Postural hypotension (faints on standing, eating, or hot bath) Resting tachycardia Urine retention Erectile dysfunction Nocturnal diarrhoea Gastroparesis (impaired gastric emptying) Delayed or incomplete bladder emptying Loss of cardiac pain (silent ischaemia) Hypoglycemic unawareness

Diabetes Flashcards by Mo Bakhtyar

Typ I Diabetes - Clinical Features

acute onset of
* polydipsia
* polyuria
* polyphagia
* weight loss
* Fatigue

Secondary enuresis
Ketoazidosis

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Typ I Diabetes - Investigation

Next step - urine dipstick
Best step - random glucose 11.1mmol/l, TPO a/b, Tissue tranglutaminase a/b

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Typ I Diabetes - Management

admit for insulin therapy
follow up: HbA1c every 3 month 7% or less)
Vaccination: Pneumococcal, Influenza, dTpa

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Typ II Diabetes - Clinical features

Asymptomatic
Metabolic Syndrome
Acanthosis nigrans (neck, axilla)
skin tags
hirsutism
recent skin/genital infection
chronic fatigue

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Typ II Diabetes - Investigation

next step: random blood glucose equal or >11.1mmol/L
best step – fasting blood glucose – equal or > 7.0 mmo/L. HbA1c equal or more than 6.5% (on two occasions).
OGTT if uncertain level of blood glucose

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Typ II Diabetes - Screening

No Risk Factors every 3 from 40 years using AUSDRISK
Aboriginal and Torres Strait Islander people should be screened annually with blood testing (FBG, RBG or HbA1c) from18 years
With Risk Factors from 30 years every 3 years ( FBG or HbA1c)
Impaired FG every 12 month ( FBG, HbA1c)

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Typ II Diabetes -AUSDRISK score

AUSDRISK score Risk of developing type 2 diabetes within five years:
** ≤5 ** 1 in 100
** 6–8 ** 1 in 50
** 9–11 ** 1 in 30
** 12–15 ** 1 in 14
** 16–19 ** 1 in 7
** ≥20 ** 1 in 3

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Typ II Diabetes - Managment

Life-style modification. Consider hypoglycemic drugs
follow up: HbA1c every 3 months (target equal or less than 7 %). Monitor late complications.
Vaccination: Pneumococcal, Influenza, dTPA.

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Typ II Diabetes- Riskfactors

AUSDRISK score of ≥12
all people with a history of a previous cardiovascular event (acute myocardial infarction
or stroke)
women with a history of gestational diabetes mellitus
women with polycystic ovary syndrome
patients on antipsychotic drugs

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Typ II Diabetes- Late complication

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Autonomic neuropathy

Postural hypotension (faints on standing, eating, or hot bath)
Resting tachycardia
Urine retention
Erectile dysfunction
Nocturnal diarrhoea
Gastroparesis (impaired gastric emptying)
Delayed or incomplete bladder emptying
Loss of cardiac pain (silent ischaemia)
Hypoglycemic unawareness

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More complications seen in Diabetes mellitus

Acute painful neuropathy: Burning pain in feet, shins, thigh.
Mononeuritis multiplex:
✓ Cranial nerves (III, IV, VI, VII).
✓ Foot drop.
✓ Meralgia paresthetica.
✓ Tarsal tunnel syndrome.
Proximal motor neuropathy (Diabetic amyotrophy) -painful, asymmetrical muscle wasting of quadriceps andpelvic girdle. Pain typically worse at night.
Diabetic cheiropathy (Prayer Sign)
Dupuytren’s contracture
Carpal tunnel syndrome
Charcot joint

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Secondary Causes
of Hyperglycemia:

Diseases of Pancreas
(Pancreatitis,Neoplasia,Cystic fibrosis,Haemochromatosis)
Endocrinopathies
(Cushing, Acromegaly, Pheocromocytoma, Hyperthyroidism)
Drug induced
(antipsychotic, thiazid diuretics, oestrogen, GCS)
Genetic syndromes
(Turner, Down, Klinefelter)

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Diabetic foot ulcer- Presentation

Caused by peripheral neuropathy (80%), peripheral
arterial disease (10%), deformity (Charcot foot).
Painless, punched – out.
Most common localisation - first metatarsal area, heel.

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Diabetic foot ulcer - Investigation

Investigations:
* Blood glucose levels
* ABPI, +/- Duplex US (to rule out arterial disease).
* Microbiology swab (if signs of infection).
* X – ray of bone (if deep ulcer based on probe to bone)

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Diabetic foot ulcer - Management

Good foot hygiene and appropriate footwear.
Glycaemic control (HbA1c < 7%).
If not infected - Surgical debridement.
If infected but no signs of cellulitis -
Amoxycillin/Clavulanate
If signs of cellulitis - Admit, Ticarcillin/Clavulanate I/V
If no improvement - consider osteomyelitis: - Next step X-ray; Best step MRI.

Goals for Diabetes Therapy

Blood pressure (no albuminuria) <140/90
Blood pressure (plus albuminuria) <125/80

Lipids
* Total Cholesterol <4mmol/l
* Triglycerid <2.0mmol/l
* HDL >1mmol/l
* LDL < 2.0mmol/l

Albumin/creatinine ratio
* < 2.5 mg/mmol– men
* < 3.5 mg/mmol - women

Diabetic Retinopathy

NON Proliferative
* Microaneurysm
* Dots & blots
* Hard and soft exudsates
* Cotton wool - infarcts
* Macular oedema

Proliferative
* Neurovascularisation (Hallmark)
* large haemorrhaeges
* retinal detatchment

Diabetic Retinopathy - Symptoms

Increasing number of floaters
Blurry vision
Noticing colours appear faded or washed out
Vision changes from blurry to clear
Seeing blank or dark areas in field of vision
Poor night vision
Losing vision

Diabetes Ketoacidosis- Symptoms

Polydipsia,
polyuria,
polyphagia,
weight loss,
fatigue,
Dehydration,
Confusion,
Drowsiness,
Coma,
Abdominal pain,
nausea,
vomiting
Kussmaul breathing,
odor of acetone.

Diabetes Ketoacidosis - Investigation

Next step – ketones in serum or urine, if glucose > 15 mmol/L
Best step – ABG: metabolic acidosis with respiratory compensation. High AG. (Na + K) – (Cl + HCO3) = 8 – 16 mEq/L Na – (Cl + HCO3) = 10 – 14 mEq/L
Other: Electrolytes (Na, K, PO4); PO; amylase/lipase, septic screen (Chest X-ray,blood culture, urine culture), ECG.

Diabetic ketoacidosis - Management

10 unit rapid acting Insulin im

Hospital admission

Rehydration (normal saline IV – 20 ml/kg/hour);
If Na corrected > 145 mmol/L – give half saline IV (look for symptoms of cerebral oedema)
Insulin short acting IV:
Monitor glucose every hour: when <15 mmol/L, start
glucose 5% IV Monitor K every 2 hours: when < 5.5. mmol/L, start KCl IV
Sodium bicarbonate if pH < 7.0
Broad spectrum a/b if evidence of infection

Hypoglycaemia - Cause

** blood glucose <3.0mmol/l*

Drugs: salicylates, nonselective B-blockers,
TCA, MAOI, ACE inhibitors.
Endocrine: Addison disease, GHdeficiency, Hypopituitarism, Insulinoma,
Septicaemia,Starvation, Reactive hypoglycaemia, Hypoglycaemia of infancy and childhood, Renal failure, (Somogyi effect)

Hypoglycaemia - Mild

**Classic warning symptoms:** * Adrenergic symptoms: sweating, tremor, palpitations, hunger, peri-oral paraesthesia. **Management:** * give something sweet by mouth (2 barley sugars, or 6 jellybeans, glass of lemonade, teaspoon of honey), followed by a snack

Hypoglycaemia - Severe

**Neuroglycopenic symptoms:** * Poor concentration, drowsiness, double vision, violent behaviour, focal neurological signs, LOC, seizure, coma. **Management:** * glucagon 1 mg im or sc * If iv line glucose 50% – 20 mL IV. * children : 10% glucose 20 – 30 ml in children (50% glucose can cause hyperosmolality and death). * Admittion * if consciousness and can swallow: orally source of carbohydrate. * Review of medications, dietary intake, driving or licensing requirements and hypoglycaemia management is mandatory.

Somogyi Effect

* Episodic hypoglycaemia at night is followed by rebound hyperglycemia. * Insulin dosage should be slowly reduced

Late Dumping

* rebound hypoglycemia * Investigation: BG, OGTT, Gastric emptying Scinti

Hyperglycaemia hyperosmolar non- ketonic coma

* Only TypII DM, especially elderly Clinic * The trigger usually is the concurrent condition causing decompensation of diabetes (infection). * insidious onset * Fatigue, polyuria, polydipsia. * Marked dehydration(hyperosmolarity, marked hyperglycaemia and hypernatremia) * Stupor coma

Hyperglycaemia hyperosmolar non- ketonic coma- Diagnostic

- negative Ketones - high urine glucose - hyperglicaemia - BG more than 55 mmol/l

Hyperglycaemia hyperosmolar non- ketonic coma- Therapy

* Rehydration with 0.45% saline. * Insulin with cautions to avoid rapid changes. * Heparin to reduce the risk of DVT. * Treat any concurrent condition. * Prognosis: mortality is higher than in DKA (50%)

Lactic Acidosis

Presentation: * marked hyperventilation ‘air hunger’ * confusion Trigger * metformin, especially if kidney function is impaired. Investigations * reveal blood acidosis with low pH, low bicarbonate, high serum lactate, absent serum ketones and a large anion gap. Management * Remove the cause. Bicarbonate therapy.

Differitial Coma

DKA * Ketones +, Glycaemia increased, Mx IV saline, Inslin-K Nonketotic hyperosmolar syndrome * Ketones -, Glycaemia increased, Mx IV saline, Inslin-K Hypoglycaemia coma * Ketones-, Glycaemia decreased,Mx IV saline, glucagon Alcoholic ketoacidosis * Ketones +, Glycaemia decreased, Mx IV saline, dextrose

metabolic Syndrome

- upper truncal obisity (102cm) or 88cm with two of the following: -triglyceride over 1.7 -low HDL under 1(m) under 1.3(f) -BP over 130/85 -high risk of developing typ2 DM

Hypoglycaemia

Classic: -sweating, tremor, palpitation, hunger, perioral paraestesia -Rapid loss of conciousness Coma: stuperosem comatose or strange behaviour

hypoglycaemia treatment

- 20-30 mL 50% glucose IV until fully conscious or 1 mL glucagon IM or SC - Admit to hospital if concerned (rarely necessary) -instruct the patient how to avoid a similar situation in the

Hypoglycaemia

assumed to be. the cause for any coma until proven otherwise