Endocrine and Metabolic Conditions Flashcards
Addison’s Disease Definition
Adrenal insufficiency is a clinical syndrome that arises due to the insufficient production of glucocorticoids and mineralocorticoids from the adrenal cortex.
It can be categorized as primary, commonly known as Addison’s disease, where the cause lies within the adrenal glands themselves, or secondary, where inadequate stimulation of the adrenal glands by the pituitary or hypothalamus is the culprit.
Difference between primary and secondary adrenal insufficiency
In primary adrenal insufficiency (Addison’s disease), the adrenal glands are damaged, while secondary adrenal insufficiency is due to dysfunction in the hypothalamus or pituitary.
Name causes of primary adrenal insufficiency
Auto-immune destruction (most common)
Surgical removal of the adrenal glands
Trauma to the adrenal glands
Infectious diseases, such as tuberculosis (more common in developing countries)
Haemorrhage (e.g., Waterhouse-Friderichsen syndrome)
Infarction
Less commonly, neoplasms, sarcoidosis, or amyloidosisAuto-immune destruction (most common)
Name causes of secondary adrenal insufficiency
Congenital disorders
Fracture of the base of the skull
Pituitary or hypothalamic surgery or Neoplasms in the pituitary or hypothalamus
Infiltration or infection of the brain
Deficiency of corticotropin-releasing hormone (CRH)
Signs and symptoms of Addison’s disease
Hypotension
Fatigue and weakness
Gastrointestinal symptoms
Syncope
Skin pigmentation due to increased ACTH which stimulates production of alpha melanocyte stimulating hormone (MSH).
In the case of auto-immune Addison’s disease, approximately 60% of patients may also have vitiligo or other autoimmune endocrinopathies.
First line investigations for Addison’s disease:
U+E and serum cortisol, where you may find:
Hyponatraemia (low sodium)
Hyperkalaemia (high potassium)
Low serum cortisol
Glucose (typically low)
What would you expect a blood gas to show in someone with Addison’s disease?
hyperkalaemic, hyponatraemic, hypoglycaemic metabolic acidosis
With less aldosterone, there is a reduced excretion of hydrogen ions, leading to their buildup in the blood. This causes an increase in the acidity of the blood, resulting in metabolic acidosis.
Name some other findings one would expect in Addison’s disease
ACTH: High in primary insufficiency, low or low-normal in secondary insufficiency
Renin (high in Addison’s disease)
Aldosterone (low in Addison’s disease)
What is the gold standard investigation
for Addison’s disease?
An ACTH (Short Synacthen) test is the gold standard investigation to confirm the diagnosis.
Name further investigations for addison’s disease:
Testing for adrenal auto-antibodies
Chest X-ray for tuberculosis
CT scan of the adrenal glands
MRI of the brain
Management of adrenal insufficiency:
Patient education on ‘sick day’ rules, carrying a steroid card, and wearing a medical alert bracelet
Doubling the regular steroid medication dose during any intercurrent illness
Replacement of both glucocorticoids (typically with hydrocortisone) and mineralocorticoids (typically with fludrocortisone)
Regular screening for complications including an adrenal crisis and osteoporosis
Management of Addison’s crisis:
Aggressive fluid resuscitation
Administration of intravenous/IM (if no access) steroids STAT
Glucose administration if hypoglycaemia is present
What is the most likely cause of Addison’s disease?
autoimmune
What does severe meningococcal infection cause with the adrenal gland?
Waterhouse-Friderichsen syndrome
Thought that meningococcal septicaemia is associated with disseminated intravascular coagulation (DIC) which leads to adrenal haemorrhage.
If someone take steroids for a long time and then suddenly stops what might this cause? (think adrenals) and what do we give?
Secondary adrenal insufficiency - give IV Hydrocortisone
what part of the adrenal gland is mineralocorticoid produced?
Zona glomerulosa
What part of the adrenal gland produces glucocorticoids?
zona fasciculata
First step of management for an adrenal crisis?
immediate administration of intravenous or intramuscular hydrocortisone 100 mg in adults
What is Cushing’s syndrome?
endocrine disorder characterized by excess glucocorticoids
What is Cushing’s disease?
glucocorticoid excess caused by an adrenocorticotropic hormone (ACTH)-secreting pituitary tumour
What are the two main category causes of Cushing’s syndrome?
ACTH-dependent disease
ACTH-independent
What causes ACTH-dependent cushings?
pituitary tumor (Cushing’s disease) or ectopic ACTH-producing tumors (e.g. lung carcinoids, thymic carcinoids, and others).
What causes ACTH-independent cushings?
C: cancer adrenal adenoma
A: adrenal nodular hyperplasia
R: Rare causes: McCune-Albright syndrome
Steroid use
What are the signs and symptoms of cushings?
Proximal myopathy
Striae and easy bruising
Osteoporosis and fractures
Glucose intolerance or diabetes mellitus
Obesity, particularly truncal or “centripetal” obesity
Hypertension
Hypokalaemia
Facial changes, such as moon face and acne
Hirsutism in women
Fat redistribution leading to interscapular and supraclavicular fat pads
Thin extremities due to muscle wasting
Thin, fragile skin
Erectile dysfunction in men
Psychological issues, such as depression or cognitive dysfunction
Osteopenia or osteoporosis
What investigations do we do for cushings?
24-hour urinary free cortisol test
Low-dose Dexamethasone suppression test
Explain the different results of low/high dose dexamethasone suppression tests?
Not suppressed by low dose - Cushing’s syndrome (e.g. exogenous steroid use)
Not suppressed by low dose but suppressed by high dose - Cushing’s disease (pituitary source)
Not suppressed by low dose or by high dose dex – ectopic ACTH (not under axis control, likely ACTH-producing tumour)
What further tests can you do to localise the source of cushings syndrome?
Plasma ACTH levels to distinguish between ACTH-dependent and independent causes
High-dose dexamethasone suppression test for suspected Cushing’s disease
Inferior petrosal sinus sampling for suspected pituitary cause if MRI does not show pituitary tumour
MRI of the pituitary and/or CT of chest and abdomen for tumor localization
Cushing’s syndrome is commonly associated with small cell lung cancer and can present with weight loss, increased skin pigmentation, and persisting respiratory symptoms
What is the medical management of cushings syndrome?
Initial therapy often involves medications to decrease cortisol levels. These include Metyrapone, an inhibitor of cortisol synthesis; Ketoconazole, an adrenolytic agent; Mifepristone, a glucocorticoid receptor antagonist; and Pasireotide, a somatostatin analog.
what is surgical management of cushings disease?
Resection of the pituitary tumor is the treatment of choice for Cushing’s disease, often after initial control of hypercortisolaemia with medical therapy to improve surgical outcomes.
When might radiotherapy be considered for Cushing’s syndrome?
May be considered for cases where hypercortisolaemia persists post-surgery, or in cases where surgery is not possible or declined.
What happens post successful treatment of Cushing’s syndrome?
Successful treatment of Cushing’s disease leads to cortisol deficiency and subsequently, steroid replacement post-operatively is essential. Patients need to carry a steroid card and ideally wear a medic alert bracelet in case of acute illness or emergency situations.
What are the three functions of cortisol? (3As)
mAke glucose in the liver
Antistress pathway
Anti-inflammatory pathway
Why does cushings cause osteoporosis?
decreases the activity and lifespan of osteoblasts and increases the activity of osteoclasts
What causes false positives of 24hr urinary free cortisol?
depression, obesity, alcohol excess and inducers of liver enzymes
In patients presenting with signs and symptoms of Cushing’s syndrome but normal diurnal variation in cortisol levels, consider pseudo-Cushing’s syndrome caused by chronic alcohol consumption.
What is the most common underlying cause of Cushing’s?
exogenous corticosteroid exposure
What are the main side effects of steroids
insomnia, mania, depression, psychosis
What is nelson’s syndrome?
in the setting of Cushing’s syndrome a bilateral adrenalectomy has taken place. As a consequence, there is a loss of feedback to the brain and we get increased Corticotrophin-Releasing Hormone from the hypothalamus leading to increased stimulation of the anterior pituitary and enlargement of the pituitary and formation of an adenoma. This leads to symptoms of mass effect with headaches, visual field defects but also hormonal issues with compression of the posterior pituitary. Primary treatment is transphenoidal surgery
define diabetes insipidus/ arginine vasopressin disorder
Arginine vasopressin disorder (formally diabetes insipidus) is an endocrine condition characterised by either an inadequate production (AVP-D) or an insufficient renal response (AVP-R) to arginine vasopressin (AVP), also called antidiuretic hormone (ADH).
Which part of the body causes AVP deficiency
cranial
Which part of the body causes AVP resistance?
kidneys
Name some causes of AVP deficiency
C: congenital defect in ADH gene
I: idiopathic
V: vascular - sickle cell disease
I: infection - meningoencephalitis
T: tumour, tuberculosis, trauma
Name some causes of AVP resistance
D: drugs - lithium
I: inherited - wolfram’s syndrome
M: metabolic - low potassium high calcium
C: chronic renal disease
Signs and symptoms of diabetes insipidus?
Large volumes of dilute urine (>3 litres in 24 hours and a urine osmolality of <300 mOsm/kg)
Nocturia
Excessive thirst
In children, additional symptoms may include:
Failure to thrive
Enuresis
Investigation for diabetes insipidus?
Urea and electrolytes (sodium may be raised)
Blood glucose (to rule out diabetes mellitus)
Urine dip
Paired serum and urine osmolality measurements
Arginine vasopressin disorder is present when the serum osmolality is raised (>295 mOsm/kg) with inappropriately dilute urine (urine osmolality < 300 mOsm/kg).
What to do if diagnosis of diabetes insipidus remains uncertain?
a water deprivation test
This should only be done if there is evidence of hypovolaemia or hypernatraemia
The patient is deprived of fluids while monitored for urine osmolality and body weight changes
In AVP-D, urine osmolality increases with ADH administration
In AVP-R, urine osmolality remains low/unchanged despite ADH administration
What does the water deprivation test also distinguish arginine vasopressin deficiency from?
primary polydipsia which is a condition characterised by similar symptoms of polydipsia and polyuria. The latter condition is usually due to a psychological cause of excessive drinking. Upon testing, urine osmolality is normal both after fluid deprivation and after desmopressin is given.
Management of arginine vasopressin deficiency?
AVP-D can be managed with desmopressin, a medication which mimics the action of endogenous ADH.
Sodium levels should be monitored routinely due to the risk of hyponatraemia.
Management of arginine vasopressin resistance?
AVP-R is managed by correcting any underlying metabolic abnormalities and discontinuing any offending drugs.
High dose desmopressin has been used with variable results.
Other potential treatments include using a thiazide diuretic (counter-intuitive, we know) and a non-steroidal anti-inflammatory drug to reduce urine volume.
What is type 1 diabetes mellitus?
Type 1 diabetes mellitus (T1DM) is an autoimmune condition characterized by the destruction of the insulin-producing beta cells within the pancreas, leading to insulin deficiency.
What is believed to cause type 1 diabetes?
combination of genetic predisposition and environmental triggers. Genes associated with the human leukocyte antigen (HLA) system contribute to susceptibility. Environmental triggers, such as viral infections, are proposed but not definitively identified.
What are the signs and symptoms of type 1 diabetes mellitus?
Polyuria
Polydipsia
Weight loss - a distinguishing factor between T1DM and T2DM
In severe cases, patients may present with diabetic ketoacidosis (DKA), characterised by hyperglycemia, metabolic acidosis, and ketonemia.
What does diagnosis of type 1 diabetes involve?
Diagnosis involves first confirming diabetes and then identifying the underlying cause as type 1
If a patient is symptomatic of type 1 diabetes name one other result needed?
Random blood glucose ≥ 11.1mmol/l or Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)
If a patient is asymptomatic of type 1 diabetes name two results which are required from different days?
Autoantibody testing: Identification of specific antibodies (e.g. anti-GAD, ICA, IAA) contributes to confirming the autoimmune nature of T1DM.
C-peptide levels: Evaluation of C-peptide production helps assess endogenous insulin secretion.
Urine ketone testing: Presence of ketones may suggest concurrent DKA.
Explain the insulin therapy management for type 1 diabetes?
Individualised insulin regimens are essential. Short-acting insulin is administered after meals and snacks, while long-acting insulin is typically given at night-time
What are the target ranges for blood glucose and HbA1c levels?
Pre-meal blood glucose: 4-7 mmol/L (72-126 mg/dL)
Bedtime blood glucose: 6-10 mmol/L (108-180 mg/dL)
HbA1c: Less than 7% (53 mmol/mol) for most adults; individualised targets for children, elderly patients, and those at risk of hypoglycemia.
Name some other management strategies for type 1 diabetes?
Lifestyle Interventions: Patients should receive guidance on nutrition, exercise, and alcohol consumption.
Blood Glucose Monitoring: Regular self-monitoring of blood glucose (SMBG) is essential.
Continuous Glucose Monitoring (CGM)
Regular Follow-Up: Patients should receive ongoing care and education from diabetic specialist nurses and healthcare providers. Monitoring HbA1c levels at least every three months is crucial to assess long-term glycemic control.
Psychosocial Support
Comprehensive Care: T1DM management should address both short-term and long-term complications. Regular screening for microvascular complications (e.g. retinopathy, nephropathy, neuropathy) and macrovascular complications (e.g. cardiovascular disease) is essential.
What is the hypoglycaemia management for type 1 diabetes?
Hypoglycemic episodes should be promptly treated with sugary drinks or snacks for conscious patients. For unconscious individuals, intramuscular glucagon or intravenous dextrose administration is necessary.
Explain the blood pressure control for type 1 diabetes
Stricter blood pressure targets are recommended for individuals with T1DM, aiming for values of less than 135/85 mmHg, or less than 130/80 mmHg in the presence of end-organ damage. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are often preferred as first-line agents.
What is the honeymoon period in type 1 diabetes?
Immediately after diagnosis, insulin requirements may be very low if the pancreas is still able to produce a significant amount of insulin. This is known as the ‘honeymoon period’. It is important that children are closely monitored during this time. This is because insulin requirements can suddenly increase as the remaining beta cells are destroyed. Additionally, as the blood glucose may be normal in this period on very low insulin doses, parents may incorrectly think that the condition has gone away.
What are the sick day rules with type 1 and 2 diabetes in terms of ACEIs, diuretics and NSAIDs
Stop treatment if there is a risk of dehydration to reduce the likelihood of acute kidney injury (AKI).
What are the sick day rules in terms of insulin therapy for type 1 and 2 diabetes?
Do not stop insulin treatment; instead, consider adjusting the dose with guidance from the specialist diabetes team.
What are the sicks rules in terms of blood glucose monitoring for type 1 and 2 diabetes mellitus?
Increase monitoring frequency to at least every 3–4 hours, including overnight.
Adjust insulin doses based on results.
Continue careful monitoring until blood glucose levels return to baseline.
Seek urgent medical advice if blood glucose remains uncontrolled.
What are the sick rules in terms of ketone monitoring for type 1 and 2 diabetes?
Check ketone levels regularly (at least every 3–4 hours, including overnight).
Seek immediate medical advice if urine ketone level is greater than 2+ or blood ketone level is greater than 3 mmol/L.
What are the sick rules for eating in terms of diabetes type 1 and 2?
Encourage maintaining regular meals and fluids, including carbohydrates, if appetite is reduced.
Fluid and Carbohydrate Replacement:
If unable to eat or vomiting, replace meals with carbohydrate-containing drinks (e.g. fruit juices, sugary drinks).
Adjust fluid intake based on blood glucose levels (sugar-free fluids for high levels, sugary fluids for low levels).
What are the associated medical conditions with type 1 diabetes mellitus?
Growth and pubertal development (delay in puberty and obesity)
Associated illnesses:
Thyroid disease (most associated; screening recommended)
Coeliac disease
What are the most common autoantibodies associated with type 1 diabetes mellitus?
Islet cell autoantibodies
What is the first line treatment in type 1 diabetes?
basal bolus insulin
What is the classical feature of chronic diabetic sensory neuropathy?
Sensory loss in a stocking distribution
This is a length dependant predominantly sensory polyneuropathy. Therefore, it presents with glove and stocking sensory loss, usually beginning in the legs (i.e. where the length of sensory neurons is the longest)
How does one work out a subcutaneous insulin regime including the basal bolus?
To do this one must work out the total 24 hour insulin requirement, then we must apply this to a basal bolus regime. The purpose of this is so simulate normal insulin secretion. There is always some insulin detectable in the blood but there are peaks corresponding to glycaemic load when meals are eaten. This is what we simulate. To work out the relative doses we consider there are 3 meals a day, so three-fifths of the total insulin for the 24 hour period should cover each of the meals in this cause 72 units. We then divide this by 3 to work out the number of short acting insulin units needed to be taken with each meal in this case 24 units. This works within 10-20 minutes and lasts for 3-5 hours. The remaining 2/5th is given as a long acting insulin like Lantus this has a much broader wave of activity lasting typically 18-24 hours
What is the primary investigation for diagnosing type 1 diabetes mellitus?
Measuring serum glucose
What does the glycemic index measure?
how quickly carbohydrate-containing foods affect blood sugars
What is type 2 diabetes mellitus?
chronic metabolic condition characterized by inadequate insulin production from pancreatic beta cells, resulting in insulin resistance. This leads to an elevation in blood glucose levels, causing hyperglycaemia.
What contributes to type 2 diabetes mellitus?
Poor dietary habits
Lack of physical activity
Obesity
Signs and symptoms for type 2 diabetes mellitus?
Polyuria
Polydipsia
Unexplained weight loss
Blurry vision
Fatigue
How does one investigate type 2 diabetes mellitus is symptomatic?
one of the following results is sufficient for diagnosis:
Random blood glucose ≥ 11.1mmol/l
Fasting plasma glucose ≥ 7mmol/l
2-hour glucose tolerance ≥ 11.1mmol/l
HbA1C ≥ 48mmol/mol (6.5%)
How do the investigations for type 2 diabetes change if asymptomatic?
If the patient is asymptomatic, two results are required from different days.
What are the lifestyle modifications for type 2 diabetes?
Advice on diet, regular physical activity, and smoking cessation
What are the pharmacological interventions for type 2 diabetes?
Initial drug treatment is usually metformin, with consideration of other agents like Pioglitazone, DPP‑4 inhibitors, sulphonylureas, or SGLT-2 inhibitors for those who cannot take metformin.
If one mono therapy and HbA1c > 58 mol/mol what do we consider in type 2 diabetes mellitus?
consider dual therapy with metformin, pioglitazone, a DPP‑4 inhibitor or a sulphonylurea (such as gliclizide).
If in type 2 diabetes mellitus dual therapy has not controlled drug glucose what do we then do?
triple therapy using the above medications can be considered. Otherwise, starting insulin may be necessary.
How often do we monitor HbA1c in type 2 diabetes mellitus?
Measure HbA1c levels at 3-6 month intervals. If the patient is on insulin or is at risk of hypoglycaemia, self-monitoring of glucose at home is necessary.
What type of basal insulin therapy do NICE recommend for type 2 diabetes?
basal insulin therapy with isophane (NPH) insulin as the first type to be used as it is most cost effective eg. Insulatard. Quick acting insulin analogues eg. Humalog, Novorapid, may be added in with meals if there is a big post meal glucose excursion.
What are the name of long acting insulin analogues?
Levemir, Lantus, Insulin Degludec and Abasaglar (a biosimilar insulin).
Why are mixed insulin combinations not used as much?
Mixed insulin combination which contain varying proportions of short and intermediate acting insulin such as Novomix 30 (30% short acting, 70% intermediate acting insulin) are more convenient because of fewer injections per day but may not be as successful.
What are the blood pressure targets in diabetes? and what drugs do we use
Blood pressure control needs to be strict in diabetes because these patients are at higher risk of macro- and microvascular complications.
NICE Hypertension Guidance [CG136] sets the same blood pressure targets as those who do not have diabetes, however in diabetics with HTN, ACE-inhibitors are first line as they are reno-protective
What are the sick day rules for metformin when you have type 2 diabetes?
Stop treatment if there is a risk of dehydration to lower the risk of lactic acidosis.
What are the sick day rules for sulfonylureas when you have type 2 diabetes?
Be cautious, as they may increase the risk of hypoglycemia, especially if dietary intake is reduced.
What are the sick day rules for SGLT-2 inhibitors when you have type 2 diabetes?
Check for ketones and stop treatment if acutely unwell and/or at risk of dehydration due to the risk of euglycemic diabetic ketoacidosis (DKA).
What are the sick day rules for GLP-1 receptor agonist when you have type 2 diabetes?
Stop treatment if there is a risk of dehydration to reduce the risk of AKI.
What is diabetic ketoacidosis characterised by? (triad)
Hyperglycemia (blood glucose >11 mmol/L)
Ketosis (blood ketones >3 mmol/L or urinary ketones ++ or higher)
Acidosis (pH <7.3 or bicarbonate <15 mmol/L)
Note: patients on SGLT-2 inhibitors may present with euglycemic DKA (where glucose is normal)
How is diabetic ketoacidosis caused?
DKA occurs due to insulin deficiency (absolute or relative) leading to hyperglycaemia
Ketones, including acetone, 3-beta-hydroxybutyrate, and acetoacetate, are produced from ketogenesis, whereby fatty acids are metabolised as an alternative energy source
These ketones are responsible for the acidosis seen
Hyperglycaemia causes an osmotic diuresis that contributes to severe dehydration as well as electrolyte imbalance
Vomiting and decreased fluid intake secondary to altered mental state also exacerbate dehydration
Name some common triggers for diabetic ketoacidosis?
Infections
Dehydration and fasting
Missing doses of insulin
Medications e.g. steroid treatment or diuretics
Surgery
Stroke or myocardial infarction
Alcohol excess or illicit drug use
Pancreatitis
Name one sign which was cause diabetic ketoacidosis to be classified as severe?
Blood ketones > 6mmol/L
Bicarbonate < 5mmol/L
Blood pH < 7
Anion gap above 16
Hypokalaemia on admission
GCS less than 12
Oxygen saturations < 92% in air
Systolic BP < 90mmHg
Brady or tachycardia (heart rate < 60 or > 100bpm)
Name some signs and symptoms of diabetic ketoacidosis?
Symptoms:
Nausea and vomiting
Abdominal pain
Polyuria
Polydipsia
Weakness
Signs:
Dry mucous membranes
Hypotension
Tachycardia
Altered mental state (drowsiness, confusion, coma)
Kussmaul’s breathing (deep, sighing breathing to compensate for metabolic acidosis by blowing off carbon dioxide)
Fruit-like smelling breath (due to ketosis)
What bedside investigations do we do for diabetic ketoacidosis?
Capillary blood glucose
Blood or urinary ketones
Urine dip +/- MSU (looking for evidence of a urinary tract infection which may precipitate DKA)
ECG (for ischaemic changes which may precipitate DKA, or changes secondary to electrolyte imbalance e.g. hypokalaemia)
What blood tests do we do for diabetic ketoacidosis?
Venous blood gas (for acid-base balance)
Urea and electrolytes (for electrolyte imbalance and AKI)
Full blood count and CRP (for infection markers)
Blood cultures (if infection is suspected)
HbA1c (to assess diabetic control over recent months)
What imaging would we consider for diabetic ketoacidosis and why?
Consider chest X-ray as part of septic screen (if signs of infection as a trigger for DKA)
What is the initial management for diabetic ketoacidosis?
Initial A to E assessment - Drowsy patients may require airway protection and an NG tube to prevent aspiration - Ensure adequate IV access - If hypotensive give up to 1L in fluid boluses then seek urgent senior input if not resolved - Consider urinary catheterisation and monitor fluid balance
What is the second step in the management of diabetic ketoacidosis?
IV fluid replacement with normal saline - A regimen of large volumes of IV fluid replacement given relatively quickly initially then over longer durations should be followed - Slower infusion rates should be considered in young adults, the elderly, those with heart or kidney failure or other serious comorbidities - An example in a healthy adult would be 1L over 1 hour, then 2x 1L over 2 hours, then 2x 1L over 4 hours, then 1L over 6 hours - Potassium replacement should be added after the first bag, depending on serum potassium levels
What is the third step of management of diabetic ketoacidosis?
After IV fluids have started, a fixed rate insulin infusion should be set up and withheld any existing insulin injections the patine is due.
This is provided as an infusion of 50 units of Actrapid in 50ml of 0.9% NaCl, at a rate of 0.1 units/kg/hour
Continue long-acting insulin if the patient is already on this
Investigation and management of any underlying triggers (e.g. septic screen and start antibiotics if evidence of infection)
What should one consider giving to a diabetic ketoacidosis patient due to dehydration?
Ensure VTE prophylaxis with low molecular weight heparin is prescribed as patients are at high risk of developing clots
What is the ongoing emergency management for diabetic ketoacidosis?
Patients should be closely monitored with hourly blood glucose and ketones - The aim is for ketones to fall by > 0.5mmol/L/hour - Blood glucose should fall by 3 mmol/L/hour - If these targets are not met, the rate of insulin infusion should be continued
At what value of blood glucose in diabetic ketoacidosis would one start a 10% glucose infusion?
14
When is diabetic ketoacidosis resolved?
once ketones are less than 0.6 mmol/L and pH is over 7.3 - If at this point they are able to eat and drink, a subcutaneous regimen of insulin should be started (usually with the input of a specialist diabetes team) - The insulin infusion should be stopped half an hour after the first dose of subcutaneous short acting insulin has been given
What is a rare but severe complication of diabetic ketoacidosis? Symptoms and signs include: headache, decline in consciousness, rise in blood pressure, drop in pulse and seizures
cerebral oedema
The first step of diabetic ketoacidosis management if the patient has a systolic blood pressure under 90mmHg
a 500ml bolus of IV 0.9% saline should be given and repeated if necessary - if not, then a rate that replaces deficit and provides maintenance would be adequate.
What is the criteria for mild diabetic ketoacidosis?
hyperglycaemia/ diagnosis of diabetes, blood ketones >3 mmol/L, urine ketones >2 + as well as a pH of 7.2-7.29, and/ or a bicarbonate of < 15 mmol/L
For children with diabetic ketoacidosis and a systolic BP below 90 what is the first step?
an initial intravenous bolus of 10 ml/kg 0.9% sodium chloride over 30 minutes
what anion gap indicates a severe DKA
> 16
What to do with short and long acting insulin when giving fixed rate intravenous insulin infusion due to diabetic ketoacidosis?
Subcutaneous short or rapid acting insulin should not be given alongside an intravenous insulin infusion. However, BSPED guidelines suggest that long acting insulin can be given alongside FRIII.
What is the first investigation we do for diabetic ketoacidosis?
Capillary blood gas and capillary blood ketones
What is diabetic retinopathy?
sight-threatening complication of diabetes mellitus, resulting from poor glycaemic control. This leads to vascular occlusion and leakage from the capillaries that supply the retina, causing retinal ischaemia, neovascularisation and, if left untreated, potential loss of sight.
What are the two stages of diabetic retinopathy?
non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR)
What are the three severity levels of non proliferative diabetic retinopathy?
Mild NPDR: Microaneurysms and dot hemorrhages on fundoscopy.
Moderate NPDR: Microaneurysms, dot and blot hemorrhages, cotton-wool spots, and hard exudates.
Severe NPDR: Beaded veins, intraretinal microvascular abnormalities (IRMA), and extensive retinal hemorrhages.
What does proliferative diabetic retinopathy include?
involves neovascularisation and fibrous proliferation on the retina or vitreous, posing a higher risk of severe vision loss.
What is the pathophysiology of diabetic retinopathy?
Chronic hyperglycaemia in diabetes mellitus causes structural changes to the retinal capillaries, including thickening of the basement membrane and loss of pericytes. This results in capillary occlusion and leakage, leading to retinal ischaemia and formation of new, fragile vessels.
What are the signs and symptoms of diabetic retinopathy?
Early stages of diabetic retinopathy may be asymptomatic. As the disease progresses, symptoms can include:
Floaters or dark spots in the vision
Blurred or distorted vision
Difficulty seeing at night
Sudden loss of vision
What are the investigations used for diabetic retinopathy?
Fundoscopy
Optical coherence tomography
Fluorescein angiography
What do you see on fundoscopy for the different severities of diabetic retinopathy?
Signs of milder disease include:
Microaneurysms
Hard exudates
Blot haemorrhages
Severe disease presents with:
Engorged tortuous veins
Cotton wool spots
Large blot haemorrhages.
In proliferative diabetic retinopathy (PDR), neovascularisation can be observed on the retina or optic disc.
What can optical coherence tomography be used to detect?
detect macular oedema
What is fluorescein angiography used to see in diabetic retinopathy?
Used in advanced cases to evaluate the extent of neovascularisation and guide treatment.
What management strategies are there for diabetic retinopathy?
Optimisation of blood glucose control
Laser photocoagulation
Intravitreal injections of anti-vascular endothelial growth factor
Vitrectomy surgery
What is laser photocoagulation used for?
proliferative diabetic retinopathy and clinically significant macular oedema.
What are anti-VEGF injections used for
diabetic macular oedema.
When would one do vitrectomy surgery?
for advanced cases with complications such as vitreous haemorrhage or retinal detachment.
What are the complications of diabetic retinopathy?
Vitreous Hemorrhage: Can cause sudden vision loss.
Tractional Retinal Detachment: May lead to blindness.
Macular Oedema: Causes central vision loss.
Neovascular Glaucoma: Can result in severe pain and vision loss.
Blindness: The ultimate complication in untreated or advanced cases.
For non-proliferative diabetic retinopathy what is the primary management?
Maintaining strict glycemic control
What retinal features are reason for immediate referral to an ophthalmologist?
proliferative retinopathy - R3 (new blood vessels), vitreous haemorrhage, advanced retinopathy with retinal detachments
What are the gastrointestinal complications of T2DM:
Gastroparesis - a result of poor glycaemic control leading to nerve damage of the autonomic nervous system. Characterized by delayed gastric emptying, early satiety, abnormal stomach wall movements, and morning nausea.
What are the neurological complications of T2DM
Autonomic Neuropathy - may lead to postural hypotension and associated symptoms like dizziness, falls, and loss of consciousness.
What are the vascular complications of T2DM:
Peripheral Arterial Disease (PAD) - patients present with foot discolouration, gangrene, intermittent claudication, rest pain, night pain and absent peripheral pulses (confirmed on doppler).
What are the foot complications of type 2 diabetes mellitus?
Diabetic Foot Infections - patients with vascular and neuropathic complications are at high risk for diabetic foot ulceration and subsequent infection.
What are the sexual dysfunction complications of T2DM
caused by a combination of factors including poor glycaemic control, neuropathy, microvascular complications, obesity, hypertension, depression, medication side effects, etc.
What are the cardiac complications of T2DM?
diabetes significantly increases the risk of cardiovascular disease, contributing to major morbidity and mortality.
What is diabetic nephropathy characterised by?
proteinuria, progressive decline in glomerular filtration rate (GFR), and high blood pressure
What is the pathogenesis of diabetic nephropathy?
hyperglycaemia-induced damage to the renal microvasculature leading to glomerulosclerosis and tubulointerstitial fibrosis. Over time, these changes result in decreased kidney function and eventually end-stage renal disease (ESRD). Histologically, it manifests as Kimmelstiel-Wilson nodules, diffuse glomerular basement membrane thickening, mesangial expansion, and arteriolar hyalinosis.
What screening should be done for diabetic nephropathy?
all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
should be an early morning specimen
ACR > 2.5 = microalbuminuria
Graphic showing choice of statin for hyperlipidaemia
What are the investigations for hyperparathyroidism?
What does a J wave look like in someone with hypothermia?
State all the BMI reference ranges and what classification they correlate to:
