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KFP study > Endocrine/Metabolic > Flashcards

Endocrine/Metabolic Flashcards

1
Q

T score values for osteoporosis?

5 answers

A

-1 and over = normal

-1 to -2.5 = osteopenia

-2.5 or lower = osteoporosis

if aged >50 + Min.Trauma# (not vertebra or hip) + T score <-1.5 then = osteoporosis

If age >50 and min.trauma# at vertebra or hip = osteoporosis

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2
Q

Pros/Cons of bisphosphonates

A

Pros
Low Cost,
Oral Dose,
Longer half life (so can be stopped and still have effect)

Cons
GI upset
absorption affected by food
Can’t be used in severe CKD
Short lasting myalgia

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3
Q

Denusomab dose?

A

Denosumab 60mg SubCut 6 monthly

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4
Q

Pros/Cons of Denusomab?

3 pros and 5 cons

A

Pros
Avoids GI upset
No renal adjustment
6 Monthly

Cons
STRICTLY 6 monthly
Therapy is indefinite
Withdrawal > 4 weeks can lead to spontaneous vertebral fractures
MAY cause hypocalcemia with CKD
Osteonecrosis of the jaw

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5
Q

When do you stop bisphosphonate therapy

A

5 years after oral versions
-continue for 10 years however in those at high risk of MT#

3 years after IV bisphosphonate
- continue for 6 if high MT# risk

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6
Q

When do you start assessing for osteoporosis?

And when do you start scanning (rebatable)?

A

Assess women > 45 and men > 55
For MT# or other conditions that effect BMD

Scan when
If W>45 or M>50 has a Minimal trauma fracture then scan

If W> 45 or M> 50 with any of the following: RA, premature menopause, hypogonadism, hyperthyrodism, hyperparathyroidsim, CKD, coeliac/malabsorption, taking glucocorticoids (>3 months dosed over 7.5mg), anti androgen therapy, then also scan and qualify for rebate.

If M or W over 70 years old then scan (DXA)

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7
Q

What are the TSH targets in thyroxine replacement?

A

< 60 years old TSH target is between 0.5-2.5 milliunits/L

Between 60-80 years old TSH target is 1-5 milliunits/L

Over 80 years old TSG target is 4-6 milliunits/L

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8
Q

General advice to give patients taking thyroxine replacement?

4 answers

A
  1. To take thyroxine on an empty stomach, 30-60 minutes before breakfast OR 3 hours after evening meal
  2. To avoid taking it with supplements that reduce absorption: iron, calcium
  3. Patient will need long term bloods done to allow for dose titration
  4. Warn of symptoms of hyperthyroidism as this indicates a dose reduction may be needed
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9
Q

Simple Steps to investigate Hyperthyroidism?

A
  1. TSH
  2. Symptomatic treatment with betablocker
  3. Retest TSH in 6-8 weeks
  4. If still hyperthyroid test for TSH-R
  5. Refer
  6. Treat
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10
Q

Treatment for severe symptoms of PRIMARY hyperthyroidism

list 3 symptoms

Give 1 example of dosing instructions

A

Symptoms include weight loss, AF, myopathy, heart failure

Carbimazole 30-45mg, orally, daily but divided into two or three doses.
Review with bloods and adjust every 4-6 weeks

or
propylthiouracil 300-450mg daily in 2-3 divided doses. Also adjust 4-6 weekly

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11
Q

Treatment for milder symptoms in PRIMARY hyperthyroidism?

A

Carbimazole 10-20mg, orally, daily in 2-3 divided doses. Adjust 4-6 weekly

PTU 100-200mg PO daily in 2-3 divided doses. Adjust 4-6 weekly

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12
Q

After remission of thyrotoxicosis with hyperthyroidism, what is the recommended follow up?

A

testing should be done every 3-4 months for the first year then annually for 5 years.

(If lifelong antithyroid medication is needed, 3-4 monthly testing is needed initially then 6 monthly thereafter)

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13
Q

During a thyroid storm, what are the management priorities and what may you use to address these ?

5 answers

A
  1. stopping thyroid hormone synthesis (with carbimazole)
  2. decreasing t4–>t3 conversion (with IV dexamethasone)
  3. Restoring hydration (IV fluids)
  4. Controlling tachycardia (beta blocker)
  5. Sedation if needed
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14
Q

What to check for on examination of a Goitre?

4 answers

A
  1. Size/shape and consistency of the goitre
  2. Presence and amount of nodules
  3. Enlarged lymph nodes
  4. Pemberton’s sign
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15
Q

If there is a Goitre with a Low TSH, which Imaging should be considered?

A

Radionucleotide scan and U/S. irrespective of remaining serology.

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16
Q

What are signs and symptoms of Hereditary Haemochromatosis?

(7)

A
  1. Loss of libido
  2. Joint Aches
  3. Abdominal pain
  4. Weight loss
  5. Tiredness/lethargy
  6. Polyuria, polydipsia
  7. Chest pain, SOB, palpitations
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17
Q

Name three pieces of advise with regards to management of HH?

A
  1. Will require therapeutic venesections if iron overloaded
  2. Will require regular Iron studies. Depends on ferritin level how often this is.
  3. Will need a specialist referral if ferritin is over 1000ul/L
  4. If found to have haemochromatosis, should offer to test family members
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18
Q

What tests should you order for an INCIDENTAL adrenal lesion?

A

1mg overnight dexamethasone suppression test

Aldosterone: Renin ratio

Plasma metanephrines

(Non Contrast Adrenal CT, if for some reason lesion found on a CTPA)

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19
Q

Signs and Symptoms of pheochromacytoma?

A

Flushing
Sweating
Palpitations
Sense of doom
Tremor
Headache
Anxiety
Constipation
Weight loss

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20
Q

Common causes of HYPOphoshpataemia ?

4 broad groups

A
  1. Redistribution form extracellular fluid to intracellular.
    (glucose IV infusions, diabetic ketoacidosis, acute respiratory alkalosis, refeeding syndrome)
  2. Poor intestinal absorption
    usually from phosphate binders. E.g. antacids.
  3. Increased kidney excretion
    (primary hyperparathyroid, PTH related protein dependent hypercalcaemia of malignancy, Intrinsic renal disease -Fanconi syndrome, Drugs: alcohol, heavy metals)
  4. Extra-renal removal
    Haemodialysis.
  5. Also from IV iron transfusion with carboxymaltose
  6. Alcoholism via multiple mechanisms: poor intake, increased GIT losses, magnesium depletion.
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21
Q

Why does an iron infusion cause low phosphate?

Which formulation is worst?

A

Occurs mainly with iron carboxymaltose.

There is inhibition of a fibroblast growth factor- a hormone that regulates phosphate metabolism, and is produced by osteoblasts/casts.
Inhibition of it reduced PCT reabsorption.

Somehow iron infusions also inhibit 1-a-hydrolyase –> low vitamin D and then low intestinal absorption of phosphate

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22
Q

What investigations to order for hypophospatemia?

(5)

A
  1. fractional excretion of phosphate (Figure 1)
  2. parathyroid hormone
  3. serum corrected calcium
  4. 1,25-dihydroxyvitamin D3
  5. 25-hydroxyvitamin D.
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23
Q

What does phosphate do in the body?
What are the symptoms of LOW phosphate?

A

Plays a key role in energy storage, metabolism and signalling within the cell through phosphorylation.

So it ends up affected multiple organ systems:
mild irritability, paraesthesia and muscle weakness, to more severe manifestations such as haemolytic anaemia, severe infection, delirium, generalised seizures, cardiac arrythmias, cardiomyopathy, respiratory failure and coma.

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24
Q

Replacement of phosphate can occur simply by oral replacement if levels > 0.3.
If severe <0.3 then IV replacement should be used,

What are the things to watch for with IV phosphate replacement?

A
  1. Hypocalcemia and the resultant cardiac arrhythmia that could occur.
  2. Kidney injury - heterotopic calcification - bone growing where it shouldn’t! like in the kidney!
  3. Vitamin D deficiency- replace as needed as this can help with phosphate levels. Can have cholecalciferol or calcitriol.
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25
Q

What are the causes for HYPERcalcemia?

What is the main cause?

A
  1. the main cause is hyperparathyroidism
  2. Cancer (from PTHrP related cancers)
  3. Medications
  4. Taking too much calcium in supplements
  5. Too much vitamin D
  6. Hyperthyroidism
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26
Q

What is the process of investigation once you find a raised Calcium?

A

Usually start by checking serum albumin or serum ionised calcium

Next is PTH

If that is high well.. you have an answer

If PTH is Low, test PTH-related protein in the plasma (PTHrP)
–> if PTH related protein high then indicates cancers like Renal carcinomas, leukemias, lymphomas, and rhabdomyosarcoma.

–> if PTHrP is low then test for Vitamin D (see flow chart)

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27
Q

Primary hyperparathyroidism is usually caused by a single parathyroid adenoma.

When is non-surgical, expectant management appropriate?

A

In patients aged 50 and older a watch and wait approach can be appropriate IF all the following are met:

  1. serum calcium corrected for albumin remains lower than 2.9
  2. There is normal renal function
  3. there is no nephrolithiasis or nephrocalcinosis
  4. BMD higher than -2.5
  5. no symptoms

Monitor every 6-12 months with serum calcium and renal function
BMD every 2 years

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28
Q

What should people with primary hyperparathyroidism be doing / not doing?

(3)

A
  1. avoid high calcium intake (from diet or supps)
  2. limit vitamin D intake as this can cause increased calcium levels . no more than the normal 1000IU/day
  3. Drink plenty of water- high water intake of 2.5 L a day, unless contraindicated for other reasons
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29
Q

What does a high PTH do to calcium and phosphate?

A

Increases Calcium resorption from bone
This also increases phosphate resorption from bone

PTH will increase Calcium reabsorption from the kidneys BUT
promotes Phosphate excretion

hence this can all lead to hypercalcemia and hypophosphatemia

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30
Q

What are the three clinical types of hyponatramia worth classifying into?

A

Hypovolemic- usually due to GI losses

Euvolemic- SIADH, medications, hypothyroidism, primary polydipsia

Hypervolemic - usually cardiac or renal, maybe liver failure

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31
Q

What are medications that can cause hyponatraemia?

A

CAR DISH

Chemo
ANTI drugs (antidepressants, antipsychotics, anti-inflammatories exp COX2)
Recreational drugs like ecstasy
Diuretics
Inhibitors (SSRIs, ACEi)
Sulfonylureas
Hormones (desmopressin) and Hyponotics (temazepam)

32
Q

what is the definition of SIADH?

(5)

A

Serum osmolality < 275
Urine osmolality > 100
Euvolemia
increased urine sodium > 20mmol/L
no other cause of hyponatraemia (medications, hypothyroidism, cortisol deficiency, marked hyperproteinaemia, hyperlipidemia)

33
Q

How to you assess someone as being euvolemic when working up for SIADH?

(5)

A

Make sure these are normal to conclude euvolemia
-Pulse
-Blood pressure
-Hydration status
-no Peripheral oedema
-no Pulmonary crackles

34
Q

When suspecting SIADH what investigations might you order?

A

obvious biochem
serum osmolality
urine osmolality
TFTs
Cortisol level, renin or ACTH or Short synacthen (if addison disease)
CT brain for neurological disease causes of SIADH
Chest XRAY for pulmonary causes

35
Q

when should someone be sent to hospital for SIADH?

A
  1. if symptoms < 48 hours
  2. If severe symptoms
  3. if serum sodium < 120mmol/L and symptomatic
36
Q

For an asymptomatic person with a sodium level of 125mmol/L what can be done?

A

patient does not need E.D

Order investigations: CT/CXR

Place on fluid restriction 800/1200ml / day

37
Q

What components make up the AUSDRISK score?

A

Age
Gender
Vegetabe intake
Waist Circumference
Hypertension
Smoking
Physical activity
Ethnicity (indigenous)
Previous high glucose reading
Place of birth

38
Q

Which people are immediately at high risk of T2DM, without the need for the AUSDRISK calculation?

A

if over 40 AND diabetic
anyone with IFG and IGT
first degree relative with Diabetes
all patients with a history of a Cardiovascular event
High risk ethnic backgrounds (PI, indian subcontinent)
History of Gestational Diabetes
PCOS
Taking anti-psychotics
ABTSI

39
Q

Who do you and how do you screen for T2DM?

A

EVERYONE from age 40
ABTSI from age 18.
Using the AUSDRISK score. A score of 12 or more is considered high risk- start testing.

40
Q

What lab values would be very much straight away give you a diagnosis of T2DM?

Do you need to repeat the test?

A

Fasting BGL > 7.0mmol/L

Random BGL > 11.1mmol/L

HBA1c > 6.5 mmol/L

(to confirm, repeat test, but use the same test and the same lab. Except if you used a random blood glucose, repeat with a FASTING BGL)

If patient is symptomatic and has abnormal result there is no need to repeat the test.

41
Q

Symptoms that suggest diabetes?

A

Tiredness
Polyuria
Polydipsia
Poor wound healing
Frequent bacterial or fungal infections
Blurred visions
Loss of sensation
Malaise
Sexual dysfunction

42
Q

What are key steps in addressing management for effective diabetes care?

A
  1. Patient education. provide initial information and resources such as NDSS, Diabetes Australia
  2. Patient centred care. Holistic approach that takes into account patient values and socioeconomic factors
  3. Emphasis on self management
  4. Involvement of other care providers/multi disciplinary approach: pharmacy, podiatry, optometry, endocrinologist if needed.
  5. Managing other cardiovascular risks: smoking, BP, cholesterol, diet, exercise
43
Q

What should be done at least every 6 months of a Diabetes cycle of care?

A

BP
Height, weight BMI
Feet check

44
Q

What should be done every 12 months as part of a diabetes Cycle of care?

A

Medication check
Diet, physical activity, smoking check
Assess control with HBA1c
Cholesterol check
Assess for albuminuria
Review and discuss complications

45
Q

What should be done at least every 2 years on a Diabetes TCA?

A

eye check, more frequent if extensive diabetic retinopathy

46
Q

How often should BGL/HBA1c be checked initially?

A

every 3 months, then eventually annually.

47
Q

What can cause an abnormally low HBA1c?

A

Anaemia
Chronic Blood loss
Haemoglobulinopathies
Chronic renal failure (variable)
Recovery from acute blood loss
Haemolytic anaemia

48
Q

What are non insulin medication options for T2DM?

A

Metformin
Sulfonylureas
SGLT2i
GLP1-RA
DDP4i

49
Q

If starting insulin what is the TOTAL insulin that should be needed?

A

0.6mg/kg (basal and bolus or any combination)

50
Q

When should you consider endocrinology referral for a person with t2DM?

A

If early onset (<40)
No adequate response with medication
Multiple co-morbidities especially CKD

51
Q

What are the main conditions that can affect the adrenal gland?

(5)

A

Addison Disease - Adrenal Insufficiency

Cushing Syndrome - Too much corticosteroids (not always due to a disease)

Conn Syndrome - HYPERaldosteronism

Pheochromocytoma

Pituitary tumours

52
Q

What are corticosteroids?

A

This is either aldosterone (a mineralocorticoid) or Cortisol (glucocorticoid).

Androgens are not usually classed as corticosteroids.

53
Q

__a____ affects __b__ to ___% of people with hypertension.

With this condition you will see a high __c___ and a low __d___ on serology. However a normal __d___ does not rule out ____a____

A

a. Primary Hyperaldosteronism

b. 5-10%

c. high Sodium

d. (low) potassium

53
Q

Sympathetic (catecholaminergic) mechanisms provide short-term, rapid changes in response to perturbations in __a__, whereas the HPA axis (via elevations in cortisol) provides a __b__ mechanism that allows continued resistance to homeostatic perturbations.

A

a. homeostasis

b. longer term

54
Q

investigations for CONN syndrome to diagnose.

how can you remember what Conn syndrome does to the sodium and potassium?

A

this is Primary Hyperaldosteronism

Aldosterone-renin ratio

Conn- cons you off potassium. so low potassium and high sodium.

55
Q

Why do you order a renin level when suspecting Addison’s disease/Adrenal insufficiency?

A

Because there isn’t enough hormonal signalling by the adrenal to raise the blood pressure, the renin system is trying to activate aldosterone to retain salt and therefore water and by extension pressure.

Expect the renin level to be raised

56
Q

What are features of Addison’s Disease?

A

Fatigue,
anorexia and weight loss,
postural hypotension, and
skin and mucosal hyperpigmentation

57
Q

What do you expect to happen with sodium and potassium in primary hyperaldosteronism vs. primary adrenal insufficiency?

A

In primary hyperaldosteronism (Conn’s syndrome). there is a decreased K+ and increased Na+ expected. Get conned of your potassium.

In primary adrenal insufficiency you can expect Higher potassium and low Sodium. Addison’s ADDS potassium

58
Q

The symptoms of
1.sweating
2. episodic headache and
3. tachycardia
make up the triad for which adrenal disease.

Despite it being present only 25% of the time.

A

Pheochromocytoma

59
Q

How do you investigate pheochromocytoma initially?

A

Plasma metanephrines or
24 hour urine metanephrine

60
Q

When administered a synacthen test and the subsequent level is raised, what does this indicate?

And what is the name of the chemical we are measuring?

A

Indicates normal result.

We are measuring the cortisol response to synacthen (which is essentially ACTH)

IF there was NO response to synacthen, i.e. cortisol level DID NOT rise, it would indicate adrenal insufficiency.

61
Q

What is the difference between Cushing disease and Cushing Syndrome?

A

Both end points are a raised/too much cortisol

Cushing Disease is specifically a pituitary adenoma

Cushing syndrome is anything else that causes a raised cortisol
exogenous drugs
ACTH pituitary tumour
ACTH ectopic tumour
Adrenal specific cortisol producing tumour

62
Q

What investigation would you use to help diagnose Cushing Syndrome?

A

1mg overnight Dexamethasone suppression test

or

Midnight salivary cortisol measured twice

or

24 hour urinary free cortisol collection

63
Q

Characteristics of cushing syndrome?

A
64
Q

What do you expect of Na and K+ in Cushing syndrome?

A

The coritsol takes over the aldosterone.
Causes sodium retention and potassium excretion (hypokalemia)

65
Q

6 main causes for hyperkalemia?

A

Psuedohyperkalemia (e.g. haemolysed RBC)

Acute renal failure

Rhabdomyolysis or crush injury

Diabetes Mellitus

Drugs; ACEi, spironolactone, ARBs, NSAIDs

Adrenal insufficiency (Addison’s Disease)

66
Q

What is the test for Addison’s disease or Adrenal insufficiency?

A

Short Synacthen test
- this is ACTH, so should produce a rise in cortisol, but if it doesn’t then it’s addison’s disease.

Renin level - should be raised. trying to get aldosterone going.

67
Q

Causes for hyperphosphatemia?

List 4

A

Artefact

HypoPARAthyroidism

Vitamin D excess

Cell leakage e.g. tumour lysis syndrome

Renal failure (though rare)

Medications: phosphate containing laxatives

68
Q

What main investigation should you order when suspected hypercalcemia?

A

PTH

as that is the most common cause

69
Q

What does hyperparathyroidism do to calcium and phosphate?

A

Increases serum calcium

but

decreases serum phosphate.

Even though there is more phosphate released from bones, there is much less getting reabsorbed from the kidneys

70
Q

Main causes for HYPOcalcemia?

(5)

A

Low albumin (check corrected calcium)

Renal failure

Hypoparathyroidism (?post surgery, also causing hypomagnesiemia)

Vitamin D deficiency

Acute pancreatitis

71
Q

Main causes for hypokalemia?

(4)

A

Acute GI losses:diarrhoea, laxative use, vomiting

Renal tubular acidosis

Mineralocorticoid excess syndromes

Inadequate intake: anorexia, alcoholism

72
Q

The main cause of hypernatraemia would be a ___(a)___ _______ or ____(b)____ excess or diabetes ___(c)____

A

a. renal disease

b. mineralocorticoid

c. diabetes insipidus

73
Q

In hyponatraemia, with a:

-decreased serum osmolarity and
-a normal to increased urine sodium and
- a HYPOvolaemic state,

what are the causes you are suspecting?

(2)

A

Diruectics

Addison’s disease

(also salt losing nephritis)

74
Q

When assessing hyponatraemia suspected to be due to cardiac failure or liver failure, what features of the hyponatraemia work up do you expect to find

(3)

A

decreased serum osmolality

decreased urinary sodium

hypervolaemic state

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