Endocrinology Flashcards

(70 cards)

1
Q

What is the cause of T1DM?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the cause of T2DM?

A

Peripheral insulin resistance + inadequate production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What antibodies are associated with T1DM?

A

GAD and IA2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the neuropathic symptoms of DM?

A

Diabetic ulcers

Charcot joint

Orthostatic hypotension

Sensory loss (proprioception, vibration, light + sharp)

Reflex loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the nephropathic symptoms of DM?

A

Glycosuria

Proteinuria

HTN.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the macrovascular complications of DM?

A

CAD, PAD, CVA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the microvascular complications of DM?

A

Retinopathy

Neuropathy

Nephropathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of DM?

A

Polyuria + polydipsia.

Lethargy

Recurrent infections + poor wound healing.

Blurred vision

Loss of sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name 4 causes of Hypoglycaemia

A

Insufficient food

Excess insulin/oral hypoglycaemics

Excess alcohol

Excessive exercise.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does Metformin work?

A

Decreased hepatic gluconeogenesis + increases insulin sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the side effects of metformin?

A

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

GIT disturbance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do sulfonylureas work?

A

Increased release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the SE of Sulfonylureas?

A

Severe hypoglycaemia

Weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do Thiazolidinediones work?

A

Bind PPAR-gamma receptors -> increase insulin sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the SE of Thiazolidinediones?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do SGLT-2 inhibitors work?

A

Inhibit glucose reuptake in kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does acarbose work?

A

Decreased carb breakdown in gut -> decreased carbs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the HBA1C target in DM?

A

<7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the LDL cholesterol in DM?

A

<2mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is the HDL target in DM?
\>1mmol/L
26
What is the total cholesterol target in DM?
\<4mmol/L
27
What is the Triglycerides target in DM?
\<2mmol/L
28
What is Du Quervains Thyroiditis? What pattern is seen?
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.
29
What are the common symptoms of thyroiditis?
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
What signs are specific to Grave's disease?
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
How can primary and secondary thyroiditis be differentiated?
TSH -\> primary has low TSH. 2nd has high TSH
32
How can the adrenergic symptoms of thyroiditis be managed?
Beta-blockers
33
How is AF managed?
NOACs or warfarin
34
What is the management for thyroiditis? (Name 3)
Anti-thyroid drugs (e.g. Carbimazole, propylthiouracil, methimazole) Thyroidectomy Radioactive iodine ablation
35
Name 4 causes of Hypothyroidism
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
What antibodies are present in Hashimoto's?
Anti-TPO
37
What are the symptoms of Hypothyroidism? (8)
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
How is hypothyroidism managed?
Thyroxine
39
What are the causes of Cushing's syndrome?
* 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
What are the symptoms of Cushing's disease?
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 **O**thers - osteoporosis, ocular (glaucoma, cataracts), proximal muscle wasting, menstrual Sx.
41
How is Cushing's diagnosed?
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
How is Cushings and Ectopic ACTH distinguished?
High dose dexamethasone suppression Supressed = Cushing’s disease. No suppression = ectopic ACTH production.
43
How is Cushing's managed? (Surgical / Medical)
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
What are the complications of Cushings?
Osteoporosis Increased CVD risk -\> HTN + glucose + hyperlipidaemia VTE risk
45
46
How do SGLT2 inhibitors work? Name one.
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
What are the side effects of SGLT2 inhibitors?
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
What is Waterhouse-Friderichsen syndrome?
Adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection. Typically, it is caused by Neisseria meningitidis.
49
What is Addison’s disease?
Autoimmune destruction of adrenals. Leads to low levels of Cortisol, Aldosterone, Sex hormones.
50
What are the three layers of the adrenals?
Zona Glomerulosa -\> Mineralcorticoids Zona Fasiculata -\> Glucocorticoids Zona Reticularis -\> Androgens
51
How is Addison's disease managed?
**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
What is the goal of treatment in Addison's disease?
Replace normal diurnal cortisol release. Right dose = dose that controls Sx but doesn’t cause Cushing’s
53
What are the Signs + Sx of Hypercalcaemia?
**Bones, groans, stones, thrones, psychogenic undertones.** Bones -\> fractures. Stones -\> renal stones Thrones -\> polyuria and constipation. Groans -\> abdo pain Psychogenic undertones -\> altered cognition, depression.
54
How is Hypercalcaemia managed?
Saline, calcitonin, and a bisphosphonate
55
What are the symptoms of Hypocalcaemia?
Tetany Seizures Prolonged QT Psych changes -\> anxious, irritable, irrational
56
How is Hypo, Hyper Natremia defined?
Hypo \< 135. Hyper \> 145.
57
How can hyponatremia be stratified?
Hypovolemic (dry) Euvolemic (polydipsia, SIADH, excessive Saline infusion) Hypervolemic (wet)
58
How is Hyper Hypo Kalaemia defined?
Hyper \> 5mmol/L. Hypo \< 3.5mmol/L
59
What 3 changes are seen in Hyperkalaemia?
Hyperacute T waves. Loss of P-wave Widened QRS
60
What 3 ECG changes are seen in Hypokalaemia?
Flattened T-wave ST depression U-wave
61
Name 5 RF for Osteoporosis
Female, white, age, fam hx, postmenopause, low calcium intake, vitamin D deficiency.
62
What T score is diagnostic of Osteoporosis?
Osteoporosis when their T-score is –2.5 or lower. Osteopenia is a T-score between –1 and –2.5
63
How is Osteoporosis managed? (3 Non-Pharma, 3 Pharma)
**_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
Elderly person with symptoms of anaemia e.g. fatigue (the most common presenting symptom) Massive splenomegaly Hypermetabolic symptoms: weight loss, night sweats etc
Myelofibrosis
65
Low T3/T4 and normal TSH with acute illness
Sick euthyroid syndrome
66
What HbA1c is diagnostic of DMII?
HbA1c ≥6.5% is diagnostic
67
What 2-hour plasma glucose is diagnostic of DMII?
\>11.1 mol/L
68
What fasting blood glucose is diagnostic of DMII on 2 occasions?
\>7.0mmol/L
69
When are SGLT2 inhibitors avoided?
Increase risk of lower extremity amputation. Avoid in patients with peripheral vascular disease and foot ulcers.
70