Diabetes Mellitus and DKA Flashcards
What is Diabetes Mellitus
A lack or insufficiency of insulin
What does insulin do?
It facilitates cellular uptake of glucose
How is DM classified?
Type 1 = insulin dependent, Type 2 = non-insulin dependent
Gestational diabetes, post-pancreatectomy, Cushing’s syndrome related, CF related, LADA, MODY, post infection
What is T1DM?
Complete insulin deficiency, autoimmune, usually onset in youth, normal BMI, family history
Aetiology of T1DM
Autoimmunity which attacks beta cells - associated with genetic factors e.g. genes with the human leukocyte antigen (HLA) (50%), the gene that codes for insulin
Aetiology of T1DM - Viruses
Rubella infection & enteroviruses - molecular mimicry (immune response activated against self-antigens that resemble viral agents due to overlap of amino acid chains)
Aetiology of T1DM - diet & gut microbiome
Early introduction of cow’s milk (contains protein similar to one in beta cells)
Pathogenesis of T1DM
Development of auto-antigens> processed & presented by antigen presenting cells > T-helper cells activated> autoantibodies activate and attack beta cells > decreased insulin secretion > glucose in circulation cannot be taken into cell
Initial symptoms of T1DM
Excessive urination (high levels of glucose cause kidneys to excrete more), thirst, dehydration, weight loss, weakness, fatigue, nausea, emesis, ketoacidosis
Chronic symptoms of T1DM
Eye damage, nerve damage, feet problems, kidney problems, heart disease, hypoglycaemia (inappropriate treatment)
T1DM Diagnosis?
Random + Fasting Glucose level (normal range for fasting is 4-5.9 mmol/l, post prandial is less than 7.8 mmol/l). Oral Glucose Tolerance Test- 75g glucose + blood sugar levels are monitored afterwards, HbA1c gives idea of the long term glucose trend (diabetic is 48> mmol/mol)
T1DM Treatment
Insulin- three types - short acting insulin(action in 30 min), rapid acting(action in 1-3 hrs), intermediate and long lasting have a retardant to slow release insulin i.e zinc. Injection of insulin between fatty and muscle layer in upper outer thigh, upper buttock. Insulin pumps are less frequently used but these administer insulin automatically.
T1DM Monitoring?
Home blood testing kits available to measure glucose levels.
What is Diabetic Ketoacidosis (DKA)?
High serum glucose due to lack of insulin - body produces ketones due to cellular starvation of glucose.
Roughly how many T1 Diabetics develop DKA?
around 4%
What is the fatality risk of DKA with timely medical intervention?
up to 5%
What are the main symptoms of DKA
Increased urine rate, thirst, abdominal pain, laboured breathing and coma.
What are the causes of DKA
Having pre-existing T1DM, not adhering to monitoring and treatment regime, infectious illness (pneuomia, flu, COVID, gastroenteritis, or UTI), having a heart attack or stroke, cocaine cause.
How is DKA diagnosed?
Measurement of blood pH (Acidosis), serum bicarbonate levels, serum glucose levels, measuring ions like sodium and potassium, measuring body’s electrolyte/water balance to check for increased osmolarity which happens when you’re dehydrated.
What is the treatment for DKA
fluid replacement via IV Drip, Infusion of Insulin, monitor ions, glucose, pH, bicarbonate and osmolarity every 1-2 hours
Gestational Diabetes
~Occurs in (late) pregnancy - usually heals after birth
~Impaired glucose tolerance - Beta cell dysfunction & chronic insulin resistance
~15% pregnancies -risk factors:overweight,PCOS, geriatric pregnancy (≥34), family history
~No cure
Gestational Diabetes Diagnosis
OGTT & serum glucose levels
T2DM Statistics
~ 10% of people >50 in ROI - 5.5% pre-diabetic
~ Economic burden
~ 87% increase in OPD visit, 52% hospital admissions, & 32% ED visists
Symptoms T2DM
Polyuria, polydipsia, lethargy, irregular menstruation, increased hunger,dark patches in skin folds, weight loss, yeast infection
T2DM
~Insulin resistance - initially causes and increased insulin production to maintain homeostasis - insulin production decreased due to increased stress on beta cells
~>45 years old - increase prevelance in youth
~ Linked with adipokine dysfunction (health regulators e.g. appetite, satiety, inflammation)
~abnornalities of gut microbiota
~Obesity
~Production of glucagon-like peptides (upregulate serum glucose conc.)
T2DM Risk Factors
Age, obesity, pre-diabetic, gestational diabetes, high BP, High cholesterol and triglycerides, low HDL, steroid use, history of heart disease, PCOS, heritage (Asian, Hispanic, Afro-Caribbean, travelling community)
T2DM pathogenisis
Insulin resistance due to beta cell dysfunction:
~Compensatory increase in insulin production (homeostasis)
~beta cells change - unable to maintain homeostasis - hyperglycaemia
~Increased abdominal visceral fat promotes insulin resistance due to inflammation and release of free fatty acids
T2DM effects on body parts
Liver: insulin resistance and increased hepatic glucose output
Pancreas: decreased insulin secretion, increased beta cell apoptosis, decreased beta cell mass, hyperglucogonaemia
Muscles: insulin resistance
Gut: impaired incretion effect
Adipocytes: increased in fatty acids circulating, hyperlipidaemia
T2DM diagnosis
Same as T1DM
HbA1c and serum glucose monitored
T2DM treatment
LIFESTYLE CHANGE - improved diet, less alcohol, no smoking, weight loss, more activity
~Some medicine uses e.g. insulin to reduce blood glucose- risk of hypoglycaemia
Diabetic Foot Syndrome
-Neuropathy occurs as a result of T1DM in eyes, ears and extremities
~Ulcers form- gangrene occurs as a result of deepening of ulcers
~Amputation
