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Phase 2 Metabolic > Diabetes > Flashcards

Diabetes Flashcards

1
Q
  1. When is insulin released?
  2. Name 4 other substances that promote insulin secretion
  3. Describe the 2 stages of insulin release
A
  1. in response to increased blood glucose
  2. amino acids, farry acids, parasympathetic stimulation, incretins
  3. initial rapid phase - release of stored insulin
    delayed slower phase - continued release of stored hormone and new synthesis
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2
Q

name 6 effects of insulin

A
  1. increased glycogenesis (production of glycogen)
  2. decreased gluconeogenesis (production of glucose)
  3. decreased glycogenolysis (breakdown of glycogen)
  4. uptake of glucose into adipose tissue
  5. amino acid uptake and protein synthesis
  6. lipogenesis
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3
Q
  1. What is glucagon secretion:
    a) stimulated by?
    b) inhibited by?
  2. what is the action of glucagon? (3)
A

1a) low blood glucose, fatty acids and amino acids
1b) insulin; somatostatin

  1. glycogenolysis, gluconeogenesis and ketogenesis
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4
Q
  1. What is the diagnostic definition of gestational diabetes?
  2. What is the pathogenesis of gestational diabetes?
  3. Name 5 risk factors for gestational diabetes
A
  1. diabetes that develops in pregnancy and goes away after pregnancy
  2. placenta produces steroids (in order to protect the foetus from maternal autoantibodies); steroids cause insulin resistance
  3. big for gestational age
    previous gestational diabetes
    family hx of gestational diabetes
    obese mother
    older mother
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5
Q

Name 4 types of conditions that diabetes can occur secondary to

A
  1. diseases associated with pancreatic beta cell destruction - pancreatitis, CF
  2. hormonal syndromes that interfere with insulin secretion - e.g. pheochromocytoma
  3. hormonal syndromes that cause peripheral insulin resistance - acromegaly, cushing’s syndrome
  4. drugs - glucocorticoids, oestrogens, atypical antipsychotics
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6
Q
  1. When does type I diabetes typically manifest?

2. What is LADA?

A
  1. childhood

2. variant of type I diabetes that presents in later life (can be difficult to distinguish from T2DM)

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7
Q
  1. Describe the pathogenesis of T1DM

2. Describe the pathophysiology of T1DM

A
  1. autoantibodies against pancreatic islet constituents (PROINSULIN, GLUTAMIC ACID DECARBOXYLASE) leads to autoimmune destruction of beta cells leading to absolute insulin deficiency
  2. insulin deficiency leads to the inability to utilise glucose in peripheral adipose and muscular tissue (causing hyperglycaemia). This stimulates the production of glucagon, which promotes gluconeogenesis, glycogenolysis and ketogenesis
    - hyperglycaemia results in osmotic diuresis
    - ketosgenesis results in acidosis
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8
Q
  1. What syndrome is T2DM a component of?

2. Name 2 aetiological factors of T2DM

A
  1. metabolic syndrome
  2. genetic predisposition
    aging, physical inactivity, dietary excess and overweight/obesity aggravate insulin resistance
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9
Q

What are the 2 main pathophysiological mechanisms in T2DM?

A
  1. desrupted beta cell function (reduced insulin secretion but not absolute insulin insufficiency)
  2. disrupted tissue insulin sensitivity
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10
Q
  1. What is MODY?
  2. What is its cause?
  3. How do patients with MODY present?
A
  1. T2DM that develops in the young
  2. autosomal dominant mutation interferes with insulin production cascade - insulin production is ineffective
  3. asymptomatic hyperglycaemia; normal BMI; negative ketones
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11
Q

What is the classic triad of symptoms of an acute presentation of diabetes?

A
  1. POLYURIA (due to osmotic diuresis that occurs when hyperglycaemia exceeds renal threshold)
  2. THIRST (due to resulting fluid and electrolyte loss)
  3. WEIGHT LOSS (due to accelerated catabolism and fluid depletion)
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12
Q

Name some other presenting features of diabetes

A
  1. lack of energy
  2. visual blurring (glucose induced changes in refraction)
  3. puritis vulvae/balanitis due to candida infection
  4. staph skin infections
  5. retinopathy
  6. polyneuropathy
  7. erectile dysfunction
  8. arterial disease
  9. Acathosis nigricans (blackish pigmentation at the nape of neck and in axillae)
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13
Q
  1. What is required for a diagnosis of diabetes in:
    a) asymptomatic patients
    b) symptomatic patients
  2. Describe the abnormal results of the 3 main tests for DM
  3. Describe the glucose tolerance test
  4. When is the glucose tolerance test used?
A

1a) 2 abnormal diagnostic test results
1b) symptoms + 1 abnormal diagnostic test result

  1. fasting plasma glucose >7
    random plasma glucose >11
    HbA1c >11
  2. measures blood glucose before and after ingestion of glucose solution
  3. borderline cases and gestational diabetes
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14
Q

Name 2 instances when HbA1c measurement is not useful and why

A
  1. pregnancy - volume expansion
  2. anaemia
    - in haemolytic anaemia, HbA1c will be falsely low
    - in iron deficiency anaemia, RBCs have an increased lifespan therefore HbA1c will be falsely high
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15
Q

Name 3 other investigative tests that can be useful in classifying diabetes

A
  1. c peptide - product of pro-insulin cleavage; if present, likely to be T2DM
  2. autoantibodies - Anti-GAD
  3. ketones - positive in T1DM
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16
Q
  1. How does ketoacidosis occur in T1DM?
  2. Name 2 consequences of ketoacidosis
  3. How does dehydration arise in DKA?
  4. How can acidosis result in hyperkalaemia?
  5. Name 4 effects of acidosis
A
  1. glucose can’t be taken up into cells because of lack of insulin. This pushes body into starvation like state. Lipids are broken down into fatty acids and fatty acids oxidised to produce Acetyl-CoA - produces ketones
  2. hyperventilation
    vomiting
  3. hyperglycaemia leads to an osmotic diuresis, resulting in fluid and electrolyte depletion
  4. Insulin stimulates Na/K ATPase. K+ leaks out of cell via potassium channels but can’t be pumped back in
  5. negative inotropic effect on cardiac muscle
    systemic hypotension
    peripheral vasodilation
    respiratory depression
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17
Q

Name clinical features of DKA

A
  • thirst, polyuria and weight loss
  • hyperventilation
  • nausea and vomiting
  • weakness
  • visual disturbances
  • somnolence/impaired consciousness
  • tachycardia
  • hypotension
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18
Q

What investigations are important for ?DKA

A
  • urine dip for glycosuria and ketonuria
  • ABG - acidosis
  • Bloods - U&E, bicarb, glucose
  • urine and blood culture
  • CXR
  • ECG
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19
Q

How is DKA managed?

A

IV fluid and variable rate insulin

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20
Q

Name 3 complications of DKA

A
  1. cerebral oedema
  2. aspiration pneumonia
  3. hypokalaemia
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21
Q
  1. What is HSS?

2. Describe its pathophysiology

A
  1. severe hyerglycaemia without significant ketoacidosis. Characteristic metabolic emergency of uncontrolled T2DM
  2. Hyperglycaemia → osmotic diuresis → hypernatraemia → profound volume contraction/hypovolaemia → ↓GFR
    endogenous insulin levels are sufficient to inhibit hepatic ketogenesis but insufficient to inhibit hepatic glucose production and promote glucose utilisation.
22
Q

Describe clinical features of HSS

A
  • polydipsia, polyuria
  • signs of hypovolaemia - tachycardia, hypotension, dry mucous membranes
  • stupor/coma
23
Q

What is the definition of hypoglycaemia (in terms of blood glucose)

  1. if the patient is symptomatic?
  2. if the patient is asymptomatic?
A
  1. ≤3.9

2. ≤3

24
Q

Give examples of the following types of symptoms of hypoglycaemia:

  1. adrenergic
  2. neuroglycopenic
A
  1. sweating, tachycardia, palpitations, tremor, anxiety, hunger
  2. irritability, aggression, confusion, slurred speech, loss of consciousness, seizures
25
Q

Name 6 causes of hypoglycaemia?

A
  • overadministration of insulin
  • decreased glucose delivery (missing meals, overnight fasting)
  • alcohol
  • exercise
  • oral hypoglycaemics (sulfonylureas)
  • Addison’s disease
26
Q
  1. What is a minor hypoglycaemic event?

2. What is a major hypoglycaemic event?

A
  1. person is able to manage the event themselves

2. person requires third party assistance to manage the event

27
Q
  1. What is hypoglycaemia unawareness?
  2. How is hypoglycaemia unawareness assessed?
  3. What is the legal implication of hypoglycaemia unawareness?
A
  1. patient unaware that they are becoming hypoglycaemic
  2. Gold Score
  3. Patients with a gold score >4 have impaired hypoglycaemia awareness; they are legally not allowed to drive.
28
Q

How is a minor hypo managed?

A

short acting carb + long acting carb; recheck sugars after 15 and 30 mins

29
Q

How is a major hypo managed?

A
  • if patient is co-operative/able to follow instructions, instruct patient in management of minor hypo
  • if patient is unable to follow instructions, give IM glucagon 1mg; then assess whether patient improves and can take food orally, or gain IV access for glucose infusion
30
Q

Describe 5 changes that characterise endothelial dysfunction

A
  1. decreased NO production
  2. increased platelet aggregation
  3. increased expression of adhesion molecules
  4. increased expression of cytokines and chemokines
  5. increased ROS production
31
Q
  1. How does hyperglycaemia result in endothelial dysfunction?
  2. How does hyperglycaemia/endothelial dysfunction promote atherosclerosis?
A
  1. endothelial cells take up much of the glucose in hyperglycaemia independent of insulin; ROS is produced as a byproduct of cellular respiration and promotes:
    - expression of VEGF leading to angiogenesis and endothelial proliferation
    - platelet aggregation
    - NFKB expression (proinflammatory)
    - ECM deposition and fibrosis
    - formation of advanced glycation end products which further contribute to oxidative stress
  2. inflammatory processes promote cellular adhesion and increased vascular permeability. Enables monocytes and LDL to infiltrate tunica intima leading to the formation of a fatty streak.
32
Q

Name 4 macrovascular complications of diabetes

A
  1. stroke
  2. MI
  3. impaired diastolic function (coronary atherosclerosis leads to muscle weakening)
  4. peripheral vascular disease
33
Q

Name 3 eye conditions that can develop as a consequence of diabetes and why

A
  1. cataracts (proteins within the lens become denatured due to osmotic changes relating to blood glucose)
  2. diabetic retinopathy (thickening of basement membrane in retinal vessels leads to vascular occlusion and increased vascular permeability)
  3. external ocular palsies (form of neuropathy affecting CN III and VI)
34
Q

name 9 changes that can occur in diabetic retinopathy

A
  1. microaneurisms
  2. blot haemorrhages
  3. hard exudates
  4. cotton wool spots
  5. venous bleeding
  6. neovascularisation
  7. fibrotic bands
  8. retinal detachment
  9. macular oedema
35
Q

Name the 3 main ways the kidneys can become damaged by diabetes

A
  1. glomerular damage (microvascular)
  2. ischaemia resulting from hypertrophy of efferent and afferent arterioles
  3. ascending infection
36
Q

How do the glomeruli become damaged in diabetic nephropathy?

A

afferent arteriole dilates more than efferent arteriole - increases intraglomerular filtration pressure which damages the glomerular capillaries. It also increases shear stress which contributes to hypertrophy and secretion of ECM leading to glomerular sclerosis
These changes make the filtration membrane ineffective causing progressive leakage into the urine

37
Q
  1. Name 2 diagnostic tests used to investigate diabetic nephropathy
  2. How is diabetic nephropathy generally managed?
A
  1. urine dip for presence of protein
    albumin: creatinine ratio of urine
  2. aggressive treatment of BP, preferably with ACE/ARBs
    avoid oral hypoglycaemics excreted by the kindye (metformin, glibenclamide)
38
Q
  1. Describe the vascular hypothesis of diabetic nephropathy

2. Describe the alternative hypothesis of diabetic nephropathy

A
  1. occlusion of vasa nevorum (blood supply to nerves)
  2. accumulation of sorbitol/fructose in schwann cells disrupts their structure and function leading to delayed conduction
39
Q

Name 4 types of diabetic nephropathy

A
  1. symmetrical, distal, sensory neuropathy
  2. avute painful neuropathy
  3. mononeuropathy and mononeuritis multiplex
  4. diabetic amyotrophy
  5. autonomic neuropathy
40
Q
  1. What is charcot foot?
  2. How does it occue?
  3. What is required for charcot foot to occur?
  4. What is a risk following the development of charcot foot?
  5. How is charcot foot prevented?
  6. What other condition is it important to differentiate charcot foot from?
A
  1. bone and joint dysfunction secondary to neuropathy, trauma and changes in bone metabolism
  2. a combo of diabetes, neuopathy, trauma and metabolic abnormalities of the bone result in an acute localised inflammatory condiion that leads to patterns of bone softening, destruction and deformity
  3. neuropathy + good blood supply (because it’s driven by an inflammatory process)
  4. callous formation (weight bearing areas of foot are not cushioned)
  5. offloading
  6. Osteomyelitis (MRI scan)
41
Q

Name the 3 processes which combine to produce diabetic foot

A
  1. ischaemia
  2. infection
  3. neuropathy
42
Q
  1. Which patients are seen by the community diabetes team?

2. Which patients are seen in secondary care? (6)

A
  1. patients with poor glycaemic control, on multiple medications or injectables
2. DKA
    pregnant women
    children
    kidney disease
    foot problems
    patients using insulin pumps
43
Q

Name the education programmes for people with:

  1. T2DM
  2. T1DM
A
  1. DESMOND (discuss diet and medication and awareness of diabetic complications)
  2. dose adjustment for normal eating (DAFNE)
44
Q

Name the 8 care processes for diabetes

A
  1. Cholesterol measurement (between 4 and 2)
  2. serum creatinine measurement
  3. smoking status
  4. BMI
  5. foot examination (inspection, pulses, sensation)
  6. blood pressure (<140/90)
  7. HbA1c
  8. urine albumin:creatinine ratio
    (9. diabetic eye screening)
45
Q

Describe psychosocial affects of T1DM

A
  • no day off
  • constant calculation of carbs and how much insulin
  • constant worry of what blood sugar is and if safe
  • fear of hypos
  • poor sleep
  • diabetic complications
  • social stigma of injections
  • weight gain associated with insulin
46
Q
  1. What is the MOA of metformin?
  2. Name 3 advantages of metformin
  3. Name 2 disadvantages of mentformin
A
  1. acts on the liver to decrease gluconeogenesis
  2. does not cause weight gain (but likewise doesnt cause weight loss)
    reduces micro and macrovascular risk
    rarely causes hypos
  3. can be poorly tolerated (causing GI side effects)
    renally excreted therefore can’t be used in those with renal impairment
47
Q
  1. what is the MOA of sulfonylureas?
  2. Name 2 examples of sulfonylureas
  3. Name 3 disadvantages of sulfonylureas
A
  1. acts on beta cells to produce insulin
  2. gliclazide, glipizide
  3. effect on glucose control wears off in long term as beta cell mass declines
    can cause hypos
    can cause weight gain
48
Q
  1. What is the MOA of pioglitazone?
  2. Name a disadvantage of pioglitazone
  3. In which patients is pioglitazone contraindicated and why?
A
  1. agonist of PPARγ - promotes upregulation of GLUT4 and insulin receptors
  2. weight gain
  3. heart failure (can cause fluid retention)
49
Q
  1. Describe the incretin effect

2. What enzyme is responsible for the breakdown of incretins?

A
  1. Incretins (GLP-1 and GIP) are produced in response to oral glucose and potentiatw the release of insulin from the pancreas
  2. DPP-4
50
Q
  1. What is the MOA of DPP-4 inhibitors?
  2. What suffix is given to DPP-4 inhibitors?
  3. Name 3 cautions for the use of DPP-4 inhibitors
A
  1. prevents the breakdown of incretins, therefore prolongs the action of endogenous insulun
  2. -gliptins
  3. acute pancreatitis; renal dysfunction; gastroparesis
51
Q
  1. What is the MOA of SGLT2 inhibitors?
  2. What suffix is given to SGLT2 inhibitors?
  3. Name 2 advantages of SGLT2 inibitors?
  4. In what group of patients can SGLT2 inhibitors not be used?
A
  1. inhibits sodium dependent glucose transporter in the proximal tubule. Inhibits the reabsorption of glucose leading to the urinary loss of glucose
  2. -flozins
  3. leads to reduced HbA1c and weight loss
    diuretic effect improves BP and CV risk
  4. GFR <40
52
Q

Describe the NICE guidelines for management of T2DM

  1. First line
  2. Second Line
  3. third line
  4. fourth line
  5. fifth line
A
  1. lifestyle modification - diet, weight control, exercise
  2. metformin
  3. dual therapy - metformin + another oral hypoglycaemic
  4. Triple therapy - metformin + sulfonylurea + another oral hypoglycaemic
  5. Insulin therapy

Phase 2 Metabolic (12 decks)

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