of Bone in Adults: A Clinical Guideline. Journal of Bone and Mineral Research. 2019;34(4):e3657.
https://asbmr.onlinelibrary.wiley.com/doi/full/10.1002/jbmr.3657
18. Answer: B
Approximately 50% of patients who have had diabetes for >25 years will develop neuropathy. The most common form of diabetic neuropathy is distal symmetric, nerve‐length‐dependent polyneuropathy. Of these, approximately 50% will have pain as a symptom of neuropathy that is painful diabetic neuropathy (PDN). The prevalence of PDN in type 2 diabetes is more than twice that seen in type 1 diabetes.
Among patients with the same degree of neuropathy, some experience more pain than others. Pain is mediated by small fibresr, which may be damaged or destroyed in diabetic neuropathy, resulting in sensory loss. However, these small fibresr have the capacity to regenerate and to lead to ectopic generation of impulses and hyperexcitability, resulting in highly painful neuropathy in some patients. Moreover, pain nociception is complex and involves various other factors. Patients with normal findings on clinical examination and small‐fibre testing may also experience painful neuropathy.
Tight glycaemic control in patients with type 1 diabetes reduced the occurrence of clinical neuropathy by 60% in 5 years according to the Diabetes Control and Complications Trial. But it appears not to be enough to ameliorate the onset and progression of the disease in patients with type 2 diabetes. One of the reasons could be that the neuropathic process starts early in type 2 diabetes. The underlying mechanisms for the development of neuropathy in type 1 diabetes and type 2 diabetes appear to be different.
Sundara Rajan R, de Gray L, George E. Painful diabetic neuropathy. Continuing Education in Anaesthesia Critical Care & Pain. 2014;14(5):230–235.
https://www.sciencedirect.com/science/article/pii/S1743181617300847?via%3Dihub
19. Answer: A
Gastroparesis is a syndrome characterised by delayed gastric emptying in the absence of mechanical obstruction of stomach. The main symptoms include post‐prandial fullness, early satiety, bloating, nausea and vomiting. Gastroparesis is a serious complication of diabetes and is reported by 5 to 12% of patients with diabetes. It typically develops after at least 10 years of diabetes, and these patients generally have additional evidence of autonomic dysfunction. Other non‐diabetic causes of gastroparesis are neurologic disorders, surgery, medication, and idiopathic causes.
Gastric emptying involves integration of fundic tone and antral phasic contractions with inhibition of pyloric and duodenal contractility. Gastric emptying requires interactions between smooth muscle, enteric nerves, vagus nerve, and specialised pacemaker cells, the interstitial cells of Cajal (ICC).
Autonomic neuropathy: Vagal neuropathy results in reduced pyloric relaxation, impaired antral contraction, disturbed antropyloric coordination, and reduced gastric secretion.
Enteric neuropathy: The enteric nervous system (ENS) is the myenteric plexus, a network of nerves that is layered between the longitudinal and circular muscle layer of the gut and coordinates gastric motor function. Pathological changes in these pathways due to hyperglycaemia affect motor control and may contribute to delay emptying, impaired accommodation, and gastric dysrhythmia.
Loss of ICC: This is the most common enteric neuropathological abnormality in diabetic and idiopathic gastroparesis. ICC generate slow waves that control smooth muscle contractility, are involved in aspects of neurotransmission, set the smooth muscle membrane potential gradient. A range of diabetes related mechanisms induce ICCs damage including insulinopaenia, IGF‐1 deficiency, and oxidative stress. Diabetes is a high oxidative stress state, which can cause loss of ICCs and delay gastric emptying.
Glucagon like peptide‐1 (GLP‐1) treatment: Known causes of iatrogenic gastroparesis include vagal inhibition and pharmacological blockade such as GLP‐1 receptor agonist in the treatment of type 2 diabetes.
Fluctuations in blood glucose: Acute increases in blood glucose may further delay gastric emptying, which in turn exacerbates blood glucose fluctuations that can then further impair gastric emptying rate. Delayed emptying can be the result of the pyloric contractions and antral hypomotility induced by the hyperglycaemic state. Once established, diabetic gastroparesis tends to persist, despite amelioration of glycaemic control.
Grover M. Gastroparesis: A turning point in understanding and treatment. Gut Published Online First: 28 September 2019.
https://gut.bmj.com/content/68/12/2238.abstract
20. Answer: B
Polycystic ovarian syndrome (PCOS) is the most common endocrinopathy in women and is associated with significant adverse sequelae that can affect overall health and well‐being. Physicians need to have a good understanding of the complications and develop strategies to prevent long‐term health morbidities for women who have been diagnosed with PCOS.
PCOS is diagnosed, after exclusion of other causes, and if the woman meets two of the following three features, including: (1) clinical and/or biochemical signs of hyperandrogenism, (2) oligo‐ or anovulation, and (3) polycystic ovaries (PCO) on abdominal USS. In adolescents or those within 8 years of menarche, ultrasound is not a reliable discriminator for PCOS. PCOS is classified into four phenotypes, which plays an important role in determining the metabolic and possibly long‐term complications of PCOS. The phenotypes are differentiated based on presence and absence of the three criteria of hyperandrogenism, ovulatory dysfunction, and ultrasound features of PCO and outlined in the table below. Phenotypes A and B account for two‐thirds of all cases.
| Hyperandrogenism | Oligomenorrhoea | Ultrasound features of PCO | |
| Type A | Yes | Yes | Yes |
| Type B | Yes | Yes | No |
| Type C | Yes | No | Yes |
| Type D | No | Yes | Yes |
Phenotypes A, B and C are associated with an increased risk of metabolic syndrome, whereas phenotype D is not associated with an increased metabolic risk as compared with the general population. Phenotypes A and B have higher rates of insulin resistance compared with the general population irrespective of BMI while the other phenotypes do not possess this characteristic, implying that hyperandrogenism contributes to insulin resistance. PCOS is responsible up to 80% of cases of anovulatory infertility. As women
