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Endocrine > Diabetes I and II > Flashcards

Diabetes I and II Flashcards

1
Q

What is type I diabetes?

A

AI, idiopathic absolute insulin deficiency secondary to beta cell destruction.

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2
Q

How may DM be diagnosed?

A
  • Symptoms + RBG >11.1mmol/L
  • FPG > 7.0 mmol/L
  • HbA1C >48 mmol/mol (6.5%)
  • OGTT @2h >11.1 mmol/L
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3
Q

Range of impaired fasting glucose?

A

FPG 6.1 - 6.9 mmol/L

(Normal =

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4
Q

Does TIIDM have a genetic component?

A

Yes:

  • MZ twin concordance up to 80%
  • 4/10 offspring and 1/3 siblings develop IGT or DM
  • Polygenic; >250 genes
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5
Q

How to distinuighs between TIDM and TIIDM?

A
  • C-peptide (endogenous insulin production)

- Anti-GAD and anti-islet cell Abs (TIDM)

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6
Q

What are the principles of TIIDM Mx?

A
  • LoW / diet & exercise
  • Oral hypoglycaemics
  • Self BSL monitoring
  • Regular surveillance microvascular complications
  • Risk reduction macrovascular complications (BP, lipids, smoking)
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7
Q

Principles of dietary management in DM?

A
  • Refer dietician
  • Weight loss (most cases)
  • Low GI carbs
  • Reduce sat fats
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8
Q

Role of exercise in Mx DM?

A
  • Increases glucose uptake into muscle
  • Improved sensitisation can last 2-3/7
  • May transiently increase (stress hormone); usually overall decrease in BSL
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9
Q

Self BSL targets in DM monitoring?

A

Fasting: 6-8mmol/L

2h post prandial: 6-10mmol/L

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10
Q

What determines HbA1C levels?

A

HbA1C is proportional to average BSL over previous 1-3 months.

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11
Q

Prognosis pre-diabetes (impaired glucose tolerance)?

A
  • 1-5% / year develop diabetes

- 50-80% revert to normal

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12
Q

Diagnostic criteria impaired glucose tolerance?

A

-FBG 6.1-6.9mmol/L

OGTT 2h: 7.8 - 11.0 mmol/L

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13
Q

What is TIIDM?

A

Syndrome of disordered metabolism and inappropriate hyperglycaemia secondary to absolute / relative deficiency of insulin, or a reduction in biological effectiveness of insulin or both.

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14
Q

What are the macrovascular complications of diabetes?

A
  • Ischeamic Heart Disease
  • Peripheral Vascular Disease
  • Cerebrovascular Disease
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15
Q

What are the microvascular complications of diabetes?

A
  • Retinopathy
  • Neuropathy
  • Nephropathy
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16
Q

What is the risk of developing diabetic complications related to?

A
  • Duration of diabetes
  • DM Control (e.g. HbA1C)
  • BP control
  • Control of CV RFx (lipids, smoking)
  • Genetic susceptibility
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17
Q

How is diabetic eye disease classified?

A
  • Non proliferative
  • Pre-proliferative
  • Proliferative
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18
Q

What other eye conditions are more common in diabetics?

A
  • Cataracts

- Glaucoma

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19
Q

What is microalbuminura?

A

Albumin excretion rate 30-300mg / 24h.

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20
Q

Screening test for diabetic neuropathy?

A

Albumin creatinine ratio:

N =

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21
Q

Progression of untreated microalbuminura (type I and II)?

A

TIDM: albuminuria increases at 10-20% / year to over neprophathy in 10-15y.
TIIDM: 20-40% progress to overt nephropathy

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22
Q

What is macroproteinuria?

A

Albumin excretion rate >300mg / 24h

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23
Q

Natural history untreated macroproteinuria? (TI and TII)

A
  • TI: ESRF 50% at 10y, 75% at 20y

- TII: 20% ESRF at 20y

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24
Q

What are the most common types of neuropathy in diabetes?

A
  • Distal symmetric polyneuropathy (glove and stocking)

- Autonomic

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25
Q

How does diabetes relate to other macrovascular risk factors?

A

Diabetes is a macrovascular RFx in itself BUT other macro RFx also more likely in diabetics (i.e. increased HTN, dyslipidemia etc)

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26
Q

Which areas are prone to ischaemia in DM patients with PVD?

A

-Great toe
-Medial surface 1st metatarsal head
-Lateral surface 5th metatarsal head
Secondary infection common

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27
Q

Why is exertion dsypnoea important to investigate in DM patients?

A

Myocardial ischaemia often silent; need high degree of clinical suspicion.

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28
Q

Prevention and treatment of diabetic retinopathy?

A
  • Regular examination (asymptomatic until visual loss occurs)
  • Laser treatment
  • Meticulous BSL control
  • Smoking cessation
  • ?RAAS blockade
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29
Q

Treatment of diabetic nephropathy?

A
  • Strict BP control (ACE, ARB)

- Strict BSL control (HbA1C

30
Q

Treatment of diabetic neuropathy?

A
  • Control BSLs
  • TCAs
  • SNRI antidepressants
  • Anti epileptics
  • Opioid analgesics (e.g. tramadol)
  • Capsaicin cream
31
Q

How should foot ulcers be prevented in high risk feet?

A
  • Foot care education
  • Daily inspection
  • Podiatry r/vs
  • Early treatment skin injury
  • Good footwear
  • Callus detection and treatment
  • Urea cream for dry feet
  • Early referral for ulcers
32
Q

What are the lipid targets for high risk patients?

A
  • LDL: 1.0 mmol/L

- TGs:

33
Q

Features suggestive of LADA cf TIIDM?

A
  • Lean build
  • Anti islet Abs
  • Rapid progression to insulin
34
Q

Where are the highest rates of TIDM?

A

Finland and other Northern European countries

35
Q

Which genes predispose to most genetic risk of TIDM?

A

HLA genes on Chr 6: highly polymorphic and modulate immune defence of body.
HIGH RISK = HLA:
-DR3 -DQ2
-DR4 -DQ8

36
Q

Distinction between TIDM and TIIDM?

A

Key distinguishing feature (T1 v TII) is presence of auto-Abs against B-cell auto-ags:

  • IAA: insulin reaction
  • GADA: glutamic acid decarboxylase —> catalyses formation of gaba-aminobutyrate; located in B cells
  • IA2A: insulinoma associated auto antigen 2 —> islet antigen 2, membrane bound in B cells
  • ZnT8A: zinc transporters.
  • C peptide
37
Q

What are the four major determinants of TIIDM?

A
  • Age
  • Obesity
  • Ethnicity
  • FHx
38
Q

Outline the inheritance component of TIIDM?

A

identical twins of DMII patients >50% chance of developing diabetes; siblings = 25%.Polygenic disorder: many susceptibilities e.g. TCF7-L2, KCNQ1.

39
Q

Environmental factors predisposing to TIIDM development?

A

Low weight at birth and 12 months associated with glucose intolerance later in life. Poor early nutrition thought to impair B-cell development.

40
Q

What is insulin resistance?

A

Failure of target tissue to respond normally to insulin (liver, muscle, adipose tissue major tissues in glucose regulation).

41
Q

What does insulin resistance lead to?

A
  • Failure to inhibit endogenous glucose production (gluconeogenesis) in liver.
  • Failure of glucose uptake and glycogen synthesis in skeletal muscle following a meal.
  • Failure to inhibit lipoprotein lipase in adipose tissue, leading to excess circulating FFAs.
42
Q

Subacute presentation of DM?

A

SUBACUTE: clinical onset several months or years, esp older patients.
-Polydipsia
-Polyuria
-LoW
PLUS
-lack of energy
-visual blurring (owing to glucose induced changes in refraction)
-pruritus vulvae or balanaitis due to Candida infection

43
Q

What is acanthosis ingrains?

A

Indicative of severe insulin resistance: blackish pigmentation of back of neck and axillae.

44
Q

Outline pathophysiology of DKA.

A
  • Occurs due to lack of insulin (first presentation, lack of compliance to insulin medication).
  • Unrestricted hepatic glucose production —> hyperglycaemia —> osmotic diuresis —> dehydration and electrolyte disruption —> decreased Na+ (water shift to ECF).
  • Fat mobilisation —> increased FFA —> ketoacids —> metabolic acidosis
  • Severe hyperglycemia exceeds renal threshold for glucose and ketone resorption —> glucosuria and ketonuria.
  • Total body depletion of K+, but serum K+ may be normal or elevated following a secondary shift from ICF to ECF due to lack of insulin —> increased plasma osmolality.
  • Total body PO34- depletion
45
Q

Ketoacidosis precipitating factors?

A
  • New onset TIDM
  • Inadequate / inappropriate insulin therapy
  • EtOH abuse
  • Infection
  • Pancreatitis
  • Drugs: corticosteroids and thiazides
46
Q

Principles of ketoacidosis management?

A

1) Rehydration
2) Identify K+ level; correct imbalance (potassium)
3) Correct hyperglycemia: Insulin therapy
4) Identify precipitant

47
Q

Fluids to be used in mx DKA?

A

-1L N saline over 30min - 2h

Change to 5% dextrose when glucose

48
Q

Principles of potassium treatment in Mx DKA?

A

Aim K+ 3.5 - 5mM:

1) K+ 5mM: withhold K+ but monitor levels

49
Q

Insulin in Mx DKA?

A

-IM: 0.1 IU/kg/h
-IV infusion: 6-8 units hourly via pump THEN ADJUST to BSLs
Continue infusion until acidosis resolved then switch to s/c insulin (basal bolus).

50
Q

How is effective osmolality determined?

A

2 (Na+) + glucose

51
Q

What is hyperglycaemia hyperosmolar state?

A

AKA hyperosmolar nonketotic coma:

  • severe hyperglycemia
  • minimal ketosis
  • profound dehydration
  • depressed sensorium / coma
  • efective osmolality >330 Osm/kg
52
Q

Mx hyperglycemia hyperosmolar state?

A
  • Fluids: 2L hypotonic saline (0.45%) over 1-2h
  • Monitor urine output and CVP if indicated
  • Insulin
  • Potassium
  • Prophylactic heparin
  • identify cause
53
Q

Broad pathogenesis of hyperosmolar state?

A

Relative lack of insulin –> hyperglycaemia –> glycosuria –> polyuria –> volume depletion –> renal insufficiency –> hyperosmolarity –> fluid shift from neutrons to ECF –> mental obtundation and coma.

54
Q

Mx of hypoglycaemia?

A
  • If possible: sugary fluids
  • Unconscious / risk of aspiration:
  • -> IV dextrose 50% (25-50mL)
  • -> IM/SC glucagon 1mg
  • Administer long acting carb
  • Recheck glucose 20-30 min later
55
Q

What may precipitate HHS?

A

-Sepsis / stroke / MI / CHF / renal failure / dialysis / recent surgery / burns

56
Q

Why is dehydration more severe in HHS than DKA?

A
  • More gradual onset =Increased duration of metabolic decompensation
  • impaired fluid intake
57
Q

What are the precipitants of DKA/

A

8Is precipitating DKA:

i) Infection
ii) Ischaemia / infarction
iii) Iatrogenic (glucocorticoids)
iv) Intoxication
v) Insulin missed
vi) Initial presentation
vii) Intra abdominal process
viii) Intra op / peri op stress

58
Q

Pathophysiology of diabetic nephropathy?

A
  • thickening of capillary BM and glomerular mesangium resulting in glomerulosclerosis and renal insufficiency
  • diffuse glomerulosclerosis more common than nodular inter capillary glomerulosclerosis (Kimmelsteil- Wilson lesions)
59
Q

Clinical features of peripheral neuropathy?

A
  • Paresthesias (tingling, burning)
  • Bilateral, symmetric
  • Decreased perception of vibration / pain / temp
  • Decreased ankle reflex
60
Q

Clinical features in motor neuropathy of DM?

A
  • Less common than sensory neuropathy
  • Delayed motor nerve conduction w/ muscle weakness/ atrophy
  • May involve one nerve trunk or more (mono neuritis complex)
  • Diabetic amyotrophy
61
Q

what is diabetic amyotrophy?

A

Pain, weakness, wasting of hip flexors or extensors

62
Q

Clinical features of diabetic autonomic neuropathy?

A
  • Postural hTN
  • Tachycardia
  • Decreased CV response to valsalva
  • Gastroparesis / alternating diarrhoea constipation
  • Urinary retention
  • Erectile dysfunction
63
Q

What is diabetic dermopathy?

A

Atrophic brown spots commonly in pretitibial region known as “shin spots”.
Secondary to increased glycosylation of tissue proteins or vasculopathy.

64
Q

Dermatologic manifestations of DM?

A
  • Diabetic dermopathy
  • Eruptive xanthomas
  • Necrobiosis lipidoica diabeticorum
65
Q

What is necrobiosis lipidoica diabeticorum?

A

Rare complication characterised by thinning skin over the shins allowing visualisation of subcutaneous vessels.

66
Q

Bone and joint manifestations of DM complication?

A
  • Juvenile cheiroarthropathy
  • Dupuytyren’s contracture
  • Bone demineralisation
  • Frozen shoulder
67
Q

Clinical features of hypoglycemia?

A
  1. Whipple’s Triad:

i) Serum glucose

68
Q

What are symptoms of neuroglycopenia?

A
  • Dizziness
  • Headache
  • Clouding of vision
  • Mental dullness
  • Fatigue
  • Confusion
  • Seizures / Coma
69
Q

What are the common causes of hypoglycaemia due to hyperinsulinism?

A
  • Exogenous insulin
  • Sulphonylurea reaction
  • AI hypoglycemia
  • Pentamidine
  • Insulinoma
70
Q

What are the common causes of hypoglycaemia without hyperinsulinism?

A
  • Severe hepatic dysfunction
  • Chronic renal insufficiency
  • Hypocortisolism
  • EtOH
  • non-pancreatic tumours
  • inborn error of carb metabolism, glycogen storage deficiency
71
Q

How is insulin infusion made up in DKA and Mx (i.e. rate and ongoing Mx)?

A
  • 50units of insulin made up to 50mLs with 0.9%NSal ==> 1UN/mL.
  • Rate of 0.1unit/kg/h up to 6 units / h.
  • When glucose
72
Q

Insulin in HHS?

A

-Initial dose insulin 0.05UN/kg (max 3 Units)
-Reduce insulin infusion when glucose 18mmol/L
Infuse 0.45% (half NS) at 250mL/h

Endocrine (21 decks)

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