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FRACP > Endocrine > Flashcards

Endocrine Flashcards

1
Q

List the hormones of the pituitary.

A

Hormones of the pituitary (FLAAGTOP):

Anterior: FSH, LH, ACTH, GH, TSH, PL

Posterior: ADH, oxytocin

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2
Q

Is IGF-1 useful in the diagnosis of GHD?

A

IGF-1 is a marker of GH levels but is NOT useful in the diagnosis for GHD owing to:

  1. May be normal despite there being GHD
  2. May be low in other conditions: malnutrition, chronic disease (CKD, liver disease), high oestrogen.
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3
Q

In a patient with epilepsy what is the most appropiate diagnostic test if GHD is suspected?

A

GHRH/arginine test is most appropiate for Dx of GHD if insulin tolerance test (gold std) is contraindicated e.g. epilepsy.

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4
Q

What is the gold standard test for GHD?

A

insulin tolerance test

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5
Q

What type of imaging is required for a microprolactinoma?

A

Pituitary MRI

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6
Q

Describe the basic electrolyte abnormalities and acid-base derangements in Addison’s vs Cushing’s disease.

A

Addison’s: metabolic acidosis / hyponatraemia / hyperkalaemic

Cushing’s: metabolic alkalosis / hypokalaemic

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7
Q

What are the effects of Conn’s syndrome on BP and serum potassium?

A

Conn’s syndrome = adrenal adenoma

HTN and hypokalaemia

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8
Q

Where do VIPomas (vasoactive intestinal polypeptide) occur?

A

Commonly: PANCREAS

Rarely (ganglioneuroblastomas): sympathetic chain and adrenal cortex

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9
Q

What is the 4 normal functions of VIP (vasoactive intestinal polypeptide)?

A
  1. Increased intestinal secretion of water and electrolytes
  2. Peripheral vasodilation
  3. Inhibition of gastric acid secretion
  4. Potentiates ACh action on salivary glands.
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10
Q

With some of the normal functions of VIP in mind, extrapolate the ‘clinical’ features of the VIPoma syndrome.

A
  1. Increased intestinal secretion of water and electrolytes

VIPoma: secretory diarrhoea, dehydration, abdominal colic, weight loss

  1. Peripheral vasodilation

VIPoma: cutaneous flushing,

  1. Inhibition of gastric acid secretion

VIPoma: achlorhydria (decreased gastric acid secretion)

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11
Q

What are 5 ‘biochemical’ features of the VIPoma syndrome.

A
  1. Hypokalaemic acidosis (due to alkaline secretions)
  2. Raised urea and calcium (dehydration)
  3. Raised VIP (obviously)
  4. Raised pancreatic polypeptide
  5. Mild rise in glucose
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12
Q 
45F with 1 year history of weight gain and intermittent sweating, What is the likely diagnosis?
A. Hypothyroidism
B. Carcinoid
C. Insulinoma
D. Lymphoma
E. Phaechromocytoma

Which DDx not on this list may also cause the above scenario?

A

C. Insulinoma = wt gain + sweating

Wt loss and sweating: phaechromocytoma, lymphoma, carcinoid.

Wt gain: hypothyroidism

DDx: primary ovarian failure

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13
Q

Patient on long-term metformin develops cognitive impairment, peripheral neuropathy and anaemia. What is the problem?

A

Metformin-associated B12 deficiency.

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14
Q

What is the MOA of denosumab? Which endogenous molecule mimics it’s activity?

A

RANK ligand inhibitor that inhibits the maturation of osteoclasts - prevents bone degeneration.

Osteoprotegerin is an endogenous RANKL inhibitor.

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15
Q

True/False: Thyrotoxicosis causes hypercalcaemia.

A

True.

Hypercalcaemia is due to increased bone turnover in thyrotoxicosis.

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16
Q

What is the triad of ‘milk-alkali’ syndrome?

A

Due to ingestion of large amounts of calcium and absorbable alkali (e.g. HCO3- for PUD):

‘Milk-alkali CAR runs on milk and alkaline batteries’

  1. Calcium - hypercalcaemia
  2. Alkalosis - metabolic alkalosis
  3. Renal impairment
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17
Q

Describe the mechanism of tertiary hyperparathyroidism in patients with CRF.

A

CRF with prolonged hypocalcaemia have parathyroids that become autonomous despite improvement to renal function (i.e. tranplantation) resulting in hypercalcaemia.

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18
Q

What is the MOA of DPPIV inhibitors, what are they used for?

A

Oral hypoglycaemics

DPPIV (dipeptidyl peptidase IV) inhibitors) prevent the degradation of incretins.

Higher levels of incretin lead to increased GLP-1, which leads to glucagon suppression (unless patient is hypoglycaemic)

Also associated with glucose-dependent insulin stimulation.

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19
Q

True/False: DPPIV inhibitors cause hypoglycaemia.

A

False.

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20
Q

What is the effect of DPPIV upon gastric motility and weight of patients with T2DM?

A

Reduced gastric motility.

Weight neutral.

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21
Q

What are bisphosphonates and what is their MOA?

A

Rx of osteoporosis.

MOA: analogue of pyrophosphate, becomes ingested by osteoclasts and kills them, slows down bone breakdown.

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22
Q

Define hyperosmolar hyperglyaemic state (HHS) in terms of serum osmolality, BSL, and ketosis.

How does HONK fit in this semantic?

How common is coma in HHS?

A

Serum osmol > 320 mOsm/kg (N = 280-300)

BSL > 30

Minimal ketosis

HONK is a subset of HHS

Coma in 1/3 of cases of HHS

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23
Q

Define DKA (it’s in the name).

A

DM: BSL > 14mmol/L

Ketosis: serum ketone > 1.5 or UA ++

Acidosis:

  • pH < 7.3 (HCO3- < 20)
  • high-AG metabolic acidosis
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24
Q

Compare the demographic of DKA and HHS.

A

DKA = young T1DM that present early with ketotic symptoms (i.e. SOB)

HHS = elderly that presents late dehydrated with AKI.

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25
Q

Patient develops cerebral oedema from aggressive IVF rehydration for DKA. How might this be treated?

A

Mannitol +/- dexamethasone

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26
Q

What are the recommendations for the treatment of DKA/HHS to avoid cerebral oedema complications (3)?

A
  1. Gradual Na+ and H2O replacement
  2. Gradual reduction of BSL (3mmol/h)
  3. Add dextrose once target BSL attained (BSL < 15)
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27
Q

How low do ketones have to be in treated DKA before a insulin infusion can be ceased?

A

ketones < 0.3 mmol/L

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28
Q

What is the target K+ level in the treatment of DKA?

A

K > 5.0 mmol/L (replacement my be ceased if K > 5.5)

Check every 2h until acidosis resolves.

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29
Q

Whilst treating a DKA, how frequently are the following monitored:

BSL
Venous pH
Ketones
Serum K+

A

BSL = q1h whilst on insulin infusion

Venous pH = q1h until pH > 7.2

Ketones = BD until ketones < 0.3 mmol/L

Serum K+ = q2h until acidosis resolves

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30
Q

Give 3 broad categories of causes of DKA/HHS.

A
  1. Infections (50%)
  2. Non-compliance or inadequate insulin (i.e. patient unwell or newly Dx)
  3. Other acute illness that causes insulin resistance (e.g. CVA, IHD, pancreatitis, hyperthyroid, EtOH)
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31
Q

At what renal threshold does glucosuria occur?

A

Threshold for renal reabsorption of glucose is 10 mmol/L, above which glucosuria occurs.

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32
Q

Measurement of which ketone is the best marker for DKA resolution?

A

Betahydroxybutyrate - most readily cleared by kidneys.

Acetone and acetoacetic acid may be noted in the urine for days post-resolution of DKA.

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33
Q

List 4 catabolic hormones that INCREASE with stress

A

GGCC:

Glucagon (body needs sugar)
GH (counterintuitive)
Catecholamines
Cortisol

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34
Q

Describe the synthesis of catecholamines in simple terms (6 molecules and 5 enzymes).

A 
Phenylalanine
(phenylalanine hydroxylase) 
Tyrosine 
(tyrosine hydroxylase)
Dopa 
(L-aromatic amino acid decarboxylase)
Dopamine
(Dopamine beta-hydroxylase)
Noradrenalin
(phenylethanolamine-N-methyl transferase, PNMT)
Adrenalin
35
Q

What is the rate limiting step of catecholamine synthesis?

A

Tyrosin to Dopa via tyrosine hydroxylase.

36
Q

When busy treating a DKA/HHS with protocol, what intercurrent treatment should not be forgotten.

A

Treat the precipitant of DKA/HHS.

Infection / non-compliance / inadequate insulin / acute illness causing insulin resistance (e.g. silent MI)

37
Q

Patient presents with DKA and lowered GCS, what prophylaxis should be instigated?

A

DVT prophylaxis.

38
Q

What is the anion gap in DKA-related metabolic acidosis?

A

High

Causes of high-AG metabolic acidosis = DRLT or MUDPILES

39
Q

True/False: upon resolution of DKA/HHS there need not be an overlap with insulin infusion and SC bolus insulin regimens.

A

False.

0.5-2h overlap recommended (varies).

40
Q

True/False: patient with resolving DKA is eating poorly, this does not preclude him from being converted to SC bolus insulin.

A

False.

Patient should remain on insulin infusion whilst not tolerating PO diet.

41
Q

Is it possible to have DKA in T2DM?

A

Yes.

Hyperglycaemic emergencies:

80%: DKA in T1DM (expected)

10%: HHS in T2DM (expected)

10%: DKA in T2DM (unexpected but as common as HHS)

42
Q

DKA occurs in T2DM, what are the DDX?

A

1/3 = autoimmune beta cell failure, actually T1DM or LADA (latent autoimmune diabetes in adults)

1/3 = non-autoimmune beta cell failure, burnt-out T2DM or pancreatic islet cell negative T1DM

1/3 = ketone prone diabetes (KPD), reversible beta cell dysfunction with severe insulin resistance that occurs in Hispanics and African Americans (usually tolerate just OHG)

43
Q

How is pancreatic beta-cell failure defined biochemically (2)?

A

Fasting: C-peptide < 0.33 nmol/L

Peak Glucagon: C-peptide < 0.5 nmol/L

44
Q

True/False: Insulin is an anabolic hormone down-regulated in stress.

A

True.

45
Q

Describe in simple terms the biochemical effect of stress on the body and how this results in insulin deficiency and hyperglycaemia.

A

Increased gluconeogenesis (hepatic and renal) and glycogenlysis (hepatic and muscle) leads to increased blood glucose and in turn relative insulin deficiency and then “hyperglycaemia”.

46
Q

For which of the following scenarios is intensive glucose control indicated:

  1. Acute MI
  2. Mixed ICU
  3. Post-CABG (cardiac ICU)
A
  1. Unclear - DIGAMI yes but DIGAMI 2 no
  2. No - risk of hypoglycaemia and increases mortality
  3. YES - decreased risk of sternal infections (PORTLAND 3)
47
Q

What BSL target range is followed in most ICUs.

A

5-10 mmol/L - not tight control.

48
Q

What are the ‘3Is’ of peri-operative BSL control

A

Cornerstone of glycaemic control (3 Is):

Intensive BSL monitoring – aim 4-10

IVF considerations – patients on insulin require IV dextrose to avoid hypoglycaemia.

Insulin – patients on insulin require insulin even when fasting, sliding scales are a guide and need daily review.

49
Q

Give 5 classes of OHGs and give 1-2 generic name example of each.

A

BIG-ASs:

  1. Biguanides e.g. metformin
  2. Incretin mimics
    DPPIV e.g Sitagliptin
    GLP-1 agonist e.g. exenatide
  3. Glitazones (thiazolidinediones) e.g. rosiglitazone, pioglitazone
  4. Alpha-1-glucosidase inhibitors e.g. acarbose
  5. Suphonylureas e.g. gliclazide, glipizide, glibenclamide, glimepiride
50
Q

Most of the oral hypoglycaemic medications can be withheld on the day of surgery, which should be withheld 24h prior?

A

Metformin (biguanide)

51
Q

For 4 types of insulin (not including pre-mixed) give 1-2 examples of each (generic names).

Over what period of time do they act?

A

Ultra short (4h): lispro insulin (humalog), aspart insulin (novorapid)

Short (6h): regular insulin (actrapid, humlin R)

Intermediate (14h): isophane insulin (protaphane, humulin NPH)

Long/basal (24h): glargine (lantus), detemir (levemir)

52
Q

For the 2 types of pre-mixed insulins what types of insulins are usually in the mix? Give examples.

A
  1. Regular/Isophane (short/intermediate) e.g. Mixtard, Humulin
  2. Lispro/Protamine: ultra short insulin with protamine which slows the onset and increases the duration insulin action e.g. Humalog.
53
Q

Of the 5 types of OHGs list one which:

  1. Do NOT cause hypoglycaemia
  2. Cause hypoglycaemia
  3. May cause hypoglycaemia if combined with other OHGs.
A

BIG-AS:

  1. NO Hypos (2):
    Biguanides (metformin)
    Glitazones (thiazolidinediones)
  2. Cause Hypos (1):
    Suphonylureas (…ides)
  3. Hypos if combined (2):
    Alpha-glucosidase inhibitors (acarbose)
    Incretin mimics (…gliptins and exenatide)
54
Q

MOA of biguanides (Metformin)?

A

Decreased hepatic production of glucose

Increased peripheral utilisation of glucose

55
Q

MOA of suphonylureas (…ides)?

A

Contains ‘S’:

Increased pancreatic insulin ‘S’ecretion

May decrease insulin resistance

56
Q

MOA of Thiazolidinediones (…glitazones)?

A

Agonist of PPAR-gamma which regulates genes involved with lipid and glucose metabolism

Increases peripheral sensitivity to insulin and decreases hepatic glucose output

57
Q

MOA of alpha-1 glucosidase inhibitors (Acarbose)

A

Delays intestinal absorption of CHO via inhibition of alpha-1 glucosidase in the SI

Decreases post-prandial hyperglycaemia

58
Q

MOA of incretin mimics (…gliptins)

A

Inhibits DPP-4 leading to increased concentrations of incretin hormones (GLP-1 and GDIP)

Increased glucose dependent insulin secretion and decreased glucagon production

Decreases HbAic

59
Q

Describe the pathophysiology of secondary hyperparathyroidism in CRF.

A

CKD causes elevation of FGF-23 (fibroblast growth factor 23) and phosphate retention:

  1. FGF23 story:
    - Elevated FGF23 leads to decreased Vit D3 which leads to low Vit 25D that causes hypocalcaemia.
    - This all results in decreased expression of the following in the parathyroid gland:

CaR (calcium sensing receptor)
FGFR (FGF receptor)
VDR (vitamin D receptor)
KLOTHO (anti-aging co-factor of FGF23)

  1. Hyperphosphataemia retention story:
  • Directly triggers release of PTH
  • Causes decreased CaR expression and indirectly triggers releas of PTH
  • Elevated PTH levels causes resistance of bone to PTH which indirectly leads to hypocalcaemia
  • Hyperphophataemi directly causes hypocalcaemia

Result of above 2 mechanism causes an elevated PTH due secondary hyperparathyroidism and hypocalcaemia.

60
Q

What neurotransmitter cause:

  1. Satiety
  2. Hunger
A

Satiety (GAP):

  • gut (4 - PCOG): PYY3-36, cholecystokinin, oxyntomodulin, GLP-1
  • adipocytes (1): leptin
  • pancreas (IPA): insulin, pancreatic polypeptide, amylin

HunGer:
- stomach (1): grehlin

61
Q

Which 2 agents are used to treat obesity, what are the MOA?

A
  1. Phentermine (Duromine): sympathomimetic amine that causes anorexia via appetit suppression through the hypothalamus.
  2. Orlistat: lipase inhibitor that causes steatoorhoea via inhibition of gastrointestinal lipases.
62
Q

What is the HbA1c target for general population?

A

= or < 7.0

63
Q

What is the HbA1c target for newly diagnosed T2DM with no CVD?

A

On metformin = or < 6.0 (more strict)
On other OHG = or < 6.5
On insulin = or < 7.0 (less strict = general population)

64
Q

What is the HbA1c target for chronic DM or with CVD?

A

= or < 7.0 (less strict = general population)

65
Q

What is the HbA1c target for patient with recurrent hypoglycaemia?

A

= or < 8.0 (least strict - relaxed)

66
Q

What is the HbA1c target for patient with major comorbidities or limited life expectancy?

A

Any.

Only treat symptomatic BSLs

67
Q

Where are CaSR (calcium sensing receptors) found in the body?

A

Mostly: parathyroid gland and renal tubules

Less importantly: thyroid C cells, bone (osteoblasts and osteoclasts), breast, brain and intestines

68
Q

What is the CaSR (calcium sensing receptors)?

A

G-coupled membrane protein that repsonde to serum calcium + amino acid levels.

69
Q

True/False: under homeostatic circumstances the parathyroid gland exerts tonic inhibition of PTH release.

A

True.

CaSR prevents PTH release when calcium is high.

70
Q

Describe the function of CaSR in the renal tubules during hypercalcaemia.

A

Overall: renal tubules promote calciuria when calcium is high.

During hypercalcaemia:
PT: inhibits phosphaturic action of PTH
LoH: inhibits salt resorption
DT: inhibits Ca reabsorption
CD: inhibits ADH action
71
Q

What is mutated in Familial Hypocalciuric Hypercalcaemia?

A

Inactivating lesion of CaSR which renders it less sensitive to rises in calcium.

Leading to a raised set point to tolerate abnormally high calcium levels.

72
Q

How is Familial Hypocalciuric Hypercalcaemia diagnoses?

A

Urinary calcium:
- hypocalciuria or inappropiately low calcium despite hypercalcaemia

Other findings:
HYPERCALCAEMIA
Normal PTH (should be low) 
Normal PO4 / Mg
Normal/high Vit D / calcitriol (should be low)
Normal renal function
73
Q

What is the opposite condition to Familial Hypocalciuric Hypercalcaemia?

What are the investigative findings?

A

Autosomal dominant Hypocalcaemia - lowers set point of CaSR making CaSR more sensitive to rises in calcium.

HYPOCALCAEMIA
High urine calcium
Recurrent nephrolithiasis
Normal PTH / Mg

74
Q

MOA of Cinecalcet?

What is the indication of its use?

A

CINNA brings down PANEM in THE HUNGER games!

Cinecalcet brings down PTH.

MOA: binds to CaSR and increases the sensitivity of CaSR to calcium, leading to reduced PTH secretion.

Used to treat primary and secondary hyperparathyroidism.

75
Q

What are the SEs of Cinecalcet?

A

GI symptoms

Hypocalcaemia - treat with calcium supplements.

76
Q

Describe the demographic of a patient with asymptomatic primary hyperparathyroidism.

A

Middle-aged / eldery

77
Q

In a patient with asymptomatic primary hyperparathyroidism, aside from mild hypercalcaemia, what other abnormalities in bloods/urine/BMD is found?

What are the DDx?

A

None.

Normal or mildly raised PTH
Normal renal function
Normal vit D
Normal urine Ca

DDx: thiazide, lithium, FHH

78
Q

What is the treatment of asymptomatic primary hyperparathyroidism?

A

Surgery to improve BMD and reduce fracture risk.

Criteria:
Ca > 0.25 above upper limit of normal
eGFR < 60
BMD suggest osteoporosis (T score < 2.5)
< 50 yrs

Other medical therapy does NOT improve BMD:

  • biphosphonates stabalise BMD
  • Calcimimetics decrease Ca but NO effect on BMD
  • Check BMD every 1-2 yrs and monitor Ca/Cr
79
Q

Which enzyme converts 25-OH vit D to 1,25-OH vit D in the renal tubules?

A

1-alpha hydroxylase

80
Q

What stimulates 1-alpha hydroxylase?

A

PTH (suggesting low Ca)

Low Ca / PO4 / FGF23

81
Q

What inhibits 1-alpha hydroxylase?

A

1,25-OH vit D (negative feedback)

Low Ca / PO4 / FGF23

82
Q

What is the mechanism for hypercalcaemia in sarcoidosis?

A

Granulomatas produce 1,25-OH vit D via extra-renal hydoxylation of vit D.

83
Q

Patient has hypercalcaemia but also elevated 1,25-OH vit D. What is the likely diagnosis?

A

Sarcoidosis

FRACP (20 decks)

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