Diabetes 2 Flashcards

1
Q

What are the diabetic neuropathies?

A
Progressive:
Symmetrical sensory polyneuropathy
Autonomic neuropathy
Reversible:
Acute painful neuropathy
Mononeuropathy and mononeuritis complex
Diabetic amyotrophy
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2
Q

What is symmetrical sensory polyneuropathy?

A

Most common form affects feet first (loss of vibration, pain and temperature)
Imapired proprioception
Ulceration
Neuropathic arthropathy (Charcot’s joints) in the ankle and knee (grossly deformed and swollen)
Wasting of the small muscles of the hand and distorted foot with a high arch and clawing of the toes

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3
Q

What is acute painful neuropathy?

A

Burning or crawling pain in the lower limbs

Symptoms are worse at night

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4
Q

What is mono neuritis and mononeuritis multiplex?

A
One or more individual nerves may be affected 
Onset may be abrupt and painful 
Carpal tunnel syndrome 
III and VI extrocular muscles
Unilateral pain, ptosis, dipoplia
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5
Q

What is diabetic amyotrophy?

A

Presents with painful wasting, usually asymmetrical of the quadriceps muscles
Knee reflexes are diminished or absent

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6
Q

What is autonomic neuropathy?

A

Affects the cardiovascular system- resting tachycardia, loss of sinus arrhythmia, postural hypotension , peripheral vasodilation
GI- diarrhoea, gastroparesis
Bladder- incomplete emptying followed by painless distended blader
Ereticle dysfunction

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7
Q

What is the management for foot lesions?

A

Swabbing of ulcers for bacterial culture and early antibiotic treatment
Good local wound care and, if necessary, surgical debridement of
ulcers
Evaluation for peripheral vascular disease by clinical examination, measurement of blood flow (by Doppler probe) and femoral angiography if clinically indicated
Reconstructive vascular surgery for localized areas of arterial occlusion.

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8
Q

What infections are diabetics prone to?

A

UTI
Cellulitis, boils and abscesses
TB
Mucocutaneous candidiasis

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9
Q

What are the skin complications that occur in diabetes?

A

Liperhypertrophy
Necrobiosis lipoidica diabeticorum (erythematous plaques, often over the shins, which gradually develop a brown waxy discoloration)
Vitiligo
Granuloma annulare–flesh-coloured rings and nodules, principally over the extensor surfaces of the fingers.

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10
Q

What is the presentation of type 2 diabetes?

A

Onset over months/years, classic triad (may be less obvious than T1DM)
Lack of energy
Visual blurring: glucose-induced refractive changes
Pruritis vulvae/balatitis: candida infection
Older patients: retinopathy, polyneuropathy, erectile dysfunction, arterial disease

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11
Q

What are causes of secondary diabetes?

A

Pancreatic disease: CF, chronic pancreatitis, pancreatic carcinoma
Endocrine: Cushing’s, acromegaly, thyroroxicosis, pheochromocytoma, glucagonoma
Drug induced: thiazide diuretics, corticosteroids, antipsychotics, antiretrovirals
Congenital disease: insulin receptor abnormalities, myotonic dystrophy, Friedreich’s ataxia

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12
Q

In which populations is the use of HbA1c inappropriate to diagnose diabetes?

A
<18yo
Acutely unwell 
Those taking medication that could raise blood sugars
Those with end-stage CKD 
Those with HIV
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13
Q

What is the pathogenesis of diabetic ketoacidosis?

A

Insulin absense –> increased hepatic glucose production (gluconeogenesis) & reduced uptake of glucose peripherally
Rising plasma glucose –> osmotic diuresis + dehydration
Lipolysis occurs in glucose-starved tissues –> elevated free fatty acids
In liver: free fatty acids –> fatty acetyl-CoA
In mitochondria to generate energy: fatty acetyl CoA –> ketone bodies
Accumulation of ketone bodies = metabolic acidosis
Respiratory compensation = hyperventilation
Acidosis: vomiting (fluid/electrolyte loss)
Renal perfusion falls: impaired excretion of raised H+ and ketones
Increased secretion of Na+ & K+

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14
Q

What is diabetes insidious characterised by?

A

High plasma osmolality
Low urine osmolality
Hypernatraemia

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15
Q

What criteria is used to diagnose HHS?

A

Hypovolaemia (due to osmotic diuresis)
Marked Hyperglycaemia (serum glucose>30mmol/L)
No significant ketonaemia/ketonuria (serum ketone <3mmol/L)
No significant acidosis (pH>7.3, bicarb >15mmol/L)
Osmolality >320mmol/kg

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16
Q

What are the 3 criteria to confirm DKA?

A

Capillary blood
glucose >11 or know diabetes
Capillary blood ketones >3 or 2+ ketonuria
Venous pH <7.3 and/or venous bicarb <15

17
Q

When do the the ITU need to be contacted with a DKA?

A
Ketone >6 
 pH < 7.1 
HCO3 <5 / anion gap > 16 
 K+ < 3.5 
 GCS < 12 
 SpO2 < 92% 
 SBP < 90, Pulse >100 / < 60
18
Q

When should potassium chloride be replaced in patients with a DKA?

A

> 5.5 NONE
3.5 – 5.5 40mmol/L
< 3.5 Senior advice

19
Q

What are the causes of hypoglycaemia (EXPLAIN)?

A
Exogenous drugs (typically sulfonylureas or insulin)
Pituitary insufficiency 
Liver failure 
Addison's disease 
Islet cell tumours (insulinomas) 
Non-pancreatic neoplasms
20
Q

What are the complications of DKA and its treatment?

A

gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury

21
Q

What causes lower than expected levels of HbA1c?

A

Sickle-cell anaemia
GP6D deficiency
Hereditary spherocytosis

22
Q

What causes higher than expected levels of HbA1c?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

23
Q

What are the features of an insulinoma?

A

Whipple’s triad of symptoms of 1) hypoglycaemia with fasting or exercise, 2) reversal of symptoms with glucose, and 3) recorded low BMs at the time of symptoms is hallmark for an insulinoma

24
Q

What are the features of gastroparesis in diabetics?

A

Bloating and vomiting after eating
Erratic blood glucose readings
Treat with metoclopramide