Jan exam stuff Flashcards
Instructions:
- Introduction to a MAXIMUM of 2-3 sentences
- Consider starting with a single sentence that summarises the answer as a whole then introduce the relevant concepts as you go along
- Answer the question as asked – and in ALL its parts - if 4 parts to address, give reasonable attention to all 4, not just single sentences for 2, and more detail for the other 2
- See Practice Paper and last year’s paper. Almost all questions tend to be multipart,
Which of the following is NOT an effect of PTH:
* Increased calcium reabsorption in the kidney
* Mobilisation of calcium in the bone
* Increased phosphate reabsorption in the kidney
* Increased calcium absorption in the gut (via calcitriol formation)
- Increased calcium reabsorption in the kidney - PTH acts to raise blood calcium levels so it does do this
- Mobilisation of calcium in the bone - PTH acts to raise blood calcium levels so it does do this
** Increased phosphate reabsorption in the kidney - to reabsorb calcium, you have to get rid of phosphate so PTH doesn’t cause this to happen (it causes the opposite)
- Increased calcium absorption in the gut (via calcitriol formation) - PTH acts to raise blood calcium levels so it does do this
Insulin insensitivity is a major feature of:
* CHI
* Diabetes insipidus
* T1DM
* T2DM
- CHI - overproduction of insulin in infants, technically the opposite of insulin insensitivity
- Diabetes insipidus - increased thirst and urine production, nothing to do with insulin
- T1DM - lack of insulin production
** T2DM - correct
An example of a secosteroid is:
* Cortisol
* Aldosterone
* Oestrogen
* Vitamin D
Secosteroid - steroid with a “broken ring”
- Cortisol - not a secosteroid
- Aldosterone - not a secosteroid
- Oestrogen - not a secosteroid
** Vitamin D - produced by sunlight, UV rays break a double bond
Which of the following is a glucocorticoid:
* Cortisol
* Aldosterone
* Insulin
* Glucagon
** Cortisol - correct
- Aldosterone - not a glucocorticoid
- Insulin - polypeptide hormone
- Glucagon - polypeptide hormone
Where is growth hormone-releasing hormone synthesised:
* Pituitary gland
* Adrenal gland
* Bone
* Hypothalamus
- Pituitary gland - GHRH acts on it, it then synthesised GH
- Adrenal gland - produces steroid hormones, not growth hormones
- Bone - nothing to do with GHRH or its axis
** Hypothalamus - correct
Calcimimetics (ie cinacalcet) are CaSR:
* Agonists
* Positive allosteric modulators
* Antagonists
* Negative allosteric modulators
CaSR - calcium-sensing receptor
- Agonists - divalent Cations (Ca²⁺, Mg²⁺), spermine, Gd³⁺, aminoglycosides (neomycin)
** Positive allosteric modulators - correct, also R568, etelcalcitide, and aromatic amino acids (L-Trp, L-Phe)
- Antagonists - N/A
- Negative allosteric modulators - Calcilytics (NPS-2143)
Which endocrine condition are biguanides and sulphonylureas commonly used to treat:
* Acromegaly
* Cushing’s disease
* Type 2 diabetes mellitus
* Multiple endocrine neoplasia type-1
- Acromegaly - Selective tyrosine kinase inhibitors, monoclonal antibodies, octreotide, etc
- Cushing’s disease - caused by a tumour so treatment is extreme - radiation, surgery, chemotherapy, etc
** Type 2 diabetes mellitus - correct, biguanides are drugs reducing blood glucose supply and sulphonylureas are insulin secretagogues
- Multiple endocrine neoplasia type-1 - early detection is useful and allows preventative measures, once onset, treat the tumour (radiation, surgery, chemotherapy, etc)
Which endocrine condition is Octeotride commonly used to treat:
* Acromegaly
* Cushing’s disease
* Type 2 diabetes mellitus
* Multiple endocrine neoplasia type-1
** Acromegaly - Selective tyrosine kinase inhibitors, monoclonal antibodies, octreotide, etc
- Cushing’s disease - caused by a tumour so treatment is extreme - radiation, surgery, chemotherapy, etc
- Type 2 diabetes mellitus - treatments revolve around insulin and glucose
- Multiple endocrine neoplasia type-1 - early detection is useful and allows preventative measures, once onset, treat the tumour (radiation, surgery, chemotherapy, etc)
Which of the following is NOT a GPCR:
* Parathyroid hormone receptor
* Glucocorticoid receptor
* Calcium-sensing receptor
* MCR2/ACTH receptor
- PTH receptor - is a GPCR
** Glucocorticoid receptor - correct
- CaSR - is a GPCR
- Melanocortin receptor 2/ACTH receptor - is a GPCR
Which of the following two mutations would likely permit chronically elevated PTH secretion:
* CaSR LoF
* CaSR GoF
* VDR LoF
* VDR GoF
- Calcium-sensing receptor loss of function - The receptor does react to blood calcium levels and so does not suppress PTH
** Calcium-sensing receptor gain of function - The receptor reacts too strongly to blood calcium levels and suppresses PTH too much
** Vitamin-D receptor loss of function - The receptor doesn’t react to PTH activating it so does not produce vitamin D which inhibits PTH through negative feedback
too strongly to blood calcium levels and suppresses PTH via negative feedback too much
- Vitamin-D receptor gain of function - The receptor reacts too strongly to PTH activating it so produces too much vitamin D which suppresses PTH via negative feedback too much
TCF7L2, KCNJ11, SLC30A8, HHEX, and CDKN2A/B have been identified as diabetes risk genes, with which of the following two factors have these genes been related:
* β-cell function
* Insulin sensitivity
* β-cell mass
* Truncal obesity
TCF7L2 - incretin signalling
KCNJ11 - kATP channel
SLC30A8 - Zn²⁺ transport
HHEX - transcription factor
CDKN2A/B - cell cycle regulator
** β-cell function
- Insulin sensitivity
** β-cell mass
- Truncal obesity
Which two of the following four T2DM treatments are shown with their correct method of action:
* SGLT2 inhibitors - insulin sensitiser
* Thiazolidinediones - increase glucose supply
* Sulphonylurea - insulin secretagogue
* GLP-1 receptor agonists - incretin therapies
- SGLT2 inhibitors - insulin sensitiser - actually reduces blood glucose supply
- Thiazolidinediones - increase glucose supply, T2DM drugs aim to lower blood sugar levels so DEFINITELY not this but also TZDs are insulin sensitisers
** Sulphonylurea - insulin secretagogue, along with metformin
** GLP-1 receptor agonists - incretin therapies along with DPP-4 and GIP-1 agonists
Which of the following is not considered a cause for pituitary tumours:
* AIP mutations
* Addison’s disease
* XLAG
* MEN-1 syndrome
- AIP mutations - Tumour suppressor gene mutation, results in promoted pituitary tumour formation
** Addison’s disease - hypoadrenalism, low adrenal cortex activity causing low cortisol and aldosterone production
- XLAG - X-linked acrogigantism, GoF mutations promoting tumour formation and then GH excess
- MEN-1 syndrome - Tumour suppressor gene mutation, results in promoted prolactinoma formation
Which two of the following pituitary tumours are correctly classified:
* Somatotroph - functional LH/FSH excess
* Corticotroph - functional ACTH excess
* Thyrotroph - functional GH excess
* Lactotroph - functional prolactin excess
- Somatotroph - functional LH/FSH excess, this would be a gonadotroph, a somatroph results in GH excess
** Corticotroph - functional ACTH excess
- Thyrotroph - functional GH excess, this would be a somatotroph, a thyrotroph results in TSH excess
** Lactotroph - functional prolactin excess
