Diabetes Flashcards
What is type 1 diabetes?
Metabolic disorder characterized by hyperglycemia due to absolute insulin deficiency
EPIDEMIOLOGY of T1DM
More common in Europeans and the west in general
Tends to start before puberty
5-10% of all DM
Etiology of T1DM
Autoimmune destruction of pancreatic beta cells
Can be due to:
Genetics - HLA DR/DQ genes
Viral: Enteroviruses + Congenital rubella
Environmental triggers in susceptible individuals
Pathophysiology of T1DM
Autoimmune destruction of pancreatic beta cell destruction
B-Cell destruction preceds sub clinically for months to years as insulitis.
Hyperglycaemia develops when 80-90% beta cells have been destroyed
Patients unable to uti9lise glucose in peripheral muscle and adipose = stimualtion of counter hormons ie glucagon + adrenaline + cortisol + growth hormone
Counter hormones promote gluconeogenesis, glycogenolysis + ketogenesis = hyperglycemia
Classification of T1DM
Classic i.e with beta cell destruction
Idiopathic i.e without beta cell destruction
Presentation of T1DM
Polyuria
Polydipsia
Young age
DKA signs = weight loss, blurred vision, nausea and vom, abdo pain, lethargy
Risk factors for T1DM
Geography mainly
Investigations to order in T1DM
Random plasma glucose: 11mmol or higher = +ve with +ve history
Fasting plasma glucose: 7mmol or higher
2 hr plasma glucose: 11mmol or higher
AC1 reflects degree of hyperglycaemia over last 3 months
Results of an OGTT and when is it required?
Required: if fasting or random glucose is borderline
Normal <7.8mmol
Diabetes >11mmol
What are some secondary causes of DM
Don’t Panic EveryOne
Drugs: steroids, antiHIV, thiazides
Pancreas: CF, pancreatitis, Ca
Endocrine: Cushings, Acromegaly, T4
Other: Glycogen storage disease
Diagnostic criteria for metabolic syndrome
Central obesity + two of:
Increased trigs
Low HDL
HTN
Hyperglyceamia
Long Term Management of DM
The 4Cs
Control: record blood glucose levels
- maintain fasting levels between 4.5-6mmol
- maintain post prandial levels between 4.5-9mmol
- maintain HBA1C <45 - 50 mM
- monitor BP + lipids
Complications: Macro and Micro
- Macro: cardio, cerebrovasc,PVD
- Micro: retinopathy, neuropathy, nephropathy
- Monitor for these problems by checking pulses, BP, eyes, ACR + U+Es + foot inspection
Competency
Coping
Lifestyle modifications in DM
DELAYS
Diet Exercise Lipids Average BP + Aspirin Yearly check up Smoking cessation
What is type 2 DM?
Progressive disorder defined by defects in insulin secretion and action + resistance and beta cell dysfunction which leads to a relative insulin deficiency
Factors which worse insulin resistance in T2DM
Obesity
Inactive life
Increasing age
Excessive alcohol
Risk factors for T2DM
PICHD
Pre diabetes Positive family history Physical inactivity Increasing age Increasing weight Gestational DM CVD HTN Dyslipidemia
Clinical presentation of T2DM
Pt may be asymptomatic May present with: -candida infection -skin infections -UTIs -fatigue -blurred vision -parasthesis
Investigations to consider in T2DM
HBA1C Fasting glucose >7 Random gluocse>11 OGTT>11 Fasting lipid profile which may show increased LDL, low HDL and increased trigs Ketones: should be negative
Management of T2DM
At diagnosis: Anti-hypertensive + statin + lifestyle changes +/- metormin
Hyperglycaemic: Insulin therapy +/- metformin
Aysymptomatic and normoglycaemic: Metformin +/- insulin if HBA1C > target
Complications of DM
KNIVES
KIDNEY: nephropathy NEUROMUSCULAR: peripheral neuropathy INFECTIVE: TB, UTIs VASCULAR: CAD, CVD, PVD EYES: Retinopathy + cataracts SKIN: diabetic dermopathy
Which severe and life threatening condition can diabetic patients present with asymptomatically?
‘Silent’ MI: due to autonomic neuropathy
Consequences of diabetic neuropathy
Charcots foot Claw toes Pes Cavus Loss of protective sensation Ulcers
Diagnosis and management of diabetic nephropathy
Microalbulinaemia where ACR >30
Start on ACEi
Refer if ACR>70
Signs in background retinopathy
Dots, Blots and Exudates
Signs in pre-proliferative retionopathy
Spots, beading and bleeds
Signs in proliferative retinopothy
New vessel formation and bleeds
Signs in maculopathy
Reduced visual acuity
3 main diabetic emergencies
DKA
HONK: Hyperosmotic hyperglycaemic non ketotic coma
Lactic acidosis
Which of type 1 or type 2 does DKA occur in?
Type 1 only due to the fact that DKA relates to an absolute deficiency of insulin
Pathogenesis of DKA
- Ketoacidosis - a decrease in insulin = increase in stress hormones like usual. A decrease in glucose utilisation leads to oxidation of fats which increases fatty acids and ATP, generating ketone bodies
- Dehydration - Decreased insulin = decreased utilisation of glucose = increased gluconeogensis = severe hyperglycaemia + osmotic diuresis = increase in ketone
Causes of DKA
The 5 S’s
S - Sepsis S - Surgery S - Sugar High (Missed insulin) S - Stress S - Substances (Alcohol , Dope)
Clinical presentation of DKA
Remember DKA
D - Diuresis, Delirium / Dizziness, Dehydration
K - Kussmaul Breathing, Ketotic Breath
A - Abd. Pain
Investigations and results seen in DKA
Ketones and K in urine ABG shows pH <7.3 + low HCO3 + CO2 retention Hyperglycemia >11 CXR may show infection as the source Check kidney function
Management of DKA
IV FLUIDS
K THERAPY
INSULIN
Hyperosmolar hyperglycaemic non ketotic coma happens to patients with which type of Diabetes?
T2DM because there is enough insulin to prevent ketosis but not enough to prevent hyperglycaemia
Causes of HONK
Infection
T2DM uncontrolled
MI
Presentation of HONK
Thirst
Polyuria
Impaired concentration
Complications of HONK
Occlusion events i.e. DVT
Management of HONK
Fluids w/ potassium
Insulin
Anticoagulation
