Diabetes Flashcards Preview

Phase 2a > Diabetes > Flashcards

Flashcards in Diabetes Deck (130)
Loading flashcards...

What causes diffuse neuropathies?

accumulation of fructose and sorbitol which disrupts the structure and function of the nerve


What are the different types of progressive neuropathy?

symmetrical sensory polyneuropathy (the most common form) and autonomic neuropathy


Symptoms of symmetrical sensory polyneuropathy?

affects the feet first, with loss of vibration, pain and temperature sensation and impaired proprioception

can lead to unrecognised trauma with vlistering leading to ulceration, neuropathic arthropathy in the ankle and knee causing a deforms and swollen joint

involvement of motor nerves can cause muscle wasting in the hand and a distorted foot with a hgih arch and clawing of the toes


Symptoms of autonomic neuropathy?

affects the CV (resting tachycardia, loss of sinus arrhythmia, postural hypotension), GI (diarrhea, gastroparesis), bladder (incomplete emptying) and erectile dysfunction


What are the different types of reversible neuropathy?

acute painful, mononeuropathy, mononeuritis multiplex, cranial nerve lesions, isolated peripheral nerve lesions, diabetic amyotrophy


Symptoms of acute painful neuropathy?

burning/ crawling pains in lower limbs, worse at night and pressure from bed clothes can be intolerable


Symptoms of mononeuropathy/mononeuritis multiplex?

where one of more nerves are affected, can be abrupt and painful lesions, more common at sites of external pressure, with pain, ptosis, diplopia and sparing of pupillary function


Symptoms of diabetic amyotrophy?

asymmetrical, painful wasting of the quadriceps, the wasting is marked and knee reflexes are diminished or absent


What foot damage can occur in diabetes?

ischemia and haemorrhage and tissue necrosis leading to ulceration, infections, gangrene, dcellulitis, abscess and osteomyelitis, bone deformity, absent dorsal pedis pulses


Prevention and treatment of feet in diabetes?

daily foot examination, comfortable shoes, no bare foot walking, regular chiropody to remove callus, relieve high pressure areas with best rest and therapeutic shoes, metatarsal head surgery, IV antibiotics for cellulitis, surgery if abscess or deep infection, good local wound care, reconstructive vascular surgery in area of arterial occlusion


What causes increased infections in diabetes?

impaired function of polymorphonuclear leucocytes particularly in urinary tract and skin, TB and mucocutaneous candidiasis are common, can leading to further loss of glycemic control and cause ketoacidosis


What effect does diabetes have on the skin?

lipohypertrophy, necrobiosis lipoidica deabeticorum (erytheatous plaques over the shins with a brown waxy discolouration), vitiligo (symmetrical white patches), granuloma annulare (flesh coloured rings and nodules over extensor surfaces of fingers)


How can lipohypertrophy be avoided?

varying the injection site of the insulin day to day


Prognosis of diabetes?

1 - good health, but increased risk of complications so must have good control, blood pressure and weight

2 - 75% die of heart disease, 15% of stroke, CV disease is 5x more common

for every 1% increase in HbA1c level there is an increase in death from diabetes by 21%


What is diabetic ketoacidosis?

hyperglycaemia (blood glucose >11mmol/L), acidaemia (pH3mmol/L) or significant ketonuria (>2 on urine stix)


When does ketoacidosis occur?

in starvation states, the body can no longer metabolize carbohydrates as the body is less efficient, there is excess glucose that cannot be taken up or metabolized due to lack of insulin so the body goes into starvation state for energy production, this produce acetone, increase in hepatic gluconeogensis, peripheral lipolysis increasing free fatty acids which is converted into acidic ketones


What increases the effect of and triggers ketoacidosis?

stress hormones (catecholamine, glucagon, cortisol) which are secreted in response to dehydration and intercurrent illness, infection, discontinuation or inadequate insulin, CV disease, steroids, menstruation, pancreatitis, chemo


In who is ketoacidosis seen?

in 4% of type 1 DM, especially in newly presenting, hospital patients, rare in DM 2 unless older, overweight, non white and newly presenting


Presentation of ketoacidosis?

polyuria, polydipsia, vomiting, dehydration, altered mental state, coma, weight loss, anorexia, weakness, lethargy, Kussmaul respiration (deep hyperventilaton) and acetone fruity breath

dry mucous membranes, dry tongue, decreased skin turgor/skin wrinkling/reduced tissue turgor, sunken eyes, slow capillary refill, tachycardia, weak pulse, hypotension


What will investigations show in ketoacidosis?

chest may have pneumonic consolidation, pericardial rub, murmurs, may have intra abdominal precipitant, altered mental status, abscess, boils, rashes

glycosuria and ketonuria, elevated glucose levels, ketonaemia, raised WCC, high sodium due to dehydration, hyperkalaemia due to acidosis, elevated urine and creatinine due to AKI

plasma osmolarity >290mOsm/kg
anion gap is >13mmol/L


How is plasma osmolarity calculated?



How is anion gap calculated?



DD of diabetic ketoacidosis?

alcoholic ketoacidosis, hyperosmolar hyperglycemic state, lactic acidosis, aspirin overdose, acute pancreatitis, sepsis without ketoacidosis, acute abdomen, ketoacidosis due to starvation


Management of diabetic ketoacidosis?

replace fluid, remove ketones, replace electrolyte loss, replace insulin, restore acid base balance, shift potassium back into cells, ABC, O2 monitor, ECG monitor, large bore peripheral IV access, urinary catheterisation to monitor urine output, LMWH and TED stockings, nasogastric tube if drowsy or vomiting, IV insulin infusion, 5% dextrose once glycemia is normal to prevent hypoglycemia, treat underlying cause, regular monitoring


What is classed as severe DKA?

1 of the following:
blood ketones >6mmol/L
bicarbonate 100 or 16


Who is DKA needs specialist input?

elderly, pregnant, 18-25, heart or kidney failure, serious comorbidities, fluid administration and deficits


Complications of DKA?

cerebral oedmea, headache, pulmonary oedema, hypoglycemia, arrhythmia, brain injury, death, hypokalaemia, metabolic acidosis, myocardial suppression, venous thromboembolism, MI, retinopathic changes, ARDS


Prognosis of DKA?

high mortality rate, but rates are decreasing, prognosis is worse with age and severe underlying causes, death mainly by cerebral oedema in the young and pneumonia, MI and sepsis in adults


Prevention of DKA?

good diabetic control, educate on risk factors and symptoms, monitoring, psychological support


What is a hyperosmolar hyperglycaemic state (HHS)?

marked hyperglycaemia (>40mmol/L) causing osmotic diuresis with hyper osmolality leading to an osmotic shift of water into the intravascular compartment causing severe intracellular dehydration

hypovolaemia and osmolality is usually >320mOsmol/kg

there is enough insulin to prevent ketogenesis but not enough to reduce blood glucose

metabolic emergency and seen in type 2