Diabetes Mellitus Flashcards

Question

Principles of insulin treatment

Answer 1

 Principles of insulin treatment:  Injections: o The needles used are very fine and sharp Even though most injections are virtually painless, patients are understandably apprehensive and treatment begins with a lesson in injection technique. o Insulin is usually administered by a pen injection device but can be drawn up from a vial into special plastic insulin syringes marked in units (100U in 1ml). o Injections are given into the fat below the skin on the abdomen, thighs or upper arm and the needle is usually inserted to its full length. o Slim adults and children usually use a 31 gauge 6mm needle and fatter adults a 30gauge 8 mm needle. o Both reusable and disposable pen devices are available together with a range of devices to aid injection. o The injection site used should be changed regularly to prevent areas of lipohypertrophy (fatty lumps) o The rate of insulin absorption depends on local subcutaneous blood flow and is accelerated by exercise, local massage or a warm environment. o Absorption is more rapid from the abdomen than from the arm and slowest from the thigh. All these factors can influence the shape of the insulin profile

Answer 2

 Complications of insulin therapy o At injection site:  Shallow injections result in intradermal insulin delivery and painful, reddened lesions or even scarring.  Injection site abscesses occur but are extremely rare  Local allergic responses sometimes occur early in therapy but usually resolve spontaneously  Generalized allergic responses are exceptionally rare  Fatty lumps known as lipohypertrophy may occur as the result of overuse of a single injection site with any type of insulin (atrophy or hypertrophy) o Insulin resistance especially with obese patients. Insulin resistance may also be associated with antibodies directed against the insulin receptor especially in patients reported with acanthosis nigricans (dark velvety skin especially in skin folds e.g. armpits). o Weight gain: Many patients show weight gain on insulin therapy, especially if the insulin dose is increased inappropriately, but this can to some extent be overcome by emphasis on the need for diet and exercise, plus addition of metformin. Patients who are in poor control when insulin is started tend to gain (or regain) most weight. o Hypoglycemia

Answer 3

 The 2 main classes of drugs used in Zambia are Sulfonylureas and biguanides.  Sulfonylureas o Glibenclamide initially can be given orally OD or in two divided doses. Usual dose is 5mg orally daily taken before breakfast up to a maximum of 20mg in divided doses before food, depending on the patient’s response. Doses above 20mg will not result in any improvement in glucose control. o Chlopropamide 250mg PO OD taken with breakfast. Dosage may be adjusted to a maximum of 500mg depending on the patients response o Sulfonylureas can be given together with biguanides.  Biguanides o This is preferred drug in obese patients in addition to dietary control and exercise. It may also be added in patients who have reached the maximum dose of a sulfonylurea without achieving control of blood sugar levels. o Metformin 500mg PO BD or TDS daily or 850mg PO BD or TDS with or after food. Maximum dose is 2.55g daily in doses.  NOTE: dosage increments in oral antidiabetic drugs should be gradual i.e. at 1 to 2 week intervals.  Withdrawal of oral (sulfonylureas and biguanides) drugs should be commenced only after the insulin therapy has been initiated. In some patients, metformin and insulin combination can be given.

Answer 4

 Use of insulin in type 2 DM:  Insulin is usually added to an oral agent when glycemic control is suboptimal at maximal doses of oral medications.  An intermediate-acting agent is used starting with a low dose and increasing as needed for glycemic control (such as 5 to 10 U of NPH increasing as needed)  Adding NPH at bedtime is generally more efficacious than using it during the day.  If using only insulin, start with an AM (morning) injection. The dose can be increased by 5U every 3 to 7 days until adequate control is achieved.  If early morning hyperglycemia is a problem, intermediate acting insulin can be given twice daily as a split dose.

Answer 5

 Points of emphasis:  Symptoms of hyper or hypoglycemia  Weight  Blood pressure  Visual acuity (+ fundoscopy), examine the eyes for cataracts and other opacities  Examine oral cavity  Examine feet  Examine injection site  Lab tests: blood or urine sugar and urine albumin or protein

Answer 6

 These can be classified as:  Acute: o Hypoglycemia o Diabetic ketoacidosis o Hyperglycemic hyperosmolar state (Non-ketotic hyperosmolar coma)  Chronic: due mainly to non-enzymatic glycosylation as well as osmotic damage  High levels of glucose are taken in by cells which do not require insulin for glucose uptake e.g. neurons. These cells have the enzyme aldose reductase which converts excess glucose to sorbitol which causes damage to these cells.  Retinopathy  Neuropathy  Nephropathy  Diabetic foot ulcer

Answer 7

 This is caused by overdose of insulin or hypoglycemic agents, missing of meal, strenuous exercise.  Clinical manifestation:  Early: one may feel the effects of sympathetic stimulation such as cold sweat, tremor, hunger or palpitations  Late: if early symptoms are neglected then symptoms of the effect of hypoglycemia on the brain such as dizziness, blurring, headache, nightmares and coma may occur

Answer 8

 Management:  Any patient with diabetes losing consciousness should always be considered hypoglycemic until proven otherwise by blood sugar determination and should be managed by rapid IV administration of glucose or PO/ NG tube administration of any concentrated sugar solution.  Prolonged unconsciousness requires continuous 10% IV glucose administration

Answer 9

 Diabetic ketoacidosis (DKA) is a medical emergency principally associated with diabetes type 1 (due to insulin deficiency) although it has also been recently reported to be associated with diabetes type 2 (due to a relative insulin deficiency).  It is an acute severe manifestation of insulin deficiency

Answer 10

 DKA is an acute metabolic crisis in patients with diabetes characterized by:  Hyperglycemia (Blood glucose >11 mmol/L (200mg/dl))  Metabolic ketoacidosis (venous bicarbonate <15mmol/L and/or venous pH <7.3)  Hypotension and features of dehydration  Hyperketonemia (>3mmol/L) and ketonuria (more than 2+ on standard urine sticks)

Answer 11

 Precipitating factors include:  Infection (30%)  Poor compliance with insulin or discontinuation of insulin (poor diabetic control)- 15%  Dehydration  Stressful conditions such as trauma, surgery, MI or of emotional crisis  Excessive alcohol ingestion  It can occur in a patient who is not known to be diabetic i.e. the presenting complaint (10%)

Answer 12

 Any event that decreases insulin availability or causes stress that increases insulin demand leads to severe insulin deficiency and the effect of counter regulatory hormones such as glucagon, cortisol, epinephrine and growth hormone to become overwhelming.  Insulin deficiency is a necessary precondition since only a modest elevation in insulin levels is sufficient to inhibit hepatic ketogenesis and stable patients do not readily develop ketoacidosis when insulin is withdrawn.  Other factors include counter-regulatory hormone excess and fluid depletion.  The combination of insulin deficiency with excess of its hormonal antagonist leads to the parallel processes seen in DKA.  The biochemical changes include:  Increased production of glucose by the liver (gluconeogenesis) and increased glycogen degradation to glucose (glycogenolysis)  Decreased glucose uptake and utilization by muscles (because of lack of insulin)  Rising glucose levels lead to an osmotic diuresis, loss of fluid and electrolytes and dehydration. Plasma osmolality rises and renal perfusion falls.  Lipolysis: enhanced breakdown of free fatty acids (beta-oxidation) and subsequent ketogenesis in mitochondria. This increases blood levels of ketone bodies such as acetoacetic acid, beta-hydroxybutyric acid, and acetone resulting in metabolic acidosis (decrease in pH and bicarbonates). Accumulation of ketone bodies causes metabolic acidosis.  The above biochemical processes result in significant hyperglycemia and ketoacidosis which are responsible for the clinical manifestations of DKA.  The excess ketones are excreted in urine but also appear in the breath, producing a distinctive smell similar to that of acetone.  Respiratory compensation for the acidosis leads to hyperventilation, graphically described as ‘air hunger’ (Kussmaul’s respiration).  As the pH falls below 7.0, pH dependent enzyme systems in many cells function less effectively. Untreated severe ketoacidosis is invariably fatal

Answer 13

 According to pH:  <7.3: Mild  <7.2: Moderate  <7.1: Severe  One of more of the following suggests severe DKA.  Clinical o Pulse >100b/min or <60b/min o Systolic BP <90mmHg o Glasgow coma Score <12 o Oxygen saturation <92% on air (if normal respiratory function)  Blood o Blood ketones >6 mmol/L o Bicarbonate <12 mmol/L o Venous/Arterial pH <7.1 o Hypokalemia on admission <3.5mmol/L

Answer 14

 Mental status changes: some patients are mentally alert at presentation but drowsiness, lethargy and confusion may evolve into coma (5%) with severe DKA.  Dehydration: dry tongue and buccal mucosa, poor skin turgor, hypotension but with an increase in heart rate. (due to osmotic diuresis)  Polydipsia, polyuria and nocturia  Kussmaul respiration: deep and fast breathing resulting from metabolic acidosis. Hyperventilation becomes less marked in very severe acidosis owing to respiratory depression.  Acetone (“fruity”) odour of breath due to acetone  Nausea and vomiting (due to gastroparesis and attempt to remove H+ ) with frequent abdominal pain (this may even be confused with surgical acute abdomen)  Leg cramps  Weight loss  Weakness (which may be extreme –prostration)  Hypothermia  Sign of infection which may precipitate DKA (pyrexia in late stages)  A history of diabetes (unless first presentation)  Cerebral edema: an extremely serious complication of DKA especially in children.

Answer 15

 Diagnosis (requires all 3)  Random blood sugar (capillary glucose): hyperglycemia (>11mmol/l) or a known diabetic  Urine dipstick for ketones: hyperketonuria (2+ ketones) or serum Ketone (≥3+ or >6mmol/L)  Arterial blood gas analysis: can diagnose metabolic acidosis which is indicated by low serum bicarbonate (<15mmol/L) or low blood pH (<7.35)  Other investigations o Urea and creatinine: raised o Serum potassium:  Hyperkalemia (>5.5 mmol/L) (In early stages due to H-K exchanger on RBCs to offset the acidosis)  Hypokalemia (<3.5mmol/L) (due to osmotic diuresis as well as hyperaldosteronism) o Serum sodium: tends to be low because of dilution as the osmotic effect of hyperglycemia increases ECF volume o Serum osmolality is high o Increased anion gap o Increased WBC o CXR, urine culture and sensitivity, blood cultures should also be done to identify an infectious process

Answer 16

 Management should be carried out in a high dependency area (preferably the ICU).  Principles:  Assess, send blood to the lab, set up IV infusion  Fluid, electrolyte and acid-base balance  Insulin replacement and glucose stabilization  Potassium  Antibiotics (or treatment of underlying cause) Management mnemonic: “SIPA” S-solutions, I-insulin, P-potassium, A-antibiotics  Fluid replacement: normal saline and 5% Dextrose are used  Given through large bore cannula.  Average loss of water is of 500mmol. Normally 6 5 - - 8L 7 liters with a sodium loss should be given in the first 24 hours.  If systolic blood press (SBP) <90mmHg give 500ml of normal saline over 15mins and repeat if required (Give 1L in 30 minutes)  If/when SBP> 90 give 1L in 1 hour then 1 liter in 2 hours, then 1L in 4 hours then 1 liter in 8 hours.  When the serum glucose level falls to <14mmol/L (13.9mmol/L) change the IV fluid to 5% Dextrosesaline to prevent hypoglycemia  If sodium level more than 150mmol/L give half strength (hypotonic) saline.  Carefully monitor the urine output  Insulin  Soluble insulin IV 0.1 U/Kg/h (5-10 units/hour) by infusion. o 50 short/rapid acting insulin in bag with normal saline made up to 50ml. If glucose remains high (>7) after 2 hours, increase dose. o Alternatively, 6IU SC every hour (8IU) for obesethis is what is used  Note: soluble insulin given as an IV bolus is rapidly destroyed within a few minutes. IV insulin must always be given as a continuous infusion.  When blood sugar levels reach 10-14 mmol/L (13.9) reduce to 0.05 units/kg/h (2-4 units/hour) or titrate against blood glucose level.  When patient is able to take oral feeds give soluble insulin 2-3 times before meals  Alternative: o 20 units IM stat followed by 5-10 units IM hourly until blood sugar is 14mmol/l. o When blood glucose is 10-14mmol/L give 8 units 4 hourly subcutaneously until the patient is able to take oral feeds. o When patient is taking food orally, change to soluble subcutaneously twice or three times before meals.  For blood glucose measure baseline and hourly initially. Aim for fall of 3- 6mmol/L (55-110mg/dl) per hour.  Potassium (KCL)  Add dosage below to each 1L of infused fluid o If plasma K <5.5mmol/L do not include potassium chloride in the first bag of fluids. Dehydration may cause AKI so that should be treated first. o If plasma K <3.5mmol/L, add 40mmol KCL o If plasma K 3.5-5.5mmol/L, add 20mmol KCL  Insulin therapy leads to uptake of potassium by the cells with a consequent fall in plasma potassium levels. Potassium is therefore given as soon as insulin is started.  Antibiotics: broad spectrum antibiotics e.g. Ceftriaxone 1g IV BD  Sodium bicarbonate: 600ml of 1.4% or 100ml of 8.4% in large cannulated vein if pH<7.0  Once stable and able to eat and drink normally, transfer the patient to 4 times daily subcutaneous insulin regimen.  Sliding-scale regimens are unnecessary and may even delay the establishment of stable blood glucose.  Other management measures:  Bladder catheter if no urine passed in 2 hours or 3 hours of hydration.  Nasogastric tube if drowsy.  Give subcutaneous prophylactic LMW heparin  Other investigations: o Blood and urine culture o Cardiac enzyme o CXR o ECG (monitor if electrolyte problems or severe DKA)

Answer 17

 Hypotension: this may lead to renal shutdown. Plasma expanders (or whole blood) are therefore given if the systolic blood pressure is below 80mmHg. A central venous pressure line is useful in this situation. A bladder catheter is inserted if no urine is produced within 2 hours, but routine catheterization is not necessary.  Coma: The usual principles apply. It is essential to pass a nasogastric tube to prevent aspiration, since gastric stasis is common and carries the risk of aspiration pneumonia if a drowsy patient vomits.  Cerebral edema: this is a rare, but serious complication and has mostly been reported in children or young adults such as 8.4% bicarbonate may sometimes be responsible. The mortality is high.  Hypothermia:severe hypothermia with a core temperature below 33oC may occur and can be overlooked unless a rectal temperature is taken with a low-reading thermometer.  Late complications: these include pneumonia and deep-vein thrombosis (DVT prophylaxis is essential) and occur especially in the comatose or elderly patient.  Complications of therapy: these include hypoglycemia and hypokalemia, due to loss of potassium in the urine from osmotic diuresis. Overenthusiatic fluid replacement may precipitate pulmonary edema in the very young or the very old. Hyperchloraemic acidosis may develop in the course of treatment since patients have lost a large variety of negatively charged electrolytes, which are replaced with chloride. The kidneys usually correct this spontaneously within a few days.

Answer 18

 Previously called non-ketotic hyperosmolar coma.  This is a condition, in which severe hyperglycemia develops without significant ketosis, it is a metabolic emergency characteristic of uncontrolled type 2 diabetes.  Patients present in middle or later life, often with previously undiagnosed diabetes.

Answer 19

 Common precipitating factors:  Consumption of glucose-rich fluids  Concurrent medication such as thiazide diuretics or steroids  Intercurrent illness such as myocardial infarction, stroke, pneumonia, sepsis etc.

Answer 20

 Symptoms:  Such patients present with several weeks history of polyuria, weight loss and diminished oral fluid intake that is followed by mental confusion, lethargy, stupor or coma (10%). o Onset over several days: generalized weakness, leg cramps, visual impairment.  Impairment of consciousness is directly related to the degree of hyperosmolality.  Physical examination:  Patients have extreme dehydration, hypotension, tachycardia and altered state of consciousness or coma. The dehydration is caused by a hyperglycemia induced osmotic diuresis, when it is not matched by adequate fluid intake.  Signs of underlying infection.

Answer 21

 Increase in glucose leads to osmotic shift out of the cells resulting in intracellular dehydration.  No ketoacidosis due to basal insulin which is sufficient to stop ketogenesis, but not to reduce glucose.  Usually it is seen in old patients and is the first presentation of diabetes.  It can be precipitated by illness and dehydration.  In rare cases mixed HHS and DKA states can occur reflecting some degree of insulin deficiency.

Answer 22

 Diagnostic criteria:  Glucose >30 mmol/L  Serum Osmolality >320 mOsm/kg  No significant ketosis: less than 3+ on urine or <3 mmol/L  Other tests: o Bloods: FBC, CRP, U&Es o Septic screen if infection is suspected o ECG o Arterial blood gases: should be normal

Answer 23

 Treatment involves:  Fluid replacement: administration of IV fluids. Rehydrate with normal saline, slower than DKA (older population). The standard fluid for replacement is normal saline. Avoid 0.45% saline, rapid dilution of the blood may cause more cerebral damage than a few hours of exposure to hypernatremia. o Frequently required 6-10 liters. o 1L in 30 minutes o 1L in 1 hour o 1L in 2 hours o 1L in 4 hours o 1L in 8 hours  Bringing down the sugar rapidly by using rapidly acting insulin preparations o Give insulin after 1 hour at half the rate of DKA as HHS is highly insulin sensitive. o Insulin is not needed if glucose dropping with fluids along. Glucose should drop by 3 mmol/hr. o It is sometimes useful to infuse insulin at a rate of 3 U/hour for the first 2-3 hours, increasing to 6U/hour if glucose is falling too slowly. o When glucose is less than 14mmol/L check for random blood sugar every 2 hours and use 5% dextrose saline.  Identifying and treating the precipitating factor:  Monitor fluid balance, glucose and U&Es. Correct electrolytes if needed  DVT prophylaxis o Low molecular weight heparin should be given to counter the increased risk of thromboembolic complications associated with this condition

Answer 24

 Cerebral edema  Pulmonary embolism  Ischemia: MI, stroke  Much higher mortality (>10%) than DKA, in part reflecting patients’ underlying poor health.

Answer 25

 Symptoms include:  Difficulty of reading  Blurring of vision  Floaters  Shadowing which may later on progress to total blindness (in advanced stages).  Signs: seen on fundoscopy or ideally, retinal photograph  Microaneurysns: earliest sign. Small red dots.  Dot and blot hemorrhages from aneurysm rupture.  Hard exudates: lipid and protein leak from vessels.  Cotton wool spots: retinal nerve fiber ischemia  Venous beading (dilation) and loops: retinal ischemia  Intraretinal microvascular abnormalities (IRMA): redomelled capillary beds.

Answer 26

 Classification:  Non-proliferative retinopathy (NPDR): formerly divided into ‘background retinopathy’-microaneurysms and hard exudates only- and pre-proliferative retinopathy-everything else. o “Mild” if there are only microaneurysms, o “Severe” if there is 4-quadrant hemorrhage/aneurysms, ≥2 quadrant venous bleeding or ≥1 quadrant IRMA o “Intermediate” for anything in-between  Proliferative retinopathy: o Defined by presence of neovascularization o Vitreous hemorrhage. May cause symptoms such as floaters, flashes and sudden painless loss of vision. o Tractional retinal detachment: appears as ‘tented’ retina.  Macular edema: o Appears as blurring of retinal layers o Present with gradual blurring of vision o Can occur in NPDR and PDR o Commonest cause of vision loss in diabetes

Answer 27

 Glucose and BP control  Laser therapy  Vitrectomy if there is vitreous hemorrhage persisting >6 months or tractional retinal detachment.  Aspirin 100mg/day prevents further occlusion of small capillaries  Surgery: viterotomy removes blood clots and fibrosis that obstruct vision

Answer 28

 Symptoms include:  Burning sensation  Numbness  ‘Pins and needles’  Constipation or nocturnal diarrhea  Impotence  Foot ulcer

Answer 29

 Classification:  Polyneuropathy: is the commonest neuropathy, characterized by distal symmetrical predominant sensory impairment which manifests with tingling sensations, numbness, burning sensation etc.  Radiculopathy: characterized by neurogenic pain, it is often self-limiting.  Amyotropy: atrophy of proximal muscles mainly around the hip girdle  Autonomic neuropathy (dysregulation): Postural hypotension, GI manifestations (gustatory sweating, gastroparesis, nocturnal diarrhea), Genitourinary manifestations (neuropathic bladder, erectile dysfunctionimpotence)  Mononeuropathy: paralysis of a specific nerve or nerves e.g. diplopia due to third and sixth nerve palsies.

Answer 30

 Management:  Symptomatic treatment: pain control  Diarrhea control  Treatment of impotence.  Painful neuropathy: TCAs are 1st line. Gabapentin or Carbamazeppine are 2nd line

Answer 31

 This is a common complication in diabetes.  Clinical features:  Periorbital edema (eye or facial puffiness), pedal edema, anasarca  Anemia, uremia and osteodystrophy in patients with end stage renal disease  Lab findings:  Progression from micro albuminuria to macroalbuminuria  Management:  Tight blood pressure control  ACE inhibitors: decreases the progression of renal disease  Renal transplantation or dialysis in End stage renal disease

Answer 32

 Foot care should be an essential part of diabetes care:  Put on comfortable shoe  Check for pebbles in shoe and do not walk barefoot (wear comfortable and spacious shoes)  Examine the foot daily to detect problems earlier  Wash and dry and oil the feet  Take caution during nail cutting  Treat athletes’ foot or any other foot infection as early as possible  Remove corn  Do not use hot water to wash the feet  Stop smoking

Diabetes Mellitus Flashcards

(73 cards)