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Endocrine system > DIABETES MELLITUS Type I&II DKA, HHS > Flashcards

DIABETES MELLITUS Type I&II DKA, HHS Flashcards

1
Q

What is diabetes?

A

Diabetes is defined as an elevation of blood glucose above a diagnostic threshold.

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2
Q

Name some pure genetic disorders associated with insulin action.

A

Donohue syndrome, Rabson-Mendenhall syndrome

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3
Q

What conditions feature insulin resistance?

A

Obesity, Type 2 diabetes, NAFLD

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4
Q

List some endocrinopathies associated with insulin resistance.

A

Cushing’s syndrome, Acromegaly, Phaeochromocytoma, Glucagonoma

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5
Q

What is a common cause of insulin resistance induced by external factors?

A

Steroid-induced, specifically by exogenous glucocorticoids

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6
Q

What are the disorders associated with insulin secretion?

A

Type I diabetes, MODY, Neonatal diabetes

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7
Q

Name some genetic disorders related to insulin secretion.

A

MODY, Neonatal diabetes

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8
Q

What are some pancreatic diseases associated with insulin secretion?

A

Alcoholic and chronic pancreatitis, Acute pancreatitis, Pancreatectomy, Pancreatic cancer, Cystic fibrosis, Haemochromatosis

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9
Q

What is the spectrum of Type 2 diabetes in terms of insulin deficiency and resistance?

A

Ranging from predominant beta cell deficiency to predominant insulin resistance

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10
Q

Is diabetes often asymptomatic?

A

Yes, especially type 2 diabetes.

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11
Q

What are the symptoms of high blood glucose?

A

Polyuria,
Thirst and polydipsia,
Blurred vision,
Genital thrush,
Fatigue,
Polyphagia Weight loss

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12
Q

Why does hyperglycemia cause blurred vision?

A

Hyperglycemia results in changes to osmotic pressures in the anterior chamber of the eye in front of the lens.

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13
Q

Name some diabetic emergencies and their associations.

A

Diabetic ketoacidosis (most commonly due to type 1), Hyperosmolar hyperglycaemic state (extreme presentation of new type 2 diabetes)

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14
Q

When might complications of diabetes present with symptoms/signs?

A

Rarely, and they may include loss of vision, retinal bleed, or retinal changes found by an optician.

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15
Q

What is the purpose of the C-peptide measurement?

A

C-peptide, co-secreted with insulin, is used to measure ‘endogenous’ insulin secretion. If present, it indicates secretion by the person’s beta cells.

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16
Q

How does HbA1c provide information about glucose exposure?

A

HbA1c reflects the amount of glycation of hemoglobin, which is proportional to glucose exposure over the last 90 days. It is used in diagnosis and monitoring of diabetes.

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17
Q

What caution is advised when interpreting HbA1c results?

A

Caution is needed in conditions of increased or reduced RBC turnover, such as haemolytic anaemia.

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18
Q

What are the diagnostic criteria for diabetes based on fasting glucose?

A

Fasting glucose ≥ 7.0 mmol/L is considered diagnostic for diabetes.

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19
Q

In gestational diabetes, how are threshold levels determined?

A

In gestational diabetes, threshold levels are not set by retinopathy risk but rather by risk to the fetus/neonate, and are much lower.

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20
Q

What are the three diagnostic criteria for diabetes?

A

Fasting glucose ≥ 7 mmol/L, Random or 2 hr (after 75g oral glucose) glucose ≥ 11.1 mmol/L, HbA1c ≥ 48 mmol/mol. If asymptomatic, a repeat confirmatory test is required.

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21
Q

Define ‘Normal glucose tolerance’ in terms of fasting glucose, 2hr glucose in OGTT, random glucose, and HbA1c.

A

Fasting glucose ≤ 6.0 mmol/L, 2hr glucose in OGTT ≤ 7.7 mmol/L, Random glucose ≤ 7.7 mmol/L, HbA1c ≤ 41 mmol/mol.

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22
Q

What are microvascular complications of diabetes?

A

Retinopathy, neuropathy.

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23
Q

What is the recommended HbA1c target for preventing microvascular complications?

A

Aim for HbA1c <53 mmol/mol to prevent microvascular complications.

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24
Q

Name some macrovascular complications of diabetes.

A

MI/ACS (Myocardial Infarction/Acute Coronary Syndrome), stroke, PVD (Peripheral Vascular Disease).

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25
Q

What preventive measures are recommended for macrovascular complications?

A

Cholesterol control, blood pressure control, antiplatelet therapy.

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26
Q

Besides blood glucose, what other complications should be screened for in diabetes management?

A

Eye disease (laser), Neuropathy (podiatry), Kidney disease (BP management, ACEi).

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27
Q

What is the primary cause of Type 1 diabetes?

A

Autoimmune destruction of pancreatic beta-cells, resulting in beta-cell deficiency and absolute insulin deficiency.

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28
Q

What are the two subtypes of Type 1 diabetes?

A

Type 1A (immune-mediated) and Type 1B (non-immune mediated).

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29
Q

What characterizes Type 1A diabetes?

A

It involves an environmental trigger in a genetically susceptible individual, mediated by an autoimmune process within the pancreatic β-cell.

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30
Q

What is LADA, and when does it typically occur?

A

LADA (Latent Autoimmune Disease in Adults) is a ‘slow-burning’ variant of Type 1A with slower progression to insulin deficiency, occurring in later life.

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31
Q

What characterizes Type 1B diabetes?

A

It involves patients with permanent insulinopenia, prone to DKA, but without evidence of β-cell dysfunction or autoantibodies.

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32
Q

What percentage of T1DM patients does Type 1B account for?

A

Approximately 5% of T1DM patients.

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33
Q

Which population is Type 1B more common in?

A

Type 1B is more common in individuals of African or Asian ancestry.

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34
Q

What are the risk factors for Type 1 diabetes in terms of age?

A

The peak incidence is in individuals under 20, with a smaller peak in the late 30s (LADA), and clinical presentation is possible at all ages up to the 9th decade.

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35
Q

How much of the familial risk of T1DM do HLA genes represent?

A

HLA genes represent approximately 50% of the familial risk of T1DM.

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36
Q

What are some high-risk HLA genotypes for T1DM?

A

DR3-DQ2 and DR4-DQ8 are high-risk HLA genotypes for T1DM.

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37
Q

What is the risk of offspring developing diabetes if both parents have susceptible HLA alleles?

A

The risk is 30%.

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38
Q

Besides HLA genes, what other genetic factors influence the risk of T1DM?

A

At least 47 non-HLA genes or gene regions influence the risk of T1DM to a minor extent.

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39
Q

What are some environmental factors associated with the risk of Type 1 diabetes?

A

Maternal factors (gestational infection and older age), viral infections (e.g., Coxsackie B4), dietary constituents (early introduction to cow’s milk, vitamin D deficiency), environmental toxins (e.g., alloxan), childhood obesity, and psychological stress.

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40
Q

What are the key steps in the pathophysiology of Type 1 diabetes?

A
  1. Genetic susceptibility, 2. Environmental trigger (often associated with a previous viral infection), 3. T-cell mediated autoimmune response with production of autoantibodies targeting and destroying β-cells, 4. Absolute insulin deficiency leading to elevated blood glucose levels.
41
Q

What is visible on β-cell biopsy in Type 1 diabetes?

A

Insulitis with a lymphocytic infiltrate is visible on β-cell biopsy.

42
Q

What are the consequences of absolute insulin deficiency in Type 1 diabetes?

A

Elevated blood glucose levels result from absolute insulin deficiency.

43
Q

What are the classic symptoms of insulin deficiency in Type 1 diabetes?

A

Polyuria, polydipsia, weight loss.

44
Q

What are the diagnostic criteria for Type 1 diabetes with symptoms?

A

Fasting glucose ≳7.0 mmol/l or random glucose ≳11.1 mmol/l with symptoms. If asymptomatic, a repeat test may be required.

45
Q

What autoantibodies are associated with Type 1 diabetes, and what do they target?

A
  • Glutamic acid decarboxylase (GAD): Targets GABA production - Islet-antigen 2 (IA-2): Unknown function - Insulin (IAA): Regulates glucose - ZnT8 transporter (ZnT8Ab): Zn function in β-cells
46
Q

What percentage of patients have GAD 65 antibodies at diagnosis of Type 1 diabetes?

A

70-80%

47
Q

What is the function of the IA-2 autoantibody in Type 1 diabetes?

A

Unknown function

48
Q

Which autoantibody is better in children with Type 1 diabetes?

A

Insulin (IAA)

49
Q

What is the recommended insulin regimen for most people with Type 1 diabetes?

A

Usually a basal (long-acting once daily) bolus (short-acting with meals) regimen aiming to mimic normal endogenous insulin production. Most people should be treated with multiple daily injections (MDI) or continuous subcutaneous insulin infusion (CSII).

50
Q

Why should insulin analogues be used in Type 1 diabetes management?

A

To reduce the risk of hypoglycemia.

51
Q

What should patients with Type 1 diabetes be educated about?

A
  • Self-monitoring of blood glucose and ketones - Matching prandial insulin dose to carbohydrate intake, pre-meal glucose, and anticipated activity - Sick day rules. Structured education courses such as DAFNE and BERTE are available. Regular contact with a Diabetes Specialist Nurse (DSN) and dietician.
52
Q

What are the components of the annual review assessment for Type 1 diabetes?

A
  • Weight - Blood pressure - Bloods: HbA1c, renal function, and lipids - Retinal screening - Foot risk assessment - Record of severe hypoglycaemic episodes or admission with DKA
53
Q

In what situations is pancreas transplant considered in Type 1 diabetes management?

A
  • Islet Transplantation: Reserved for those with episodes of severe hypoglycemia, severe and progressive long-term complications despite maximal therapy, or uncontrolled diabetes despite maximal treatment. Goal is to prevent severe hypoglycemia, and about 50-70% achieve insulin independence after 5 years. - Whole-Pancreas Transplantation: Most often undertaken in people with T1DM and end-stage kidney disease, either at the same time as a kidney transplant or after a kidney transplant. Indications include severe hypoglycaemia/metabolic complications or incapacitating clinical or emotional problems.
54
Q

What is hypoglycemia?

A

Hypoglycemia is a metabolic condition characterized by an abnormally low blood glucose level, typically defined as less than 4.0 mmol/L. It is the most common side effect of insulin therapy.

55
Q

What are the common causes of hypoglycemia in insulin therapy?

A
  • More insulin injected than needed - Irregular eating habits - Unusual exertion - Alcohol excess - Insulin errors - Variation in insulin absorption, e.g., due to lipohypertrophy. The times of greatest risk are before meals, during the night, and during or after exercise.
56
Q

What are the clinical features of hypoglycemia?

A

Pallor, sweating, tremor, palpitations, confusion, nausea, hunger, cognitive impairment, coma.

57
Q

How should mild hypoglycemia be managed when the patient is conscious?

A
  • ABCDE approach - Consumption of 15-20g of fast-acting carbohydrate such as glucose tablets, a small can of non-diet soda, sweets, or fruit juice. - Avoid chocolate due to its slower absorption. - Consume slower-acting carbohydrates afterwards (e.g., toast).
58
Q

How should severe hypoglycemia be managed, especially if seizures or unconsciousness occur?

A
  • ABCDE approach - Administration of 200ml 10% dextrose IV - 1mg glucagon IM if no IV access (note: this will not work if the cause is acute alcohol ingestion due to its action in blocking gluconeogenesis). - Management of seizure if prolonged or repeated.
59
Q

What considerations should be taken for aftercare of hypoglycemia?

A
  • Consideration of medication changes - Investigation of non-drug causes if necessary.
60
Q

What is the etiology of type 2 diabetes (T2DM)?

A

T2DM results from a combination of insulin resistance and less severe insulin deficiency. It accounts for 90-95% of diabetes cases, with the highest prevalence in lower and middle-income countries. The condition is polygenic, influenced by environmental factors, insulin resistance, and obesity.

61
Q

What are the non-modifiable risk factors for T2DM?

A
  • Age (usually occurs later in life, >45 years) - Genetics (polygenetic disease with 400 genetic variants identified) - Ethnicity (individuals of South Asian, African, and Afro-Caribbean descent are at greater risk)
62
Q

What are the modifiable risk factors for T2DM?

A
  • Obesity (9 out of 10 people with T2DM are overweight/obese, BMI of 25 or above) - Diet (high dietary fat, saturated fat, red and processed meat, fried food, increased intake of white rice and sugary drinks) - Physical inactivity and sedentary behaviors
63
Q

How does insulin resistance develop in T2DM?

A

Insulin resistance in T2DM is developed through: -
Central obesity leading to increased plasma levels of free fatty acids and impaired insulin-dependent glucose uptake- Increased tyrosine kinase activity in liver, fat, and skeletal muscle cells, resulting in decreased activation of downstream proteins and decreased expression of GLUT channels, leading to decreased cellular glucose uptake.

64
Q

What abnormalities of insulin secretion are seen in T2DM?

A
  • Early T2DM is often associated with insulin hypersecretion as a response to insulin resistance. - Loss of the first phase of the normal biphasic insulin secretion is an early sign. - The compensatory increased insulin is insufficient to restore glucose homeostasis, leading to persistent hyperglycemia. - Hyperglycemia and increased levels of FFAs and adipokines are toxic to β-cells, resulting in decreased insulin production.
65
Q

What hormonal abnormalities are observed in T2DM?

A
  • Increased glucagon secretion due to decreased intra-islet insulin, leading to increased gluconeogenesis. - Decreased incretin effect in T2DM.
66
Q

What are the clinical features of T2DM?

A

Symptoms: Gradual onset, majority are asymptomatic. When symptomatic, characteristic features of hyperglycemia may not be severe. Signs: Acanthosis nigricans, which is insulin-driven epithelial overgrowth seen in hyperinsulinemic states (severe insulin resistance).

67
Q

How can symptomatic patients be diagnosed with diabetes based on blood glucose levels?

A

Symptomatic patients can be diagnosed based on one positive result, and a second test may be performed to confirm. The criteria include: - Random blood glucose ≥ 11.1 mmol/l - Fasting plasma glucose ≥ 7 mmol/l - 2-hour glucose tolerance ≥ 11.1 mmol/l - HbA1c ≥ 48 mmol/mol (6.5%)

68
Q

How is the diagnosis of diabetes approached in asymptomatic patients?

A

In asymptomatic patients, the diagnosis of diabetes should not be based on a single abnormal HbA1c or fasting plasma glucose level. At least one additional abnormal HbA1c or plasma glucose level is essential.

69
Q

What other investigations are conducted for diabetes management?

A
  • Blood pressure - Ketones (if random blood glucose > 15 mM) - Cholesterol - Pancreatic autoantibodies
70
Q

What lifestyle changes are recommended for managing type 2 diabetes?

A

At diagnosis, a 10-15% weight loss can result in remission of type 2 diabetes.

71
Q

What is the first-line medical management for type 2 diabetes?

A

Metformin + lifestyle management is first line in all patients with T2DM.

72
Q

What is the medical management for diabetic patients with atherosclerotic CVD?

A

Diabetic patients with atherosclerotic CVD (e.g., previous MI) should be given metformin + GLP-1 receptor antagonist.

73
Q

What is the medical management for diabetic patients with heart failure or chronic kidney disease?

A

Diabetic patients with heart failure or chronic kidney disease should be given metformin + an SGLT2 inhibitor as first line (GLP-1 receptor antagonist second line).

74
Q

What are the other medical management options for type 2 diabetes?

A

Other medical management options include DPP4 inhibitors, sulfonylureas (SUs), TZDs.

75
Q

What is the recommended HbA1c target for individuals with type 2 diabetes?

A

A target HbA1c of 7.0% (53 mmol/mol) among people with type 2 diabetes is reasonable to reduce the risk of microvascular and macrovascular disease. Targets should be set with individuals to balance benefits with harms, especially hypoglycemia and weight gain.

76
Q

How can weight loss contribute to the prevention of type 2 diabetes?

A

Weight loss in people with a BMI >30 significantly reduces the risk of developing type 2 diabetes.

77
Q

What is diabetic ketoacidosis (DKA)?

A

DKA is a disordered metabolic state that usually occurs in the context of an absolute or relative insulin deficiency accompanied by an increase in counter-regulatory hormones such as glucagon, adrenaline, cortisol, and growth hormone.

78
Q

What are the common causes of insulin deficiency leading to DKA?

A

Insulin deficiency leading to DKA can be caused by the initial presentation of unknown diabetes or non-adherence to insulin/poor self-management.

79
Q

What conditions can increase insulin demand and contribute to DKA?

A

Conditions that increase insulin demand and contribute to DKA include infections (pneumonia, UTIs, cellulitis), inflammatory conditions (pancreatitis, cholecystitis), intoxication (alcohol, cocaine, salicylate, methanol), infarction (acute MI, stroke), and iatrogenic factors (steroids, surgery).

80
Q

How are ketone bodies formed in the context of DKA?

A

Ketone bodies, mainly acetoacetate and 3-hydroxybutyrate, are formed in the liver mitochondria from acetyl-CoA, which is derived from the beta-oxidation of fats. They diffuse into the bloodstream and peripheral tissues, serving as important energy metabolism molecules for the heart muscle and renal cortex.

81
Q

What is the role of insulin in inhibiting ketone formation?

A

Insulin normally inhibits lipolysis, reducing the risk of ketone body overload. In T1DM, DKA is a risk if insulin supplementation is missed, leading to hyperglycemia and a shift to fatty acid oxidation. In T2DM, DKA is rarer due to some inhibition of lipolysis, but it can occur with increasing insulin resistance and deficiency.

82
Q

What are the consequences of excessive accumulation of ketone bodies?

A

Excessive accumulation of ketone bodies can lead to acidosis. High glucose excretion causes osmotic diuresis, resulting in electrolyte loss and dehydration, which decreases renal function and exacerbates acidosis. DKA can progress to coma and, if untreated, can be fatal.

83
Q

What are the osmotic-related clinical features of diabetic ketoacidosis?

A

Osmotic-related clinical features include thirst, polyuria, and dehydration.

84
Q

What are the ketone body-related clinical features of diabetic ketoacidosis?

A

Ketone body-related clinical features include flushed appearance, vomiting, abdominal pain and tenderness, increased respiratory rate (Kussmaul’s respiration), and a distinctive smell on the breath (not present in all individuals).

85
Q

What are some associated conditions with diabetic ketoacidosis?

A

Associated conditions with diabetic ketoacidosis include underlying sepsis and gastroenteritis.

86
Q

How is the diagnosis of diabetic ketoacidosis confirmed?

A

The diagnosis of diabetic ketoacidosis is confirmed by demonstrating hyperglycemia with ketonemia or heavy ketonuria, and acidosis. The criteria include: - Ketonaemia ≳3 mmol/L, or significant ketouria (≳2 on standard urine stick) - Blood glucose > 11.0 mmol/L or known DM - Bicarbonate < 15 mmol/L and/or venous pH < 7.3

87
Q

What are some other biochemistry findings in diabetic ketoacidosis?

A

Other biochemistry findings in diabetic ketoacidosis include: - Potassium often > 5.5 mmol/L but drops as soon as insulin is given - Creatinine often raised - Sodium often low or low end of normal - Amylase often raised (rarely pancreatitis, origin can be salivary) - White cell count raised (median 25) - does not always equate to infection, sign of inflammatory response

88
Q

How is fluid replacement managed in diabetic ketoacidosis?

A

Fluid replacement involves administering 1000mL NaCl 0.9% in the first hour, 20000mL NaCl by the end of hour 2, and 30000mL NaCl by the end of hour 4. Once blood-glucose concentration falls below 14 mmol/litre, IV glucose 10% should be given in addition to the sodium chloride 0.9% infusion.

89
Q

How is electrolyte replacement managed in diabetic ketoacidosis?

A

Electrolyte replacement involves administering NaCl 0.9% as described in fluid replacement. IV potassium is also given, and phosphate is rarely replaced.

90
Q

How is acid-base balance restoration managed in diabetic ketoacidosis?

A

Acid-base balance restoration involves rarely replacing bicarbonate, as once the circulating volume is restored, the metabolic acidosis is rapidly compensated.

91
Q

How is insulin replacement managed in diabetic ketoacidosis?

A

Insulin replacement involves administering IV insulin at 0.1 units/kg per hour to suppress ketogenesis, lower glucose, and correct electrolyte disturbance. Continue ‘usual’ subcutaneous daily basal insulin. Continue IV insulin until ketoacidosis is resolved; to prevent hypoglycemia, give 10% glucose IV alongside the 0.9% NaCl once blood-glucose concentration falls below 14 mmol/L.

92
Q

What monitoring measures are taken in the management of diabetic ketoacidosis?

A

Monitoring involves checking blood-ketone and blood-glucose concentrations hourly and blood gas and electrolytes every 2-4 hours.

93
Q

What are some other measures taken in the management of diabetic ketoacidosis?

A

Other measures include seeking the underlying cause, such as infection if suspected, considering a nasogastric tube as patients may aspirate vomit, and providing prophylactic low molecular weight heparin (LMWH) to reduce the risk of thromboembolism.

94
Q

How can recurrence of diabetic ketoacidosis be prevented?

A

Prevention of recurrence involves education and support before discharge, providing the patient with a ketone meter, arranging diabetes specialist nurse (DSN) follow-up, and informing the general practitioner (GP).

95
Q

What are some complications of diabetic ketoacidosis?

A

Complications of diabetic ketoacidosis include cerebral edema (mostly in children/young adults), hypokalemia (which can cause cardiac arrest and paralytic ileus), aspiration pneumonia, and acute respiratory distress syndrome (ARDS).

96
Q

How does the pathophysiology of hyperglycaemic hyperosmolar syndrome (HHS) differ from diabetic ketoacidosis (DKA)?

A

In HHS, there are still small amounts of insulin being secreted by the pancreas, which is sufficient to prevent DKA by suppressing lipolysis and, in turn, ketogenesis. However, the insulin level is not high enough to lower blood glucose to a safe level. The pathophysiology of HHS is characterized by marked dehydration and loss of electrolytes due to predominating hyperglycemia and osmotic diuresis, similar to DKA.

97
Q

What are the clinical features of hyperglycaemic hyperosmolar syndrome?

A

Clinical features of HHS include dehydration due to polyuria, polydipsia, nausea, vomiting, and stupor/coma. The degree of impaired consciousness is directly related to the level of osmolarity.

98
Q

What are the key investigations used to diagnose hyperglycaemic hyperosmolar syndrome?

A

HHS is characterized by profound hyperglycemia (glucose > 33.3 mmol/L), hyperosmolality (serum osmolarity > 320 mmol/kg, measured directly or calculated as 2 x Na+ + glucose + urea), and volume depletion in the absence of ketoacidosis (pH > 7.3 and bicarbonate > 15 mmol/L). Other features may include significant renal impairment, and sodium levels are often high normal or raised.

99
Q

How is the management of hyperglycaemic hyperosmolar syndrome approached?

A

The management of HHS involves assessing the severity of dehydration and using 0.9% saline for fluid replacement without insulin, as fluids alone will reduce osmolarity. Care should be taken to avoid fluid overload. Sodium should be managed to avoid rapid fluctuations, and if dropping too quickly, consider 0.45% saline. Monitoring and charting blood glucose, osmolarity, and sodium is essential. Low-dose IV insulin is started only if significant ketones (>1) or blood glucose is falling at a slow rate. Comorbidities are more likely, so screening for vascular events (e.g., silent MI) and using LMWH for all patients (unless contraindicated) is recommended. High risk of foot complications should also be considered.

Endocrine system (12 decks)

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