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PHA 332 > diabetes pathophysiology pavreen > Flashcards

diabetes pathophysiology pavreen Flashcards

1
Q

how many glands are in the pancreas?

A

the pancreas is two glands in one. the digestive gland and the endocrine gland

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2
Q

what is the function of the digestive gland in the pancreas?

A

digestion. it secretes alkaline pancreatic rich juice digestive enzymes into the duodenum through the pancreatic duct to aid digestion

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3
Q

what does the endocrine gland in the pancreas consist of?

A

Endocrine tissue of the pancreas consists multiple small clusters of cells scattered throughout the gland called the pancreatic islets or Islets of Langerhans which discharge secretions directly into the bloodstream

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4
Q

what is an islet? and what are they composed of?

A

small clusters of cells in the gland.

they consist of several different types of cells : alpha beta delta and f cells

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5
Q

what do f cells secrete?

A

they secrete pancreatic polypeptides

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6
Q

what does the core and the mantle consists of ?

A
  • The core islets for producing beta cells and mantle consists of other cells a,d,f
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7
Q

what are pancreatic acini?

A

the are multiple cells surrounded by capillaries which allows exchange of larger molecules

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8
Q

where are these acini found most commonly?

A

in areas that require large exchanges between blood and tissues

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9
Q

what are the 3 main types of cells in the pancreas?

A

islet alpha, beta and delta

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10
Q

what is the function of islet alpha cells? where is it found?

A
  • secrete glucagon
  • raises blood glucose
  • Located at the periphery of the islet
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11
Q

what is the function of islet beta cells? where are they found?

A
  • secrete insulin
  • lowers blood glucose
  • Predominate cell type found in the core of theislets
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12
Q

what is the function if islet delta cells?

A
  • Produce gastrin and somatostatin

* Somatostatin inhibits secretion of glucagon and insulin

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13
Q

what is the difference between type one and type two diabetes? (cause)

A
  • Type 1 Diabetes; cause is insulin deficiency
  • Type 2 Diabetes; typically an adult-onset diabetes; cause is inadequate response to insulin; becoming more common in children
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14
Q

what is hyperglycemia?

A

Manifestation is elevated glucose levels in blood called hyperglycemia

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15
Q

what occurs when there is low blood glucose?

A

a cells secrete glucagon
they act on hepatocytes to produce glycogenolysis and glycogeneogenesis
this release of glucose by hepatocytes increases blood sugar level to normal
if blood glucose continues to inc hyperglycaemia inhibits glucagon secretion

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16
Q

what hapoens when there is high blood glucose?

A

stimulates beta cells to secrete insulin
this accelerates faculitated diffusion of glucose into cells
inc conversion of glucose to glycogen- glycogenesis
inc uptake of amino acids and inc protein synthesis
inc synth of fatty acids
dec glycogenolysis and gluconogenesis
therefore dec blood glucose levels
if blood glucose levels continues to drop

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17
Q

what are the regulatory hormones and counter-regulatory hormones for diabetes?

A

regulatory- insulin
counter regulatory- glucagon, ad, glucocorticosteroids
, growth hormone

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18
Q

what does insulin do?

A

increases glucose uptake, glycogen synthesis, decrease glycogenolysis and glucogenesis
overal decreases lood glucose

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19
Q

how is insulin made up?

A

small protein- 551 amino acids which are linked y disulphide bridges
a chain has 21 aa
b has 30 and c is synthesised as a prohormone

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20
Q

what is proinsulin?

A

long single chain molecule and is processed into beta cells, packed into granules and it is hydrolised into connecting segment called the C peptide
pro insulin is released as insulin and c-peptide

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21
Q

what regulates insulin secretion?

A

insulin is the main regulator

amino acids, ketones, nutrients and neurotransmitters allso affect the rate

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22
Q

what rate is glucose released from the pancreas?

A

glucose is released at a low rate from the pancreas and at a higher rate after stimulation such as glucose

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23
Q

what is an insulin secretory burst?

A

usually in response to a stimulus. rapid first stage preformed insulin from granules in b cells
longer phase is consequence of a newly synthesized insulin,

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24
Q

how does the insulin dependent glucose transporter work?

A

insulin binds to insulin receptor of the cell membrane
generation of intracellular signal
insertion of GLUT-4 receptor from its active site into the cell membrane
transport of glucose across the cell membrane

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25
Q

why are GLUT transporters needed?

A

as cell membranes are impermeable to glucose

faster rate than diffusion alone

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26
Q

what are the different types of GLUT transporters?

A

glut 4,2 1

27
Q

what is GLUT 4 responsible for?

A

Insulin dependant glucose transporter for skeletal muscle and adipose tissue. It is inactive and inside the cell membrane; active when insulin causes it to move from its inactive site to the cell membrane

28
Q

what is GLUT 2 responsible for?

A

Major transporter of glucose into beta cells and liver cells. It has low affinity for glucose and acts when glucose plasma glucose level are high

29
Q

what is GLUT 1 responsible for?

A

Present in all tissues . Does not require actions of insulin and important for transport of glucose into the cells of the nervous system.

30
Q

how is diabetes aetiology classified?

A

Type 1 (β-cell destruction usually leading to absolute insulin deficiency)•Autoimmune T-cell mediated (type 1A)•Idiopathic (type 1B)

Type 2 (ranges from predominantly insulin withrelative insulin deficiency secretory defect with orwithout insulin)

other

31
Q

what is the insulin dependent glucose transporter process?

A

1-binding of insulin to insulin receptor on the surface of the cell membrane
2-generation of intracellular signal
3-insertion of GLUT 4 receptor from its inactive site into the cell membrane
transport of glucose across cell membrane

32
Q

what are the clinical features of type 1 diabetes?

A 
beta cell destruction
islet cell antibodies present
strong genetic link
age onset usually less than 30
faster onset of symptoms
insulin must be administered
body weight normal or low
extreme hyperglycaemia causes diabetic ketoacidosis
33
Q

what are the clinical features of type 2 diabetes/

A 
no beta cell destruction
no islet cell antibodies present
very strong genetic link
age of onset usually greater than 40
slower onset of symptoms
diet control and oral hypoglycemic agents
body weight usually obese
extreme hyperglycemia causes hyperosmolar non-kenotic hyperglycaemia
34
Q

what is the mechanism of islet

beta cell destruction ?

A

t cells react against beta cell antigens resulting in cell damage
t helpers activate macrophages directed at beta cells
cytotoxic t cells directly kill beta cells
locally produced cytokines damage b cells
autoantibodies against beta cells and insulin are detected in 70-80% of patients

35
Q

what are the factors involved in the development of type 1 A diabetes?

A

genetic predisposition
hypothetical triggering event involving an environmental agent that incites an immune response
immunologically mediated beta cell destruction

36
Q

what are the factors involved in the development of type 1 b diabetes?

A

cases of beta cell destruction in which no evidence of autoimmunity is present
strongly inhertied
episodic ketoacidosis due to varying degrees of insulin deficiency

37
Q

what does lack of insulin cause?

A

decreased anabolism
increased catobolism
increased sec of glycagon, cortisol, GH and catecholamines

38
Q

what does a decrease in anabolism cause

A

hyperglycaemia ( fatigue)
glycosuria ( vulvitis balantis)
osmotic diuresis ( poly polysipsia)
salt and water depletion ( tachycardia and hypotension)

39
Q

what does increased catabolism cause?

A 
inc in glycogenolysis
increase glyconeogenesis-wasting
inc lipolysis- weight loss
hyperketonaemia
acidosis- hyperventilation and peripheral vasodilation
diabetic ketoacidosis
40
Q

what factors cause a suboptimal response to insulin in type 2 diabetes?

A

obesity, genetic predisposition, physical inactivity

41
Q

what is the difference between metabolic syndrome and type 2 diabetes?

A

metabolic syndrome: –Triglycerides–HDL–Hypertension–Systemic inflammation–Fibrinolysis–Abnormal function ofthe vascularendothelium–Macrovascular disease

t2 diabetes: Obesity and insulinresistance
•Increased resistance tothe action of insulin
•Impaired suppressionof glucose productionby the liver
•Hyperglycemia andhyperinsulinemia

42
Q

how do you diagnose diabetes?

A

the three polys of diabets
Polyuria
–Excessive urination•Polydipsia–Excessive thirst•Polyphagia–Excessive hunger

WHO method- glucose concentrations in blood

43
Q

when do you initiate for oral glucose test?

A

Fasting plasma glucose 6.1-7.0mmol/l (110-126mg/dl)

Random plasma glucose 7.8- 11.1 mmol/l (140- 199mg/dl)

44
Q

what is HbA1c and how is it used in diabetes?

A

Elevatedglycated haemoglobin levels (HbA1c)- key test used to monitor long –term glycaemia control in diagnosed patients
good to check compliance and long term control

45
Q

what is hypoglycaemia?

A
  • Occurs in those treated with insulin and occasionally in those with a sulphonyl urea drug and rarely with metformin.
  • Decreased glucose in serum (< 3.5 mmol/l or 63mg/dl) is termed as hypoglycemia.
  • Excessive treatment of hyperglycaemia may result inhypoglycaemia.
46
Q

what are the symptoms of Hypoglycaemia?

A

Autonomic: •Sweating •Trembling •Tachycardia •Palpitations
•Pallor

Neuroglycopenic:
•Faintness
•Loss of concentration
•Drowsiness
•Visual disturbances
•Abnormal behaviour (agitation, aggressiveness)
•Confusion
•Coma

Other
•Hunger
•Headache
•Tiredness

47
Q

what are the causes of hypoglycaemia and what action should you take to combat it?

A

Missed , delayed or inadequate meal↓ carbohyrate intake, ↓ glucose level

↑ dose of insulin↑ uptake of glucose into cells ; ↑ storage of glucose as glycogen
↑ Exercise ↑ uptake of glucose into cells
increased alcohol consumption: Impaired gluconeogenesis
Liver disease Impaired gluconeogenesis & glucogenolysis
Introduction of other blood lowering drugs to oral agents Enhanced hypoglycaemic effect

48
Q

how do you treat hypoglycaemia?

A
  • Early treatment carbohydrate meal.•10-20g of rapidly absorbing carbohydrates
  • Process repeated in 15-20 minutes if glucose concentration remains <60 mg/dl or if patient is symptomatic.
49
Q

what is the recommended iv dextrose to be given to children?

A

•The recommended dose of i.v. dextrose in children is0.2g/kg.

50
Q

what are the cardinal biochemical features of Diabetic Ketoacidosis?

A
  • Hyperglycaemia
  • Hyperketonaemia
  • Metabolic acidosis
51
Q

what are the signs and symptoms of diabetic ketoacidosis?

A

Polyuria, thirst
Weight loss Weakness Nausea, vomiting Leg cramps Blurred vision Abdominal pain

Dehydration Hypotension Cold extremities Tachycardia Air hunger Smell of acetone Hypothermia Confusion, drowsiness, Coma

52
Q

how is ketoacidosis managed?

A 
Fluid replacement•0.9% sodium chloride
•Fluid volume expansion
•Infusion of Insulin
•Correction of hyperglycaemia and presence of ketones
•Potassium
•Prevention of hypokalemia
•None in first hour unless <3.0mmol/l
•Treatment for any associated infection
53
Q

what is Hyperosmolar non-ketotic hyperglycaemia?

A 
•No ketone production or severe acidosis
•Due to  severe osmotic diuresis
•Causing dehydration
•Increase blood viscosity
•May lead to thromboembolism
associated with type 2 diabetes
54
Q

how does HNKH Differ from diabetic ketoacidosis (DKA)?

A

•In the degree of insulin deficiency (more profoundin (DKA)•The elevation of glucose levels and degree of fluiddeficiency (more marked in HNKH)

55
Q

what are the Synergistic factors of HNKH?

A
  • Insulin deficiency
  • Increased levels of counter-regulatory or stresshormones
  • Increased gluconeogenesis and glycogenolysis
  • Inadequate use of glucose by peripheral tissue
56
Q

what is HNKH characteristed by?

A
  • Characterized by a lack of ketosis
  • Proinflammatory mediators (TNF-α, IL-6, IL-1 also promote insulin resistance and release of counterregulatory hormones insulin resistance and hyperglycaemia
  • Because of this the amount insulin required to inhibit fat breakdown is less than that needed for effective glucose transport
57
Q

what are the diagnostic features of HNKH?

A
  • Non-ketotic hyperglycaemia (often in a regionof 55mmol/l)
  • Mild acidosis without ketone production
  • Slight confusion to coma
  • Sometimes seizures
  • Plasma Na+and K+usually normal
  • Creatinine is high
  • Fluid deficit is 10L; lead to circulatory collapse
58
Q

what is the treatment for HNKH?

A
  • Fluid replacement
  • Stabilize BP ; improve circulation and urineoutput
  • Sodium Chloride 0.9% or 0.45%
  • Potassium added if required
  • Insulin given but not aggressive
  • Because fluid replacement also lowers plasmaglucose levels
  • Prophylaxis treatment for thromboembolism
59
Q

what are some of the diabetic complications?

A 
reinopathy- impaired vison
neuropathy- impared  renal function
cornary heart disease
peripheral vascular disease
cerebrovascular disease
60
Q

what is the drug treatment for diabetes?

A

1- single non-insulin blood glucose lowering therapy
2- 2 non-insulin blood lowering therapies in comb
3- 3 non0insulin therapy or any treatment combination containing insulin

61
Q

what if HbA1c rises to 48mmol/mol?

A

standard release metformin- if not tolerated try MR

62
Q

what happens if HbA1c rises to 58mmol/mol?

A 
add sulfonylurea
add pioglitazone
add DPP4 inhibitor
add SGLT 2 inhibitor
support the person to aim to 53mmol/mol
63
Q

what is triple therapy?

A 
1SGLT2
2sulfonlyurea
SGLT2
3 sultonylurea
SGLT2

or insulin based treatment

64
Q

what if metformin not tolerated?

A

DPP-4i, pioglitazone or SU

PHA 332 (42 decks)

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