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Y4 Medicine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are incretins?

A

Hormones produced by the GI tract which are secreted in response to a big meal and reduce blood glucose levels. They;
- Increase insulin secretion
- Inhibit glucagon production
- Slow glucose absorption by the GI tract

Main incretin = GLP-1

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2
Q

Which enzyme inhibits incretins?

A

DPP-4 (dipeptidyl peptidase - 4)

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3
Q

Metformin

A

MOA = increases insulin sensitivity + decreases hepatic gluconeogenesis
SE = GI upset / Lactic acidosis
Contraindications = eGFR < 30

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4
Q

Sitagliptin

A

Type = DPP-4 Inhibitor (Increases levels of GLP-1)
SE = GI upset / URTI symptoms / Headaches / Inc risk of pancreatitis

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5
Q

SLGT-2 Inhibitors

A

Dapagliflozin / empagliflozin
MOA = Inhibit SGT in the PCT which increases glucose excretion.
SE = Increased UTIs/Thrust / Fourniers gangrene / Can cause DKA!
Pros = causes weight loss

*NOTE - dapagliflozin is also licensed in the management of HF.

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6
Q

Liraglutide / Exanatide

A

GLP-1 Agonists
SC Injection + also licensed for weight loss
SE = Hypoglycemia!!! N&V / GI upset / Dizziness
May increase risk of pancreatitis

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7
Q

Piaglitazone

A

Thiazolidinedione
MOA = Activates PPAR-gamma receptors in adiopcytes which increases insulin sensitivity + decreases hepatic gluconeogenesis
SE = Fluid retention / HF / CKD / Anemia / Liver dysfunction / Inc risk of bone fractures / WEIGHT GAIN / can inc risk of bladder cancer

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8
Q

Sulfonylureas

A

Gliclazide
MOA = Inhibits K+ channels on beta cells leading to insulin secretion
SE = HYPOGLYCEMIA / weight gain / Hyponatremia / bone marrow toxicity
Contraindications: avoid post MI or Renal failure

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9
Q

Which diabetic agents cause weight gain

A

Pioglitazone + sulfonylureas (gliclazide)

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10
Q

Which diabetic agents can cause DKA

A

SGLT-2 inhibitors

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11
Q

Which diabetic agents are most likely to cause Hypoglycemia

A

GLP-1 Agonists
Sulfonylureas

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12
Q

Which diabetic agents can aid weight loss

A

GLP 1 agonists + SLGT-2 inhibitors

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13
Q

Central diabetes insipidus

A

Decreased secretion of ADH from posterior pituitary

Causes = Idiopathic or secondary to pituitary surgery, head injury, haemochromatosis, CNS infection, Craniopharyngiomas .

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14
Q

Nephrogenic diabetes insipidus

A

A failure of the Collecting ducts to respond to ADH

Causes = tubulo-interstitial nephritis / Lithium therapy / avpr2 mutation / hypercalcemia / hypokalemia / Sjogren’s syndrome

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15
Q

Which cancer is hashimoto’s thyroiditis associated with?

A

MALT lymphoma

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16
Q

Hashimoto’s thyroiditis autoantibodies

A

Anti-TPO + Anti-thyroglobulin (Anti-Tg)

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17
Q

Which drug most commonly exacerbates hyperthyroidism

A

Amiodarone

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18
Q

Functions of cortisol

A

Increases alertness
Increases blood glucose
Increases metabolism
Inhibits the immune system
Inhibits bone formation

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19
Q

ABG/VBG findings in Cushing’s disease

A

Hypokalemic metabolic alkalosis + Hypernatremia

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20
Q

Blood findings in Addison’s disease

A

Hyponatremia + Hyperkalemia

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21
Q

Management of acromegaly in a patient who cannot undergo surgery

A

GH antagonists (pegvisomant)
Somatostatin analogue (Ocreotide) - inhibit GH release
Dopamine agonists (Bromocriptine)

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22
Q

Advice for pregnant women with hypothyroidism

A

Increase levothyroxine dose by 50%

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23
Q

Digoxin causes gynaecomastia, true or false?

A
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24
Q

MEN type 1

A

Parathyroid
Pituitary
Pancreas

+ Adrenal + Thyroid

Often presents as hypercalcemia (hyperparathyroidism) or recurrent hypoglycemia (insulinoma) or recurrent gastric ulcers (gastrinoma)
Mutation = MEN1 gene

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25
Q

MEN type 2

A

Parathyroid
Phaeochromocytoma
Medullary thyroid cancer

RET oncogene mutation

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26
Q

MEN type 3

A

Medullary thyroid cancer
Pheochromocytoma

Marfinoid
Neuromas

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27
Q

Main side effects of carbimazole

A

Agranulocytosis (infections)
Acute pancreatitis

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28
Q

Visual field defects seen in prolactinoma’s

A

Bitemporal hemianopia
Bitemporal superior quandrantopia

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29
Q

Hashimoto’s thyroiditis antibodies

A

Anti-TPO

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30
Q

Grave’s disease antibodies

A

TSH antibodies

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31
Q

First line treatment for cerebral mets

A

Dexamethasone

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32
Q

Hyperthyroidism management in pregnant ladies

A

First trimester = propylthiouracil
2nd + 3rd trimester = carbimazole

33
Q

Diagnostic glucose measurements for diabetes

A

Fasting glucose >7mmol/L
Random glucose >11.1 (or after OGTT)

34
Q

Pre-diabetes glucose measurements

A

Fasting glucose 6.1 - 6.9
Glucose tolerance / random plasm glucose 7.8 - 11.1

35
Q

Features unique to T1DM (not seen in T2DM)

A

Low C peptide
Weight loss
Autoantibodies
Ketonuria

36
Q

Primary Hypothyroisim

A

Low T4/T3
High TSH

Causes;
- Hashimoto’s
- Iodine deficiency
- Lithium
- Amiodarone
- Overtreatment of hyperthyroidism

37
Q

Secondary hypothyroidism

A

Low T4/T4
Low TSH

Causes;
- Pituitary adenoma
- Pituitary surgery / trauma / radiotherapy
- Sheehan’s syndrome

38
Q

Myxoedema coma

A

Severe hypothyroidism leading to decreased conciousness + coma

39
Q

Management of myxoedema coma

A

IV fluids
IV levothyroixine
IV hydrocortisone

40
Q

Sick Euthyroidism

A

T3/T4 low
TSH = innapropriately low / normal

Pt will typically have pneumonia / other illness at the same time

41
Q

Grave’s disease Features

A

Autoimmune hyperthyroidism
- Bilateral expothalmus
- Opthalmoplegia
- Pretibial myxoedema
- Acropacy (clubbing)

May have a gotire
Scintigraphy shows increased uptake

42
Q

Gotire with firm nodules and scintigraphy reveals patchy uptake

A

Multinodular goitre

43
Q

Painful gotire with reduced, patch iodine uptake on scintigraphy

A

De quervain’s thyroiditis

44
Q

De quervain’s thyroiditis

A

Initially causes a transient hyperthyroidism and then hypothyroidism.
Usually caused by a viral infection.

45
Q

Medical management of hyperthyroidism

A

1st line = Carbimazole
2nd line = Propylthiouracil

Symptomatic relief with beta-blockers
Radioactive iodine if multinodular goitre

46
Q

Thyrotoxic storm

A

Acute severe form of hyperthyroidism
Sx = hyperpyrexia + tachycardia + agitation

Tx = propylthiouracil + hydrocortisone + propanolol

ECG may show lateral T wave inversion

47
Q

Most common type of thyroid cancer

A

Papillary

48
Q

Management of papillary / Follicular thyroid cancers

A

Total thyroidectomy + radioiodine
Yearly TFTs/Calcitonin levels (as thats how a medullary one would present)

49
Q

Causes of Hypoparathyroidism

A

Primary = usually due to thyroidectomy (Hypocalcemia + Low PTH + high phosphate)
Pseudo-hypoparathyroidism = resistance to PTH (would cause a hypocalcemia + raised PTH)

50
Q

Symptoms of hypocalcemia

A

Tetany
Peri-oral parasthesia
Trousseau’s sign - BP cuff
Chvostek’s sign - parotid gland

51
Q

Causes of cushing’s syndrome

A
  1. Exogenous steroid use (primary adrenal excess)
  2. Cushing’s disease (pituitary adenoma - secondary adrenal excess)
  3. Adrenal adenoma (primary)
  4. Paraneoplastic syndrome (ectopic ACTH release)
52
Q

Clinical Features of cushings

A

Round moon face
Central obesity
Proximal limb muscle wasting
Buffalo hump
Abdominal striae

HTN + Cardiac hypertrophy + Hyperglycemia can all occur from high cortisol

53
Q

Investigations & Findings in Cushing’s.

A

1st line = dexamethasone suppression test.
Low dose = no supression of cortisol
High dose = allows you to determine the cause of the cushing’s
- Cortisol + ACTH are suppressed = Cushing’s disease
- Just ACTH suppressed = Adrenal adenoma
- Neither suppressed = Ectopic cause (SCLC)

54
Q

Causes of Adrenal Insufficiency

A

Primary = Addison’s disease
Secondary = Pituitary surgery/inf/radiation/sheehan’s
Tertiary = Long term steroid use (can suppress the hypothalamus)

55
Q

Presence of what clinical feature indicates a primary adrenal insufficiency rather than secondary/tertiary

A

Hyperpigmentation - as this suggests raised ACTH

56
Q

1st line investigation for adrenal insufficiency

A

Short syncathen test (ACTH stimulation test)
= Failure for cortisol to rise

57
Q

Which antibodies are seen in Addison’s disease

A

Adrenal cortex antibodies + 21-hydrozylase antibodies

58
Q

Management of addison’s disease

A

Hydrocortisone
Fludrocortisone

59
Q

Addisonian crisis presentation + management

A

Reduced consciousness
severe hypotension
Hyponatremia + Hyperkalemia
Hypoglycemia

Management = IV hydrocortisone + IV fluids + IV dextrose - monitor + treat hyperkalemia as required

60
Q

Medical Management of acromegaly

A

Pegvisomant (GH antagonist)
Octreotide (Somatostatin analogue)

61
Q

Causes of Hyperaldosteronism

A

Primary;
- Bilateral adrenal hyperplasia
- Conn’s syndrome (adrenal adenoma)
- Familial hyperaldosteronism

Secondary;
- Renal artery stenosis /obstruction
- HF

62
Q

How to differentiate between causes of hyperaldosteronism

A

Renin:Aldosterone ratio
in primary there is a Low renin + high aldosterone
In secondary there is a high renin + high aldosterone

63
Q

Blood/ABG/VBG findings in Hyperaldosteronism

A

pH = Alkalosis
Hypokalemia

64
Q

Symptomatic relief of hyperaldosteronism

A

Spirinolactone

65
Q

Causes of SIADH

A

Ectopic production - paraneoplastic syndrome (SCLC, Pancreatic + prostate cancer)
Meds - thiazides, NSAIDs etc
Neurological - stroke, head injury etc
Infection
Post op

66
Q

Diagnostic findings of SIADH

A

High urine sodium + High urine osmolality + Hyponatremia + Euvolemia

67
Q

Tolvaptan

A

ADH receptor blocker

68
Q

Histology of papillary thyroid cancer

A

Cells with empty nuclei
Orphan annie eyes
Psammoma bodies (ca deposits in papillary cells)

69
Q

Waterhouse Friedreichsen syndrome

A

Severe adrenal failure due to severe infection (often neisseria meningitis)
Essentially causes severe addisonian crisis + DIC + Shock

70
Q

Increased uptake on scintigraphy in a well defined sphere shape

A

Most likely a thyroid adenoma - grave would cause a more diffuse increased uptake and a multinodule goitre causes patchy uptake

71
Q

Which insulin is used in an insulin pump

A

Insulin lispro

72
Q

What would an ECG of hypocalcemia show

A

Isolated QTc elongation

*can occasionaly cause torsades de pointes but not as common as QT elongation.

73
Q

Causes of hypophosphatemia

A

DKA
Alcohol excess
Acute liver failure
Refeeding syndrome
Primary hyperparathyroidism
Osteomalacia

Consequences = Haemolysis + WBC dysfunction + Muscle weakness + Rhabdomylosis + CNS dysfunction.

74
Q

Management of hypophosphatemia in DKA

A

Hypophosphatemia is a common complication of insulin therapy in DKA (as it causes an intracellular shift of phosphate).
You should never stop the insulin infusion because of this, just transfuse some phosphate if its severe (i.e levels < 0.3)

75
Q

What type of malignancy is associated with Hashmimoto’s thyroiditis

A

MALT lymphoma

76
Q

Treatment of acute severe symptomatic hyponatemia

A

Hypertonic saline solution (e.g 3% Sodium chloride)

77
Q

Treatment of acute severe symptomatic hyponatemia

A

Hypertonic saline solution (e.g 3% Sodium chloride)

78
Q

Central pontine myelinolysis

A

Occurs from rapid correction of hyponatemia (too fast) leading to brainstem damage.
Features = spastic quadriparesis, Pseudobulbar palsy and emotional lability.
If severe can lead to confusion, coma and even locked in syndrome.

Y4 Medicine (22 decks)

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