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MBBS 3: Internal Medicine > Diabetes I > Flashcards

Diabetes I Flashcards

1
Q

Describe insulin synthesis?

A
  1. Insulin is synthesized as pre-pro-insulin and processed to pro-insulin.
  2. Pro-insulin is then converted to insulin and C-peptide and stored in secretary granules awaiting release on demand
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2
Q

How is insulin secreted?

A
  1. glucose from GI tract
  2. activates GLUT 2 receptors of beta cells
  3. increase in ATP closes ATP-gated K+ channels to stop it flowing out
  4. depolarization
  5. Ca2+ entry and insulin granule exocytosis
  6. once secreted acts to trigger glucose uptake from blood
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3
Q

Where is insulin produced?

A

beta cells of pancreatic islets

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4
Q

Describe the biphasic nature of insulin secretion?

A
  1. there is a readily releasable pool of insulin filled granules that can be released without nutrients
  2. there is a reserve pool of insulin filled granules that is strictly metabolic dependent - this acts as the reserve pool
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5
Q

Describe the tissue distribution and function of the GLUT 1 transporter?

A
  • found in most cells
  • helps in basal glucose uptake
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6
Q

GLUT 2?

Location and functions

A
  • found in liver, beta cells, hypothalamus, basal lateral membrane small intestine
  • carrier for glucose and fructoose in liver and intestine
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7
Q

GLUT 3?

Location and functions

A
  • found in neurons, placenta, testes, brain
  • used for basal glucose uptake
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8
Q

GLUT 4?

Tissue distribution and functions

A
  • found in skeletal and cardiac muscle, fat
  • activity increased by insulin
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9
Q

GLUT 5?

A
  • found in the mucosal surface in small intestine, sperm, kidneys
  • involved in fructose transport
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10
Q

Where does glucose in the blood come from?

A
  1. our diet - Sugary foods and drinks, starchy food and carbohydrate are digested and absorbed into the blood as glucose
  2. gluconeogenesis - glucose is made by the liver and exctreted into the blood
  3. glycogenolysis - glycogen is broken down releasing glucose into the blood
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11
Q

How is glucose stored?

A

stored in the muscle as glycogen

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12
Q

How is glucose normally regulated?

A
  1. blood glucose rises
  2. pancreas produces insulin
  3. tissues of the body remove glucose from the blood and use it or fuel it
  4. blood glucose falls
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13
Q

What is diabetes?

A

A disorder of metabolism where the body is no longer able to regulate the glucose (sugar) levels in the blood
- results from defects in insulin secretion, action or both

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14
Q

Consequences of diabetes?

A

This usually leads to high sugar levels in the blood which ultimately leads to damage of blood vessels and organs of the body.

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15
Q

Pathogenesis of diabetes?

A

pancreatic beta cell apoptosis

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16
Q

Type 1 diabetes pathogenesis?

A

Auto-immune reactions leading to islet cells destruction

17
Q

Type 2 diabetes pathogenesis?

A
  1. Genetic predisposition coupled with excessive exposure to glucose and fatty acids (Gluco-lipotoxicity) → oxidative stress in the mitochondria and abnormal folding of protein in the ER
  2. Glucotoxicity also down-regulates GLUT4 levels in insulin-responsive cells
18
Q

What goes wrong in diabetes?

A
  1. blood glucose rises
  2. pancreas can not produce insulin or tissues cannot respond to insulin
  3. tissues of the body have no glucose for fuel
19
Q

Consequences of raised blood glucose?

A
  1. high glucose in the blood passes into the urine
    - polyuria, dehydration , thirst
  2. cellular metabolism stops
    - weakness, weight loss, fatigue
  3. cells of the body’s immune system cannot work properly
    - increased risk of infections
  4. glucose molecules in the blood bind on to proteins lining the blood vessels and damage the blood vessels
    - stroke, retinopathy, nephropathy, neuropathy, heart disease
20
Q

Types of diabetes?

A
  1. type 1
  2. type 2
  3. gestational diabetes
  4. other
21
Q

Pathogenesis of type I DM?

A
  1. genetic HLA-DR3/DR4/environment/viral infection
  2. autoimmune insulitis
    - antibodies against glutamic acid decarboxylase and insulin
  3. beta cell destruction
  4. severe insulin deficiency
22
Q

Clues to type 1 DM?

A
  1. thin
  2. short history
  3. ketones ++ in plasma and urine
23
Q

Latent autoimmune diabetes of adults?

A
  • Slow onset type I DM occurring in the middle aged (> 30 yrs)
  • Initially controlled with nutrition and exercise
  • Gradually dependent on insulin
24
Q

Diagnosis of LADA?

A
  1. Positive auto-antibodies (Anti-GAD)
  2. Low C-peptide levels
  3. Usually no family history
25
Q

Hypergluconaemia and how it causes DM2?

A
  • insulin has a suppressive effect on Alpha cells and glucagon(binding of the insulin receptor on alpha cells)
  • the most common cause of increased glucagon is an absence or deficiency of the restraining influence of insulin on glucagon production
26
Q

Why DKA is not common in DM2?

A

DKA is not common in DM2 because the little insulin secretion in the circulation is not sufficient to suppress the hepatic glucose production effects of glucagon

27
Q

Impaired incretin effect and how it causes DM2?

A
  • The hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are responsible for the incretin effect.
  • Phenomenon whereby insulin secretion increases more in response to an oral compared with an intravenous glucose challenge.
  • In DM2 there is loss of insulinotropic effects of GLP-1 & GIP
28
Q

Peripheral tissue resistance to insulin and how it causes DM2?

A
  • GLUT 4 primarily found in adipose, skeletal and cardiac muscles
  • In DM2 there is decreased translocation of GLUT 4 to the membrane as a result the insulin in circulation can not be able to bind the IR
29
Q

Maturity onset DM in the young (MODY)?

A

Single gene defects
- Autosomal dominant inheritance
- multiple generations affected

30
Q

Features of MODY?

A
  1. Early onset <25 years
  2. Absence of obesity, no ketosis & no evidence of beta cell destruction
  3. Hyperglycaemia often corrected by diet
31
Q

Drugs that cause secondary diabetes?

A
  1. corticosteroids (prednisolone)
  2. thiazide diuretics
  3. stavudine
32
Q

Diseases that cause secondry diabetes?

A
  1. Pancreatic disease
    eg CA pancreas, previous pancreatitis
  2. Liver disease
  3. Endocrine disease
    eg Cushing’s syndrome
33
Q

Risk factors?

A
  1. overweight (BMI ≥ 25kg/m2)
  2. waist circumference ≥90 cm in women and ≥ 100 cm in men
  3. family history
  4. diabetes in previous pregnancy
  5. smokers: current and former
  6. heavy/at risk drinking
34
Q

Diagnosing diabetes?

A
  • Symptoms AND an abnormal blood sugar
  • If the patient has NO symptoms they need TWO abnormal blood glucose measurements to make the diagnosis
  • If they have one abnormal and one normal result check again after 3 months
35
Q

Interpretation of blood glucose values?

A

Normal FBG is <126 mg/dl OR 7 mmol/L
Normal RBG is <200 mg/dL OR 11.1 mmol/L

36
Q

Glycated hemoglobin A1c that indicates diabetes?

A

> 6.5%

37
Q

Clinical presentations of diabetes?

A
  1. typical symptoms of high sugar
  2. subacute- weeks, months or years
  3. acute/severe (DKA)
  4. infections
  5. complications
    eg visual loss, cataracts or foot numbness/sores
  6. incidental finding screening
    eg hypertensive patients
38
Q

Typical symptoms of high sugar?

A
  1. Frequent urination (polyuria)
  2. Excessive thirst (polydipsia)
  3. Dizziness
  4. Weight loss
  5. Tiredness
  6. Blurred vision
  7. Numbness and/or burning pain in the legs
39
Q

Infections associated with diabetes?

A
  1. Skin infections
  2. fungal (thrush oral or genital)bacterial (cellulitis, abscesses and boils)
  3. UTI
  4. Pneumonia
  5. TB
  6. Foot infection

MBBS 3: Internal Medicine (72 decks)

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