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PHA223 > diabetes pathophysiology > Flashcards

diabetes pathophysiology Flashcards

1
Q

2 glands of the pancreas

A

digestive

endocrine

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2
Q

digestive function of the pancreas

A

exocrine tissue

secretes alkaline pancreatic juice into duodenum through the pancreatic duct to help digestion

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3
Q

Do islets have ducts/how do they secrete?

A

no ducts

secrete directly into bloodstream

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4
Q

cells of islets

A

alpha
beta
delta
F cells

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5
Q

What do F cells secrete?

A

pancreatic polypeptides

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6
Q

structure of islet cells

A

core - insulin producing beta cells

mantle - A, D, F cells

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7
Q

What do alpha cells secrete and what happens?

A

glucagon

raises blood glucose

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8
Q

What do beta cells secrete and what happens?

A

insulin

lowers blood glucose

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9
Q

What do delta cells produce and what happens?

A

gastrin and somatostatin

somatostatin inhibits secretion of glucagon and insulin

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10
Q

cause of T1DM

A

insulin deficiency

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11
Q

What is T2DM?

A

inadequate response to insulin

adult onset

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12
Q

manifestation of diabetes

A

hyperglycemia (high blood glucose levels)

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13
Q

How many chains long is insulin?

A

2

A and B chain

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14
Q

What is insulin’s pro hormone called?

A

pro insulin

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15
Q

What connects the A and B chain of insulin?

A

disulfide bridges and a C peptide (connecting)

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16
Q

How does the GLUT-4 transporter work?

A
  1. insulin binds to the cell membrane
  2. intracellular signal is sent
  3. GLUT-4 transporter inserted into the cell membrane from its inactive state
  4. transport of glucose across the membrane
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17
Q

How is glucose transported across the cell membrane?

A

using carriers called glucose transporters

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18
Q

Where are GLUT-4 transporters?

A

skeletal muscle

adipose tissue

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19
Q

What is GLUT-4 transporter dependent on?

A

insulin

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20
Q

When is GLUT-4 transporter active and inactive?

A

inactive inside the cell membrane

active when insulin causes it to move from its inactive site to the membrane

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21
Q

Where are GLUT-2 transporters?

A

beta cells

liver cells

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22
Q

When are GLUT-2 transporters used?

A

when glucose levels are high

has a low affinity for glucose

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23
Q

Where are GLUT-1 transporters?

A

in all tissues

important for the nervous system

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24
Q

Do GLUT-1 transporters require the action of insulin?

A

no

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25
Q

Which GLUT transporter needs insulin to become activated?

A

GLUT-4

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26
Q

2 types of T1DM?

A

type 1A - autoimmune T-cell mediated

type 1B - idiopathic

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27
Q

What causes gestational diabetes?

A

excess hormone production during pregnancy causes insulin resistance

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28
Q

risks of gestational diabetes

A 
macrosomia
microsomia
neonatal hypoglycemia
polycythemia
electrolyte disorders
respiratory distress syndrome
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29
Q

beta cell destruction in T1 vs T2

A

T1 yes

T2 no

30
Q

islet antibodies in T1 vs T2

A

T1 yes

T2 no

31
Q

genetic link in T1 vs T2

A

T1 strong

T2 very strong

32
Q

age of onset of T1 vs T2

A

T1 < 30

T2 >40

33
Q

onset of symptoms in T1 vs T2

A

T1 fast onset

T2 slower onset

34
Q

management of T1 vs T2

A

T1 insulin administered

T2 diet control and oral hypoglycaemic agents

35
Q

body weight in T1 vs T2

A

T1 low or normal

T2 obese

36
Q

extreme hyperglycaemia in T1 vs T2

A

T1 causes diabetic ketoacidosis

T2 causes hyperosmolar non-ketotic hyperglycaemia

37
Q

What causes T1DM?

A

severe lack of insulin caused by autoimmune mediated destruction of islet beta cells

38
Q

mechanism of beta cell destruction

A

T cells damage beta cells
- T helpers activate macrophages
- cytotoxic T cells directly kill beta cells
cytokines (macrophages and cytotoxic Ts) damage beta cells
autoantibodies against beta cells and insulin found in 70-80% of patients

39
Q

difference between type 1A and B

A

1A
- immunologically mediated beta cell destruction
- environmental agent that excites an immune response
1B
- no autoimmunity present for beta cell destruction
- African/Asian descent
- strongly inherited

40
Q

causes of T2DM

A

metabolic syndrome:

  • triglycerides
  • HDL
  • hypertension
  • systemic inflammation
  • macrovascular disease
  • obesity
  • insulin resistance
  • impaired suppression of glucose by the liver
41
Q

diagnosis (3 polys)

A

polyuria (excess urination)
polydipsia (thirst)
polyphagia (hunger)

42
Q

3 diabetic emergencies

A
  • hypoglycaemia
  • diabetic ketoacidosis
  • hyperosmolar non-ketotic hyperglycaemia
43
Q

What is hypoglycaemia?

A

glucose levels < 3.5 mm/l or 63 mg/dl

44
Q

causes of hypoglycaemia

A
  • missed/delayed/inadequate meal
  • increased dose of insulin
  • increase exercise
  • increased alcohol consumption
  • liver disease
  • blood lowering drugs with oral agents
45
Q

treatment of hypoglycaemia

A

10-20g carbohydrate meal

repeat after 10-20 mins if glucose <60 mg/dl or symptomatic

46
Q

foods with 15g carbs

A
  • half cup of orange/grapefruit/apple juice or soda
  • 1 cup fat free milk
  • 1/3 cup grape/cranberry juice
  • 1tbsp sugar
  • 5/6 pieces lifesavers
  • 3/4 glucose tabs
47
Q

hypoglycaemia if unable to swallow

A
  • IV glucose (30-50ml dextrose 20-50%)
  • children IV dextrose 0.2 mg/kg
  • viscous glucose gel to mouth or jam/honey
48
Q

3 signs of diabetic ketoacidosis

A
  1. hyperglycaemia
  2. hyperketoanaemia
  3. metabolic acidosis
49
Q

treatment for diabetic ketoacidosis

A
  1. fluid replacement - 0.9% NaCl
  2. infusion of insulin
  3. potassium (not in 1st hr unless <3 mmol/l)
  4. treatment of any associated infection
50
Q

What causes hyperosmolar non-ketotic hyperglycaemia?

A

osmotic diuresis

51
Q

symptoms of osmotic diuresis

A

dehydration
increased blood viscosity
can lead to thromboembolism

52
Q

differences between DKA and HNKH

A

DKA has more insulin deficiency

HNKH has higher glucose levels and more fluid deficiency

53
Q

What is HNKH characterised by?

A

lack of ketosis

pro-inflammatory mediators promote insulin resistance

54
Q

symptoms of HNKH

A

confusion to coma

sometimes seizures

55
Q

bloods for HNKH

A

K and Na normal

creatinine high

56
Q

treatment for HNKH

A
  1. fluid replacement - NaCl 0.9% or 0.45%, K if needed
  2. insulin - not aggressive (fluid replacement lowers glucose)
  3. treatment for thromboembolism
57
Q

What age group does HNKH occur in?

A

middle aged or elderly people

58
Q

synergistic factors for HNKH

A
  • insulin deficiency
  • increased levels of counter-regulatory or stress hormones
  • increased gluconeogenesis and glyconeolysis
  • inadequate use of glucose by peripheral tissue
59
Q

What causes insulin resistance in HNKH?

A
  • proinfmalatory mediators like TNF-alpha, IL-6, IL-1
  • they release counter regulatory hormones
  • cause insulin resistance and hyperglycaemia
60
Q

What can insulin levels do and not do in HNKH?

A

insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly

61
Q

diagnosis for HNKH? (7)

A
  • non-ketotic hyperglyaemia
  • mild acidosis without ketone production
  • slight confusion to coma
  • sometimes seizures
  • plasma Na and K normal
  • creatinine high
  • fluid deficit is 10L (can lead to circulatory collapse)
62
Q

How does fluid replacement help in HNKH?

A

stabilises BP

improves circulation and urine output

63
Q

other diabetic complications

A
  • impaired vision/retinopathy/cataract/glaucoma
  • nephropathy: renal failure
  • sensory loss, motor weakness
  • postural hypotension
  • GIT problems
  • foot disease
  • MI/ischaemia
  • TIA/stroke
  • dental
  • increased infection risk
64
Q

diabetes drug treatment (basic 3 steps)

A
  1. monotherapy: single non-insulin blood glucose lowering therapy
  2. dual therapy: 2 therapies (non-insulin)
  3. triple therapy: 3 non insulin OR any treatment combination containing insulin
65
Q

T2DM - when is metformin given?

A

HbA1c rises to 48 mmol/mol

on lifestyle interventions

66
Q

When to add on treatment to metformin?

A

HbA1c rises to 58 mmol/mol

67
Q

When is triple therapy considered?

A

HbA1c rises to 58 mmol/mol

68
Q

HbA1c aim for dual therapy?

A

53 mmol/mol

69
Q

HbA1c aim for triple therapy?

A

53 mmol/mol

70
Q

What is added in dual therapy? (metformin)

A

either:

  • sulfonylurea
  • pioglitazone
  • DPP4 inhibitor
  • SGLT-2 inhibitor
71
Q

first line therapy if metformin is c/i or not tolerated

A

DPP-4i
pioglitazone
sulfonylurea

PHA223 (43 decks)

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