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AMC MCQ > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Typ I Diabetes - Clinical Features

A

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

Secondary enuresis
Ketoazidosis

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2
Q

Typ I Diabetes - Investigation

A
  • Next step - urine dipstick
  • Best step - random glucose 11.1mmol/l, TPO a/b, Tissue tranglutaminase a/b
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3
Q

Typ I Diabetes - Management

A
  • admit for insulin therapy
  • follow up: HbA1c every 3 month 7% or less)
  • Vaccination: Pneumococcal, Influenza, dTpa
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4
Q

Typ II Diabetes - Clinical features

A
  • Asymptomatic
  • Metabolic Syndrome
  • Acanthosis nigrans (neck, axilla)
  • skin tags
  • hirsutism
  • recent skin/genital infection
  • chronic fatigue
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5
Q

Typ II Diabetes - Investigation

A
  • 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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6
Q

Typ II Diabetes - Screening

A
  • 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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7
Q

Typ II Diabetes -AUSDRISK score

A

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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8
Q

Typ II Diabetes - Managment

A
  • 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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9
Q

Typ II Diabetes- Riskfactors

A
  • 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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10
Q

Typ II Diabetes- Late complication

A
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11
Q

Autonomic neuropathy

A
  • 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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12
Q

More complications seen in Diabetes mellitus

A
  • 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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13
Q

Secondary Causes
of Hyperglycemia:

A
  • 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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14
Q

Diabetic foot ulcer- Presentation

A
  • 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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15
Q

Diabetic foot ulcer - Investigation

A

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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16
Q

Diabetic foot ulcer - Management

A
  • 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.
17
Q

Goals for Diabetes Therapy

A
  • 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

18
Q
A
19
Q

Diabetic Retinopathy

A

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

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

20
Q

Diabetic Retinopathy - Symptoms

A
  • 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
21
Q

Diabetes Ketoacidosis- Symptoms

A
  • Polydipsia,
  • polyuria,
  • polyphagia,
  • weight loss,
  • fatigue,
  • Dehydration,
  • Confusion,
  • Drowsiness,
  • Coma,
  • Abdominal pain,
  • nausea,
  • vomiting
  • Kussmaul breathing,
  • odor of acetone.
22
Q

Diabetes Ketoacidosis - Investigation

A
  • 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.
23
Q

Diabetic ketoacidosis - Management

A

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
24
Q

Hypoglycaemia - Cause

A

** 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)
25
Q

Hypoglycaemia - Mild

A

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

26
Q

Hypoglycaemia - Severe

A

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.

27
Q

Somogyi Effect

A
  • Episodic hypoglycaemia at night is followed by rebound hyperglycemia.
  • Insulin dosage should be slowly reduced
28
Q

Late Dumping

A
  • rebound hypoglycemia
  • Investigation: BG, OGTT, Gastric emptying Scinti
29
Q

Hyperglycaemia
hyperosmolar non-
ketonic coma

A
  • 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

30
Q

Hyperglycaemia
hyperosmolar non-
ketonic coma- Diagnostic

A
  • negative Ketones
  • high urine glucose
  • hyperglicaemia
  • BG more than 55 mmol/l
31
Q

Hyperglycaemia
hyperosmolar non-
ketonic coma- Therapy

A
  • 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%)
32
Q

Lactic Acidosis

A

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.

33
Q

Differitial Coma

A

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

34
Q

metabolic Syndrome

A
  • 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
35
Q

Hypoglycaemia

A

Classic:
-sweating, tremor, palpitation, hunger, perioral paraestesia

-Rapid loss of conciousness

Coma: stuperosem comatose or strange behaviour

36
Q

hypoglycaemia treatment

A
  • 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
37
Q

Hypoglycaemia

A

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

AMC MCQ (55 decks)

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