedione’s
- examples of drugs in class
- action
- side effects

A
  • pioglitazone
  • increase peripheral insulin sensitivity, decrease gluconeogenesis in the liver
  • SE’s- weight gain, fluid retention, HF

notes:
- DOES NOT CAUSE HYPOGLYCAEMIA
- contraindicated in HF due to fluid retention

32
Q

Diabetes management: Sulfonylurea’s
- examples of drugs in class
- action
- side effects

A
  • gliclazide, glimepinide, glipizide, tolbutamide

stimulate insulin secretion

SE’s- weight gain, hypoglycaemia

notes:
- increased CVD risk if used as a monotherapy

33
Q

Diabetes management: DPP-4 inhibitors
- examples of drugs in class
- action
- side effects

A

sitagliptin, linagliptin, saxagliptin

inhibit DPP4 enzyme- hence increasing the activity of GLP-1 (an incretin)

SE’s- GI upset, URTI, dizziness

34
Q

Diabetes management: GLP-1 mimetics
- examples of drugs in class
- action
- side effects

A

exanitide, lixisenatide, dilaglutide

mimic the action of GLP-1 (an incretin)

SE’s- WL, dizziness, GI upset, hypoglycaemia

35
Q

action of incretins

A

produced in GI tract
increase insulin secretion
decrease glucose production
slow GI absorption

36
Q

Diabetes management: SGLT-2 inhibitors
- examples of drugs in class
- action
- side effects

A

empagliflozin, canagliflozin, dapagliflozin

cause glucose secretion in urine

SE’s- glycosuria causes recurrent UTI’s, WL, DKA

37
Q

what is Trousseau’s sign and what is it seen in?

A

Trousseau’s sign: carpal spasm on inflation of BP cuff to pressure above systolic

hypocalcaemia

38
Q

why is C-peptide used to differentiate between T1DM and T2DM?

A

C-peptide will be low in individuals with type 1 diabetes mellitus (as the pancreas is not making enough insulin precursor, which breaks down to form C-peptide and insulin) , and normal or high in individuals with type 2 mellitus.

39
Q

DM- if a patient develops CVD (has an MI etc) what medication must be started?

A

In patients with T2DM, SGLT-2 (dapagliflozin) should be introduced at any point they develop CVD, a high risk of CVD or chronic heart failure

side effect of SGLT-2- glucosuria- thrush

40
Q

acute DKA- insulin regime

A

In the acute management of DKA, insulin should be fixed rate (0.1 units/kg/hour) whilst continuing regular injected long-acting insulin but stopping short actin injected insulin

41
Q

Addisons- how is the steroid (hydrocortisone) dose split?

A

Patients with Addison’s disease require steroid replacement therapy to manage their condition. This usually takes the form of standard-release hydrocortisone for glucocorticoid replacement and fludrocortisone for mineralocorticoid replacement. Standard-release hydrocortisone is usually given as two doses, with the larger dose being given in the morning as this more closely resembles the natural daily variation in cortisol secretion from the adrenal glands. A smaller dose is given in the evening.

42
Q

complication of DKA Tx

A

cerebral oedema

43
Q

cushings- metabolic abnormality

A

hypokalamic metabolic alkalosis

44
Q

DM- cause of sudden visual loss

A

vitreous haemorrhage

45
Q

DM- if need to stop metformin, what monotherapy can be used?

A

linagliptin

46
Q

management of proliferative retinpoathy in diabetes

A

panretinal laser photocoagulation
intravitreal VEGF inhibitors

47
Q

management of a thyrotoxic storm

A

beta blockrs, propylthiouracil and hydrocortisone

48
Q

pregnant woman presents with hyperthyroidism in first trimester- management?

A

In pregnant woman who develop hyperthyroidism in the first trimester, propylthiouracil is preferred over carbimazole due to lower risk of foetal malformation

49
Q

first line investigation of a thyroid nodule

A

Ultrasonography is the first-line imaging of choice when investigating thyroid nodules

FINALS- random flashcards per system (16 decks)

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