Diabetes Flashcards

(39 cards)

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
Signs in pre-proliferative retionopathy
Spots, beading and bleeds
26
Signs in proliferative retinopothy
New vessel formation and bleeds
27
Signs in maculopathy
Reduced visual acuity
28
3 main diabetic emergencies
DKA HONK: Hyperosmotic hyperglycaemic non ketotic coma Lactic acidosis
29
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
30
Pathogenesis of DKA
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
Causes of DKA
The 5 S's ``` S - Sepsis S - Surgery S - Sugar High (Missed insulin) S - Stress S - Substances (Alcohol , Dope) ```
32
Clinical presentation of DKA
Remember DKA D - Diuresis, Delirium / Dizziness, Dehydration K - Kussmaul Breathing, Ketotic Breath A - Abd. Pain
33
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 ```
34
Management of DKA
IV FLUIDS K THERAPY INSULIN
35
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
36
Causes of HONK
Infection T2DM uncontrolled MI
37
Presentation of HONK
Thirst Polyuria Impaired concentration
38
Complications of HONK
Occlusion events i.e. DVT
39
Management of HONK
Fluids w/ potassium Insulin Anticoagulation