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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
Which GLUT transporter needs insulin to become activated?
GLUT-4
26
2 types of T1DM?
type 1A - autoimmune T-cell mediated | type 1B - idiopathic
27
What causes gestational diabetes?
excess hormone production during pregnancy causes insulin resistance
28
risks of gestational diabetes
``` macrosomia microsomia neonatal hypoglycemia polycythemia electrolyte disorders respiratory distress syndrome ```
29
beta cell destruction in T1 vs T2
T1 yes | T2 no
30
islet antibodies in T1 vs T2
T1 yes | T2 no
31
genetic link in T1 vs T2
T1 strong | T2 very strong
32
age of onset of T1 vs T2
T1 < 30 | T2 >40
33
onset of symptoms in T1 vs T2
T1 fast onset | T2 slower onset
34
management of T1 vs T2
T1 insulin administered | T2 diet control and oral hypoglycaemic agents
35
body weight in T1 vs T2
T1 low or normal | T2 obese
36
extreme hyperglycaemia in T1 vs T2
T1 causes diabetic ketoacidosis | T2 causes hyperosmolar non-ketotic hyperglycaemia
37
What causes T1DM?
severe lack of insulin caused by autoimmune mediated destruction of islet beta cells
38
mechanism of beta cell destruction
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
difference between type 1A and B
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
causes of T2DM
metabolic syndrome: - triglycerides - HDL - hypertension - systemic inflammation - macrovascular disease - obesity - insulin resistance - impaired suppression of glucose by the liver
41
diagnosis (3 polys)
polyuria (excess urination) polydipsia (thirst) polyphagia (hunger)
42
3 diabetic emergencies
- hypoglycaemia - diabetic ketoacidosis - hyperosmolar non-ketotic hyperglycaemia
43
What is hypoglycaemia?
glucose levels < 3.5 mm/l or 63 mg/dl
44
causes of hypoglycaemia
- missed/delayed/inadequate meal - increased dose of insulin - increase exercise - increased alcohol consumption - liver disease - blood lowering drugs with oral agents
45
treatment of hypoglycaemia
10-20g carbohydrate meal | repeat after 10-20 mins if glucose <60 mg/dl or symptomatic
46
foods with 15g carbs
- 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
hypoglycaemia if unable to swallow
- IV glucose (30-50ml dextrose 20-50%) - children IV dextrose 0.2 mg/kg - viscous glucose gel to mouth or jam/honey
48
3 signs of diabetic ketoacidosis
1. hyperglycaemia 2. hyperketoanaemia 3. metabolic acidosis
49
treatment for diabetic ketoacidosis
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
What causes hyperosmolar non-ketotic hyperglycaemia?
osmotic diuresis
51
symptoms of osmotic diuresis
dehydration increased blood viscosity can lead to thromboembolism
52
differences between DKA and HNKH
DKA has more insulin deficiency | HNKH has higher glucose levels and more fluid deficiency
53
What is HNKH characterised by?
lack of ketosis | pro-inflammatory mediators promote insulin resistance
54
symptoms of HNKH
confusion to coma | sometimes seizures
55
bloods for HNKH
K and Na normal | creatinine high
56
treatment for HNKH
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
What age group does HNKH occur in?
middle aged or elderly people
58
synergistic factors for HNKH
- insulin deficiency - increased levels of counter-regulatory or stress hormones - increased gluconeogenesis and glyconeolysis - inadequate use of glucose by peripheral tissue
59
What causes insulin resistance in HNKH?
- proinfmalatory mediators like TNF-alpha, IL-6, IL-1 - they release counter regulatory hormones - cause insulin resistance and hyperglycaemia
60
What can insulin levels do and not do in HNKH?
insulin levels are sufficient to prevent excessive lipolysis but not to use glucose properly
61
diagnosis for HNKH? (7)
- 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
How does fluid replacement help in HNKH?
stabilises BP | improves circulation and urine output
63
other diabetic complications
- 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
diabetes drug treatment (basic 3 steps)
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
T2DM - when is metformin given?
HbA1c rises to 48 mmol/mol | on lifestyle interventions
66
When to add on treatment to metformin?
HbA1c rises to 58 mmol/mol
67
When is triple therapy considered?
HbA1c rises to 58 mmol/mol
68
HbA1c aim for dual therapy?
53 mmol/mol
69
HbA1c aim for triple therapy?
53 mmol/mol
70
What is added in dual therapy? (metformin)
either: - sulfonylurea - pioglitazone - DPP4 inhibitor - SGLT-2 inhibitor
71
first line therapy if metformin is c/i or not tolerated
DPP-4i pioglitazone sulfonylurea

PHA223 (43 decks)

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