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Jonah's Med Notes > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the cause of T1DM?

A

Absolute insulin deficiency, 2nd to immune mediated destruction of pancreatic B-cells

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2
Q

What is the cause of T2DM?

A

Peripheral insulin resistance + inadequate production

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3
Q

What antibodies are associated with T1DM?

A

GAD and IA2

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4
Q

Why does Insulin requirement occur in T2DM?

A

B-cell dysfunction -> initial increased insulin production to compensate -> eventual exhaustion -> cell death + dysfunction. Glucotoxicity + lipotoxicity -> cell death.

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5
Q

How can DM be assessed in a Long Case? (DICER)

A
  • D - degree of disease
    • Length of dx. Sx.
  • I - Impact of disease.
  • C - Complications
    • Macrovascular -> past stroke, MI, PVD. BP.
      • Sx -> SOB, angina, claudication.
    • Microvascular ->
      • Retinopathy -> vision changes. Ophthal r/v?
      • Neuropathy -> paraesthesias or foot ulcer. Podiatrist?
      • Nephropathy -> eGFR? ACR? CKD? GP r/v?
      • Infections + diabetic foot
  • E - Efficacy of tx
    • Current tx. Who do they see?
    • Monitoring -> measurement of BGL, recent BGLs, range of BGLs. HbA1c.
  • R - RFs
    • Diet + exercise, obesity. Smoking + alcohol. Lipids.
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6
Q

What are the neuropathic symptoms of DM?

A

Diabetic ulcers

Charcot joint

Orthostatic hypotension

Sensory loss (proprioception, vibration, light + sharp)

Reflex loss

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7
Q

What are the retinopathic symptoms of DM?

A

Decreased visual acuity

Non proliferative changes -> dot + blot haemorrhages, cotton wool spots, hard exudates.

Proliferative changes -> neovascularisation

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8
Q

What are the nephropathic symptoms of DM?

A

Glycosuria

Proteinuria

HTN.

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9
Q

What are the macrovascular complications of DM?

A

CAD, PAD, CVA

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10
Q

What are the microvascular complications of DM?

A

Retinopathy

Neuropathy

Nephropathy

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11
Q

What are the symptoms of DM?

A

Polyuria + polydipsia.

Lethargy

Recurrent infections + poor wound healing.

Blurred vision

Loss of sensation

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12
Q

Name 4 causes of Hypoglycaemia

A

Insufficient food

Excess insulin/oral hypoglycaemics

Excess alcohol

Excessive exercise.

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13
Q

How does Metformin work?

A

Decreased hepatic gluconeogenesis + increases insulin sensitivity.

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14
Q

What are the side effects of metformin?

A

Lactic acidosis (contra w/ GFR < 30, hepatic, alcoholic)

GIT disturbance.

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15
Q

How do sulfonylureas work?

A

Increased release of insulin

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16
Q

What are the SE of Sulfonylureas?

A

Severe hypoglycaemia

Weight gain

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17
Q

How do Thiazolidinediones work?

A

Bind PPAR-gamma receptors -> increase insulin sensitivity

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18
Q

What are the SE of Thiazolidinediones?

A

Weight gain, increased risk of HF, bladder cancer, fractures.

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19
Q

How do SGLT-2 inhibitors work?

A

Inhibit glucose reuptake in kidneys.

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20
Q

How does acarbose work?

A

Decreased carb breakdown in gut -> decreased carbs.

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21
Q

How do GLP-agonists work?

A

GLP-1 agonist -> exanatide.

Increases GLP-1 (glucagon like peptide) -> increases insulin secretion in response to hypoglycaemia.

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22
Q

How do DDP4 Inhibitors work?

A

DDP-4 degrades GLP-1, therefore inhibits GLP-1’s degradation.

GLP-1 (glucagon like peptide) -> increases insulin secretion in response to hypoglycaemia.

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23
Q

What is the HBA1C target in DM?

A

<7%

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24
Q

What is the LDL cholesterol in DM?

A

<2mmol/L

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25
Q

What is the HDL target in DM?

A

>1mmol/L

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26
Q

What is the total cholesterol target in DM?

A

<4mmol/L

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27
Q

What is the Triglycerides target in DM?

A

<2mmol/L

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28
Q

What is Du Quervains Thyroiditis? What pattern is seen?

A

Transient inflame following viral infection (adenovirus, mumps, coxsachie virus) -> damages follicular cells -> release of stored T3/4.

Therefore:

4-6wks Hyper-thyroid -> 4-6mo Hypo-thyroid -> recovery.

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29
Q

What are the common symptoms of thyroiditis?

A

Weight loss w/ increased appetite. Diarrhoea.

Increased symp -> tremor, tachy, palpitations, warm/sweaty skin

Heat intolerance. Fatigue

Agitation + irritability

Thymic enlargement -> nodule, multi-nodular, diffuse.

30
Q

What signs are specific to Grave’s disease?

A

Diffuse + soft goitre.

Exophthalmos -> auto-immune process against extra-ocular muscles, increased inflame in retro-orbital space.

Periorobital oedema

Pre-tibial myxoedema -> deposition of polysaccharides w/ infiltrative disease.

31
Q

How can primary and secondary thyroiditis be differentiated?

A

TSH -> primary has low TSH.

2nd has high TSH

32
Q

How can the adrenergic symptoms of thyroiditis be managed?

A

Beta-blockers

33
Q

How is AF managed?

A

NOACs or warfarin

34
Q

What is the management for thyroiditis? (Name 3)

A

Anti-thyroid drugs (e.g. Carbimazole, propylthiouracil, methimazole)

Thyroidectomy

Radioactive iodine ablation

35
Q

Name 4 causes of Hypothyroidism

A

Hashimoto’s thyroiditis
Iatrogenic -> 2nd to Iodine ablation, surg, or anti-thyroid drugs
Iodine deficiency
Transient thyroiditis -> De Quervains, post-partum
Infiltrative disease -> Sarcoidosis, amyloidosis, haemochromatosis
2nd hypothyroidism -> TSH deficiency

36
Q

What antibodies are present in Hashimoto’s?

A

Anti-TPO

37
Q

What are the symptoms of Hypothyroidism? (8)

A

Mnemonic - SLUGGISH:

S - sleepiness/lethargy

L - loss of memory

U - unusually dry skin

G - goitre

G - gradual personality changes

I - increased weight

S - sensitivity to cold

H - hair loss

38
Q

How is hypothyroidism managed?

A

Thyroxine

39
Q

What are the causes of Cushing’s syndrome?

A
  • ACTH-dependent (85%) – bilateral adrenal hyperplasia and hypersecretion due to:
    • ACTH-secreting pituitary adenoma (Cushing’s disease; 80% of ACTH-dependent)
    • Ectopic ACTH-secreting tumour (e.g. small cell lung carcinoma, bronchial, carcinoid, pancreatic islet cell, pheochromocytoma, or medullary thyroid tumours)
  • ACTH-independent (15%) - long-term use of exogenous glucocorticoids
40
Q

What are the symptoms of Cushing’s disease?

A

CUSHINGO

C - Characteristic findings -> moon facies, buffalo hump, central obesity, “lemon on sticks”

U - Urinary free cortisol

S - Striae + supressed immunity

H - Hyperglycaemia, HTN, hypercholesterolaemia. Hirsutism.

I - iatrogenic causes

N - neoplastic causes

G - glucose intolerance

Others - osteoporosis, ocular (glaucoma, cataracts), proximal muscle wasting, menstrual Sx.

41
Q

How is Cushing’s diagnosed?

A

2/3 +ve -> dx.

  1. 24hr urinary free cortisol excretion
  2. Midnight salivary cortisol level
  3. Low dose dexamethasone suppression test -> normally supresses cortisol, but in cushings cortisol remains high.
42
Q

How is Cushings and Ectopic ACTH distinguished?

A

High dose dexamethasone suppression

Supressed = Cushing’s disease.

No suppression = ectopic ACTH production.

43
Q

How is Cushing’s managed? (Surgical / Medical)

A

Cushing’s disease -> trans-sphenoidal surgery. 70-80% cure.

Ectopic ACTH -> surgery of site

Adrenal enzyme inhibitors:

Ketoconazole -> blocks all three cotricosteroids

Metyrapone -> blocks only glucocorticoid releas

44
Q

What are the complications of Cushings?

A

Osteoporosis

Increased CVD risk -> HTN + glucose + hyperlipidaemia

VTE risk

45
Q
A
46
Q

How do SGLT2 inhibitors work? Name one.

A

SGLT-2 inhibitors reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.

Examples include canagliflozin, dapagliflozin and empagliflozin.

47
Q

What are the side effects of SGLT2 inhibitors?

A

Urinary and genital infection (secondary to glycosuria). Fournier’s gangrene has also been reported
Normoglycaemic ketoacidosis
Increased risk of lower-limb amputation

Weight loss

48
Q

What is Waterhouse-Friderichsen syndrome?

A

Adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection.

Typically, it is caused by Neisseria meningitidis.

49
Q

What is Addison’s disease?

A

Autoimmune destruction of adrenals.

Leads to low levels of Cortisol, Aldosterone, Sex hormones.

50
Q

What are the three layers of the adrenals?

A

Zona Glomerulosa -> Mineralcorticoids

Zona Fasiculata -> Glucocorticoids

Zona Reticularis -> Androgens

51
Q

How is Addison’s disease managed?

A

Glucocorticoid replacement:
Short acting -> hydrocortisone. Large dose morning, small dose bed-time.
Long acting -> pred or dex
Mineralcorticoid replacement:
Fludrocortisone.
Monitor BP, K+, renin
Androgen replacement:
DHEA replacement, in women, w/ significant Sx.

52
Q

What is the goal of treatment in Addison’s disease?

A

Replace normal diurnal cortisol release. Right dose = dose that controls Sx but doesn’t cause Cushing’s

53
Q

What are the Signs + Sx of Hypercalcaemia?

A

Bones, groans, stones, thrones, psychogenic undertones.

Bones -> fractures. Stones -> renal stones

Thrones -> polyuria and constipation. Groans -> abdo pain

Psychogenic undertones -> altered cognition, depression.

54
Q

How is Hypercalcaemia managed?

A

Saline, calcitonin, and a bisphosphonate

55
Q

What are the symptoms of Hypocalcaemia?

A

Tetany

Seizures

Prolonged QT

Psych changes -> anxious, irritable, irrational

56
Q

How is Hypo, Hyper Natremia defined?

A

Hypo < 135. Hyper > 145.

57
Q

How can hyponatremia be stratified?

A

Hypovolemic (dry)

Euvolemic (polydipsia, SIADH, excessive Saline infusion)

Hypervolemic (wet)

58
Q

How is Hyper Hypo Kalaemia defined?

A

Hyper > 5mmol/L.

Hypo < 3.5mmol/L

59
Q

What 3 changes are seen in Hyperkalaemia?

A

Hyperacute T waves.

Loss of P-wave

Widened QRS

60
Q

What 3 ECG changes are seen in Hypokalaemia?

A

Flattened T-wave

ST depression

U-wave

61
Q

Name 5 RF for Osteoporosis

A

Female, white, age, fam hx, postmenopause, low calcium intake, vitamin D deficiency.

62
Q

What T score is diagnostic of Osteoporosis?

A

Osteoporosis when their T-score is –2.5 or lower.

Osteopenia is a T-score between –1 and –2.5

63
Q

How is Osteoporosis managed? (3 Non-Pharma, 3 Pharma)

A

Non-Pharma

Diet -> adequate calcium, vitamin D, protein
Weight bearing exercise
Smoking cessation + moderate alcohol

Pharm

Oral or IV bisphosphonate (inhibit differentiation into osteoclasts, + deactivate osteoclasts.)
Denosumab (Monoclonal antibody, inhibits RANKL.)
Raloxifene (SERM)

64
Q

Elderly person with symptoms of anaemia e.g. fatigue (the most common presenting symptom)
Massive splenomegaly
Hypermetabolic symptoms: weight loss, night sweats etc

A

Myelofibrosis

65
Q

Low T3/T4 and normal TSH with acute illness

A

Sick euthyroid syndrome

66
Q

What HbA1c is diagnostic of DMII?

A

HbA1c ≥6.5% is diagnostic

67
Q

What 2-hour plasma glucose is diagnostic of DMII?

A

>11.1 mol/L

68
Q

What fasting blood glucose is diagnostic of DMII on 2 occasions?

A

>7.0mmol/L

69
Q

When are SGLT2 inhibitors avoided?

A

Increase risk of lower extremity amputation.

Avoid in patients with peripheral vascular disease and foot
ulcers.

70
Q
A

Jonah's Med Notes (8 decks)

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