Revise Notes Endo Flashcards

Question

Answer 1

Clinical Features Polyuria Polydipsia Other symptoms may include: Nocturia Dehydration Fatigue. Investigations Hypernatraemic with dilute volume (high plasma osmolality with low urine osmolality) 24 hour urine volume = > 3L/day Fluid deprivation testing (distinguishes from psychogenic polydipsia): Plasma osmolality rises >305mOsm/kg and continue to produce large volumes of dilute volume despite fluid deprivation See table below to distinguish cranial vs nephrogenic DI Need to investigate cause i.e. MRI head for cranial DI

Answer 2

Management Maintain adequate fluid input and monitor sodium for hyper/hyponatramiae Cranial DI Managed with desmopressin (synthetic ADH) Nephrogenic DI Treatment depends on underlying cause- may require dietary modifications, discontinuation of offending medications, or treatment of underlying conditions. High dose desmopressin and thiazide diuretics can also be considered Complications Electrolyte imbalances Cognitive impairment Hypernatremic coma

Answer 3

) 1. Underlying Pathophysiology Deficiency of antidiuretic hormone (ADH) due to hypothalamic or pituitary dysfunction Renal resistance to ADH, resulting in impaired water reabsorption in the kidneys 2. Causes Idiopathic, tumors, trauma, infection, haemorrhage, haemochromatosis, autoimmune disorders affecting hypothalamus or pituitary Genetic mutations (e.g., in the AVPR2 or AQP2 genes), medications (e.g., lithium, demeclocycline), renal diseases (post-obstructive uropathy), hypercalcaemia

Answer 4

Diabetes Mellitus Background Diabetes is a metabolic disorder characterised by hyperglycaemia which occurs as a result of insulin resistance, insulin deficiency or a combination of the two. Type 1 diabetes Absolute insulin deficiency resulting from the autoimmune destruction of the beta cells of the pancreatic islets of langerhans, which are responsible for insulin production Type 2 diabetes Hyperglycaemia driven by insulin resistance, and a relative insulin deficiency. Often occurs as part of metabolic syndrome. Insulin resistance can develop as a result of by diet, a sedentary lifestyle and obesity.

Answer 5

Age < 18 Hemoglobinopathies HIV Pregnancy Regular medication which can induce hyperglycaemia (e.g. steroids) End-stage renal disease

Answer 6

A single abnormal fasting BM A single abnormal HbA1c If the patient is asymptomatic, arrange repeat testing (with the same test) to ensure persistent hyperglycaemia, before making a diagnosis.

Answer 7

: Weight loss TATT Polyuria, polydipsia Blurred vision Recurrent infections (e.g. candidiasis, UTIs)

Answer 8

Hyperglycaemia is defined as: HbA1c >/= 48 mmol/mol (6.5%) Fasting BM >/= 7.0 mmol/L Random BM >/= 11.1 mmol/L (or post OGTT) in the presence of symptoms

Answer 9

Common in poorly controlled or long-standing diabetics Painful sensory neuropathy Glove and stocking distribution No motor loss May have autonomic dysfunction - gastroparesis, orthostatic hypotension Management via: Optimising glycaemic control Neuropathic agents for analgesia (amitriptyline/gabapentin/pregbablin/duloxetine) Pathophysiology Nerve damage due to prolonged chronic hyperglyaemia causing microvascular damage, metabolic imbalances and inflammation Epidemiology Common- affecting up to 50% of patients with diabetes

Answer 10

Risk factors Poorly controlled diabetes Longer diabetes duration (Type 1 diabetics) Obesity Smoking History Peripheral neuropathy Numbness, tingling, burning pain, or loss of sensation in the extremities - commonly in the feet Autonomic neuropathy Altered gastric stasis (gastroparesis) Diarrhoae especially at night Urinary dysfunction or syncopal episodes (orthostatic hypotension)

Answer 11

Examination Findings Sensory deficits often in the glove and stocking distribution in limb extremities Reduced or absent reflexes Muscle weakness Normal power in myotomes (no motor deficit!) Investigations HbA1c to assess glycaemic control Bloods including UEs, TFTs, B12/folate to exclude other causes of peripheral neuropathy Nerve conduction studies or electromyography may be required to assess the severity and type of neuropathy.

Answer 12

Management Optimization of glycaemic control Analgesia - as per for neuropathic pain Amitriptyline Gabapentin Pregabalin Duloxetine If one does not work stop and try another Consider pain team or topical capsaicin if above measures fail Regular monitoring/screening Complications Diabetic foot ulcers Infections Charcot neuroarthropathy Autonomic dysfunction including erectile dysfunction, and orthostatic hypotension

Answer 13

Asymmetrical loss of proximal motor function Severe burning, neuropathic pain in the lower limbs Wasting and atrophy of the lower limbs muscles

Answer 14

Monitoring - HbA1c Targets HbA1c should be monitored every 3-6 months until stable, and then every 6 months. Targets (L/S Measures or one drug) Lifestyle measures alone OR a single non-hypoglycemic drug (e.g. metformin) Target: 48 mmol/mol Treatment involving one or more hypoglycaemic drug (e.g. gliclazide) OR on two or more drugs: Target: 53 mmol/mol Intensifying treatment If HbA1c rises to 58 mmol/mol consider intensifying diabetic treatment

Answer 15

Step 1: (Metformin +/- SGLT2i) If HbA1c > 48 despite lifestyle measures 1st Line: Commence standard release metformin. Titrate dose over several weeks to reduce risk of SEs. Adverse effects - gastrointestinal upset (diarrhoea, urgency), B12 deficiency If not tolerated, trial modified release metformin Contraindications: CKD (eGFR < 30)

Answer 16

Determine if the patient would benefit from dual therapy with an SGLT-2 inhibitor (alongside metformin) as 1st line treatment. Indications include: Chronic heart failure Established cardiovascular disease High risk of developing cardiovascular disease (QRISK > 10%) T2DM with CKD and proteinuria (see later*)

Answer 17

First, introduce metformin, gradually titrate Once tolerating metformin, commence SGLT-2i

Answer 18

Figure 269: Management of T2DM Step 2: Add a second line drug If HbA1c rises to 58 mmol/mol despite metformin (+/- SGLT2i) Intensify antidiabetic treatment with one of the following second line options. Choose from: DPP-4 inhibitors - sitagliptin Thiazolidinediones – pioglitazone Sulfonylureas - gliclazide SGLT-2 inhibitor - dapagliflozin

Answer 19

Step 3: If HbA1c rises to 58 mmol/mol despite two drugs: Consider commencing triple therapy by adding a third drug from the above list or.. Consider insulin therapy Nb. Initiation/intensification of insulin therapy commonly results in weight gain

Answer 20

BMI is > 35 OR BMI < 35 but.. insulin therapy would have significant occupational implications (e.g. HGV driver) Weight loss would benefit co-morbidities

Answer 21

Only continue the GLP-1 agonist after 6 months if there is BOTH a: Decrease in HbA1c of 11 mmol/mol (1%) and.. Weight loss of 3% Note - if commencing a GLP-1 agonist, discontinue any DPP-4 inhibitors.

Answer 22

Step 1: Commence one of: SGLT2 inhibitor (empagliflozin) (1st line if HF/CVD/QRISK>10%) DPP-4 inhibitor (gliptins) Thiazolidinedione (pioglitazone) Sulfonylurea (gliclazide)

Answer 23

Step 2: If HbA1c rises to 58 despite one drug, commence another from the above list: sulfonylurea + DPP-4 inhibitor sulfonylurea + thiazolidinedione DPP-4 inhibitor + thiazolidinedione

Answer 24

Step 3: Consider insulin therapy

Answer 25

SGLT2-inhibitors in CKD NICE recommend dapagliflozin in patients with CKD with an eGFR of 25-75 when commencing treatment and have either: Type 2 diabetes mellitus Or urine ACR > 22.6 mg/mmol It must be used as an add-on to highest tolerated dose of ACEi/ARB