Diabetes Flashcards

1
Q

What is type 1 diabetes?

A

Metabolic disorder characterized by hyperglycemia due to absolute insulin deficiency

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2
Q

EPIDEMIOLOGY of T1DM

A

More common in Europeans and the west in general
Tends to start before puberty
5-10% of all DM

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3
Q

Etiology of T1DM

A

Autoimmune destruction of pancreatic beta cells

Can be due to:
Genetics - HLA DR/DQ genes
Viral: Enteroviruses + Congenital rubella
Environmental triggers in susceptible individuals

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4
Q

Pathophysiology of T1DM

A

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

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5
Q

Classification of T1DM

A

Classic i.e with beta cell destruction

Idiopathic i.e without beta cell destruction

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6
Q

Presentation of T1DM

A

Polyuria
Polydipsia
Young age

DKA signs = weight loss, blurred vision, nausea and vom, abdo pain, lethargy

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7
Q

Risk factors for T1DM

A

Geography mainly

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8
Q

Investigations to order in T1DM

A

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

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9
Q

Results of an OGTT and when is it required?

A

Required: if fasting or random glucose is borderline

Normal <7.8mmol
Diabetes >11mmol

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10
Q

What are some secondary causes of DM

A

Don’t Panic EveryOne

Drugs: steroids, antiHIV, thiazides
Pancreas: CF, pancreatitis, Ca
Endocrine: Cushings, Acromegaly, T4
Other: Glycogen storage disease

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11
Q

Diagnostic criteria for metabolic syndrome

A

Central obesity + two of:

Increased trigs
Low HDL
HTN
Hyperglyceamia

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12
Q

Long Term Management of DM

A

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

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13
Q

Lifestyle modifications in DM

A

DELAYS

Diet
Exercise
Lipids
Average BP + Aspirin
Yearly check up
Smoking cessation
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14
Q

What is type 2 DM?

A

Progressive disorder defined by defects in insulin secretion and action + resistance and beta cell dysfunction which leads to a relative insulin deficiency

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15
Q

Factors which worse insulin resistance in T2DM

A

Obesity
Inactive life
Increasing age
Excessive alcohol

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16
Q

Risk factors for T2DM

A

PICHD

Pre diabetes
Positive family history
Physical inactivity
Increasing age
Increasing weight
Gestational DM
CVD
HTN
Dyslipidemia
17
Q

Clinical presentation of T2DM

A
Pt may be asymptomatic
May present with:
-candida infection
-skin infections
-UTIs
-fatigue
-blurred vision
-parasthesis
18
Q

Investigations to consider in T2DM

A
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
19
Q

Management of T2DM

A

At diagnosis: Anti-hypertensive + statin + lifestyle changes +/- metormin

Hyperglycaemic: Insulin therapy +/- metformin

Aysymptomatic and normoglycaemic: Metformin +/- insulin if HBA1C > target

20
Q

Complications of DM

A

KNIVES

KIDNEY: nephropathy
NEUROMUSCULAR: peripheral neuropathy 
INFECTIVE: TB, UTIs
VASCULAR: CAD, CVD, PVD
EYES: Retinopathy + cataracts
SKIN: diabetic dermopathy
21
Q

Which severe and life threatening condition can diabetic patients present with asymptomatically?

A

‘Silent’ MI: due to autonomic neuropathy

22
Q

Consequences of diabetic neuropathy

A
Charcots foot
Claw toes
Pes Cavus
Loss of protective sensation
Ulcers
23
Q

Diagnosis and management of diabetic nephropathy

A

Microalbulinaemia where ACR >30
Start on ACEi
Refer if ACR>70

24
Q

Signs in background retinopathy

A

Dots, Blots and Exudates

25
Q

Signs in pre-proliferative retionopathy

A

Spots, beading and bleeds

26
Q

Signs in proliferative retinopothy

A

New vessel formation and bleeds

27
Q

Signs in maculopathy

A

Reduced visual acuity

28
Q

3 main diabetic emergencies

A

DKA
HONK: Hyperosmotic hyperglycaemic non ketotic coma
Lactic acidosis

29
Q

Which of type 1 or type 2 does DKA occur in?

A

Type 1 only due to the fact that DKA relates to an absolute deficiency of insulin

30
Q

Pathogenesis of DKA

A
  1. 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
  2. Dehydration - Decreased insulin = decreased utilisation of glucose = increased gluconeogensis = severe hyperglycaemia + osmotic diuresis = increase in ketone
31
Q

Causes of DKA

A

The 5 S’s

S - Sepsis
S - Surgery
S - Sugar High (Missed insulin)
S - Stress
S - Substances (Alcohol , Dope)
32
Q

Clinical presentation of DKA

A

Remember DKA

D - Diuresis, Delirium / Dizziness, Dehydration
K - Kussmaul Breathing, Ketotic Breath
A - Abd. Pain

33
Q

Investigations and results seen in DKA

A
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
34
Q

Management of DKA

A

IV FLUIDS
K THERAPY
INSULIN

35
Q

Hyperosmolar hyperglycaemic non ketotic coma happens to patients with which type of Diabetes?

A

T2DM because there is enough insulin to prevent ketosis but not enough to prevent hyperglycaemia

36
Q

Causes of HONK

A

Infection
T2DM uncontrolled
MI

37
Q

Presentation of HONK

A

Thirst
Polyuria
Impaired concentration

38
Q

Complications of HONK

A

Occlusion events i.e. DVT

39
Q

Management of HONK

A

Fluids w/ potassium
Insulin
Anticoagulation