Diabetes

Question 1

Typ I Diabetes - Clinical Features

Answer 1

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

Secondary enuresis
Ketoazidosis

Question 2

Typ I Diabetes - Investigation

Answer 2

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

Question 3

Typ I Diabetes - Management

Answer 3

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

Question 4

Typ II Diabetes - Clinical features

Answer 4

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

Question 5

Typ II Diabetes - Investigation

Answer 5

• 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

Question 6

Typ II Diabetes - Screening

Answer 6

• 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)

Question 7

Typ II Diabetes -AUSDRISK score

Answer 7

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

Question 8

Typ II Diabetes - Managment

Answer 8

• 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.

Question 9

Typ II Diabetes- Riskfactors

Answer 9

• 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

Question 10

Typ II Diabetes- Late complication

Question 11

Autonomic neuropathy

Answer 11

• 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

Autonomic neuropathy is a type of nerve damage that affects the autonomic nervous system (ANS), which controls involuntary body functions such as heart rate, blood pressure, digestion, and bladder function.

1. Causes:
   
   • Diabetes: The most common cause of autonomic neuropathy, particularly in long-term, poorly controlled diabetes.
   • Other Conditions: Can also be caused by autoimmune diseases, infections, certain medications, and inherited disorders.
2. Symptoms:
   
   • Cardiovascular:
     
     • Orthostatic Hypotension: Dizziness or fainting when standing up due to a sudden drop in blood pressure.
     • Resting Tachycardia: Abnormally high heart rate at rest.
   • Gastrointestinal:
     
     • Gastroparesis: Slowed movement of food through the stomach, causing nausea, vomiting, bloating, and unpredictable blood sugar levels.
     • Constipation or Diarrhea: Alternating or persistent issues with bowel movements.
   • Genitourinary:
     
     • Bladder Dysfunction: Difficulty starting urination, incontinence, or incomplete emptying of the bladder.
     • Sexual Dysfunction: Erectile dysfunction in men and vaginal dryness in women.
   • Sweating Abnormalities:
     
     • Excessive sweating (hyperhidrosis) or lack of sweating (anhidrosis), affecting temperature regulation.
   • Pupillary Response:
     
     • Issues with the pupils adjusting to light changes, leading to problems with vision in low light.
3. Diagnosis:
   
   • Clinical Evaluation: Based on symptoms and medical history, particularly in people with conditions like diabetes.
   • Tests:
     
     • Heart Rate Variability Tests: To check how the heart responds to deep breathing or other changes.
     • Tilt Table Test: To evaluate blood pressure and heart rate response when moving from lying down to standing.
     • Gastric Emptying Study: To assess for gastroparesis.
     • Urine Tests: To evaluate bladder function.
4. Treatment:
   
   • Managing Underlying Conditions: The best way to treat autonomic neuropathy is to control the underlying condition, such as managing blood sugar levels in diabetes.
   • Medications:
     
     • Blood Pressure Medications: To manage symptoms like orthostatic hypotension.
     • Digestive Aids: Such as prokinetic agents for gastroparesis.
     • Medications for Bladder Control: Including anticholinergics for overactive bladder or catheters for severe cases.
     • Erectile Dysfunction Medications: Like phosphodiesterase inhibitors (e.g., sildenafil).
   • Lifestyle Changes:
     
     • Dietary Adjustments: Eating smaller, more frequent meals and avoiding large amounts of fat for gastroparesis.
     • Physical Therapy: To help manage symptoms and improve quality of life.
   • Symptomatic Treatment: Addressing specific symptoms like sweating abnormalities or visual disturbances.
5. Prognosis:
   
   • Autonomic neuropathy can significantly impact quality of life and may lead to serious complications if not managed effectively. However, early diagnosis and treatment of the underlying cause can help manage symptoms and slow progression.

Autonomic neuropathy is nerve damage that affects the involuntary functions of the body, such as heart rate, digestion, and bladder control. It is commonly caused by diabetes but can result from other conditions as well. Symptoms vary depending on the affected organs but can include dizziness, digestive problems, bladder issues, and sexual dysfunction. Treatment focuses on managing the underlying condition and relieving symptoms to improve quality of life.

Question 12

More complications seen in Diabetes mellitus

Answer 12

• 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

Question 13

Secondary Causes
of Hyperglycemia:

Answer 13

• 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)

Question 14

Diabetic foot ulcer- Presentation

Answer 14

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

Question 15

Diabetic foot ulcer - Investigation

Answer 15

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)

Question 16

Diabetic foot ulcer - Management

Answer 16

• 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.

Question 17

Goals for Diabetes Therapy

Answer 17

• 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

Question 19

Diabetic Retinopathy

Answer 19

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

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

Question 20

Diabetic Retinopathy - Symptoms

Answer 20

• 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

Question 21

Diabetes Ketoacidosis- Symptoms

Answer 21

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

Question 22

Diabetes Ketoacidosis - Investigation

Answer 22

• 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.

Question 23

Diabetic ketoacidosis - Management

Answer 23

• Rehydration (normal saline IV – 20 ml/kg/hour);
  If Na corrected > 145 mmol/L – give half saline IV (look forsymptoms 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

Question 24

Hypoglycaemia - Cause

Answer 24

** 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)

Question 25

Hypoglycaemia - Mild

Answer 25

**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

Question 26

Hypoglycaemia - Severe

Answer 26

**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.

Question 27

Somogyi Effect

Answer 27

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

Question 28

Late Dumping

Answer 28

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

Question 29

Hyperglycaemia hyperosmolar non- ketonic coma

Answer 29

* Only TypII DM, espesialy 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).

Question 30

Hyperglycaemia hyperosmolar non- ketonic coma

Answer 30

* 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.

Question 31

Lactic Acidosis

Answer 31

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.

Question 32

Differitial Coma

Answer 32

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