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Diabetes - pathophysiology

Morgan Morgan Medicine, Surgery & Radiology University Englisch 4,3Durchschnittliche Bewertung 4,3 von 5 (3 Bewertungen) 49 Karten

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  1. 1The pancreas contains two glands called the?The endocrine gland and the digestive gland.
  2. 2The endocrine tissue consists of cells called ? What do they do?Islets of Langerhans
    Discharge secretions directly into the blood stream.
  3. 3Each islet is composed of three types of cells?Alpha, beta and delta cells
  4. 4Alpha cells secrete a hormone called? Which?glucagon, which raises blood glucose.
  5. 5Beta cells ? Which?Beta cells secrete insulin in response to a rise in blood glucose after eating - this restores blood glucose to normal.
  6. 6Delta cells produce a hormone called ? Which?somatostatin which inhibits secretion of both glucagon and insulin.
  7. 7Insulin promotes entry of glucose into ...................................... and stores the glucose as.....................liver and muscle cells
    glycogen
  8. 8Where is glucose stored?Liver
  9. 9In adipose tissue, insulin converts glucose into?fat (triglyceride) and storage of the newly formed triglyceride within fat cells.
  10. 10Insulin dependent diabetes (type 1) usually results from?Damage or destruction of the pancreatic islets, leading to reduction or absence of insulin secretion.
  11. 11Diabetes is associated with which disease? The onset of diabetes follows a ?Specific human leuckocyte antigen autoimmune disease.
    Viral infection in some cases
  12. 12Insulin also promotes the entry of ?amino acids into the cells and stimulates protein synthesis.
  13. 13Insulin cannot be given to ?Pregnant women, as it is a growth hormone.
  14. 14Type 1 diabetes occurs primarily in ? There is a ................................. .............................. to type 1 diabetes. Body weight?Children and young adults.
    Hereditary predisposition.
    Usually normal or underweight;often recent weight loss.
  15. 15Diabetic Ketoacidosis is caused by a? What happens?Lack of insulin
    This happens when a severe lack of insulin means the body cannot use glucose for energy, and the body starts to break down other body tissue as an alternative energy source. Ketones are the by-product of this process. Ketones are poisonous chemicals which build up and, if left unchecked, and will cause the body to become acidic – hence the name 'acidosis'.
  16. 16In patients with diabetic ketoacidosis their breath smells of?Pear drops
  17. 17Non-insulin-dependent (type 2) usually affects ?older overweight and obese adults
  18. 18The islets secrete? but the tissues are?normal or increased amounts of insulin
    but the tissues are relatively insensitive to the action of insulin and are unable to respond appropriately (Insulin Resistance).
  19. 19The impaired response to insulin is linked to?Obesity
  20. 20A hyperosmolar coma results from ?marked hyperglycemia.
  21. 21Type 2 is a?hereditary disease.
  22. 22Treatment for Type 1 patients? Treatment for Type 2 patients?Patients require treatment with insulin.
    Patients require treatment with healthy eating and activity, plus oral medication and/or insulin as the disease progresses.
  23. 23Random or 2 hour post glucose load test?The doctor gives the patient a litre of a sugary drink and 2 hours later he tests the patient's blood glucose levels.
  24. 24What is the main test to diagnose diabetes?HbA1c or glycated haemoglobin
  25. 25HbA1c measures?Average plasma glucose concentration. The control of the sugar level for the 3 months prior to testing.
  26. 26The ideal level is? There is a ... to....% reduction in risk of ..................disease with every....% (10mmol/mol) reduction of hemoglobin A1c.Less than 7%/<53 mmol/mol
    10 to 20%, vascular disease, 1%
  27. 27Symptoms of Hyperglycaemia in Type 1 diabetes?Polyuria
    Polydipsia
    Lethargy
    Weight loss
  28. 28Polyuriagoing to the loo a lot. Glucose above renal threshold.
  29. 29PolydipsiaDehydration. Thirst.
  30. 30ProteinuriaProtein in urine.
  31. 31LethargyHyperglycaemia
  32. 32Weight loss due to?Fat and protein breakdown
  33. 33Type 2 diabetes is associated with?obesity (truncal), hypertension, lipid abnormalities (high cholesterol) and low levels of physical activity.
  34. 34Patients with Type 2 are on?aspirin, anti-hypertensions and statins.
  35. 35Recommendations? Blood pressure? Cholesterol? HbA1c?<130/80MMhg
    <4.5
    <53 mmol/mol (7%)
  36. 36Insulin resistance precedes Type 2 diabetes by up to 20 years. >......% of Type 2 diabetes patients are insulin resistant.90%
  37. 37Secondary causes of diabetes 4Pancreatic, e.g. cancer, cystic fibrosis, surgery
    Drug induced, e.g. corticosteroids, thiazide diuretics
    Endocrine, e.g. acromegaly, Cushing's syndrome
    Associated with stress, e.g. myo cardial infarction, CVA, severe infection
  38. 38Gestational diabetes What type of test is required? Treated with? Aim?Appears during pregnancy
    Oral glucose tolerance test is needed for diagnosis.
    Healthy eating +- insulin.
    Tight blood glucose control.
  39. 39The overall effect of diabetes? Social Psychological Physical ManagementCareer choice/work
    Social events
    Changes to routine
    Complications
    Depression
    Fear of hypos
    Threat of stigma
    Disease process/management
    Complications
    Adopting health behaviour
    Self-adjustment to treatment
    Self-monitoring
    Identifying hypo and hyper
    Surveillance
  40. 40MODY stands for? What type of diabetes? Onset (age)? Cause?Maturity Onset Diabetes of the Young
    Rare subgroup of Type 2 diabetes
    Onset generally <25 years old
    Primarily due to an islet beta cell defect
  41. 41What are the three main drug options for treating type 2 diabetes?Metformin
    A Sulfonylurea
    A thiazolidinedione
  42. 42METFORMIN activates?The enzyme AMP-kinase, which is involved with regulating cellular energy metabolism.
  43. 43How do you administer insulin?By a pen injection device into the fat below the skin on the abdomen, thighs or upper arms. The needle is usually inserted to its full length.
  44. 44What is hypoglycemia?Hypoglycemia occurs when the level of glucose present in the blood falls below a set point:
    Below 4 mmol/L (millimoles per litre)
  45. 45How to treat hypoclycemia? Mild case? Serious case?A mild case of hypoglycemia can be treated through eating or drinking approximately 10-20g of sugar (i.e. carbohydrates). Some diabetics carry glucose tablets for this express purpose.
    Serious hypoglycemia will require medical attention. In this instance, paramedics will use glucagon or provide glucose intravenously. Some diabetics have glucagons injections at home, in the form of glucagons kits.
    This allows immediate treatment and the possibility of avoiding hospital. For those diabetics that experience regular hypoglycemia, blood sugar levels should be tested regularly.
  46. 46Low density lipids function?The main carrier of cholesterol, and deliver it both to the liver and to peripheral cells. They need to be minimised as they are a risk factor for cardiovascular disease.
  47. 47High density lipids are produced in? It transports ?High density lipids are produced in both the liver and intestine. It transports cholesterol away from the periphery.
  48. 48Which drug minimises LDL?Statins
  49. 49Polyol pathway stepsHyperglycaemia results in the production of:
    Aldose Reductase (enzyme found in nerve cells, retinal cells, glomerulus and kidney tubules and blood vessel walls)
    Which reduces to Sorbitol (oxidised by sorbitol dehydrogenase to fructose)
    Sorbitol does not easily diffuse across the cell membrane and this causes damage due to osmotic stress.
    The damage causes activation of protein Kinase C and the promotion of advanced glycation endproduct formation (AGEs). AGEs are formed by the reaction of glucose and other glycating compounds with proteins. Early glycation products are reversible.
    But eventually they undergo irreversible change through cross-linking.
    *Leading to thickening and stiffening of blood vessels (less permeable and elastic).
    *Proteins bind to specific receptors - monocytes, macrophages, glomerular cells, endothelial cells

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University Medicine, Surgery & Radiology Karteikarten am Diabetes - pathophysiology, erstellt von Morgan Morgan am 20/12/2014.
Erstellt von
Morgan Morgan
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Durchschnittliche Bewertung 4,3 von 5 (3 Bewertungen)

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