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metabolic diseases > diabetes > Flashcards

diabetes Flashcards

1
Q

type 1 patho

A

autoimmune destruction of the pancreatic β cells

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2
Q

what other diseases is type 1 associated with

A

autoimmune thyroid disease, Addison’s disease and pernicious anaemia

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3
Q

clinical presentation of type 1

A

polyuria, polyphagia, polydipsia, blurred vision, glycosuria, macrovascular and microvascular disease, acetone breath, weight loss, Kussmaul breathing, nausea and vomiting

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4
Q

kaussmauls breathing

A

laboured breathing - metabolic acidosis

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5
Q

why weight loss in type 1

A

fluid depletion and breakdown of fat and muscle secondary to insulin deficiency

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6
Q

dietary advice to type 1

A

low sugar, high carb, low fat

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7
Q

conservative measures for type 1

A 
BMI measurement 
Smoking cessation 
Decrease alcohol intake 
Regular blood glucose 
encourage excersize
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8
Q

what should be monitored on type 1

A

HbA1c monitoring

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9
Q

type 1 insulin

A

Short-acting (soluble) insulins
Short-acting insulin analogues
Longer-acting insulins

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10
Q

investigations for type 1

A

Fasting plasma glucose
Random plasma glucose
HbA1c

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11
Q

clinical features of type 2

A

polyuria, polyphagia, polydipsia, blurred vision, glycosuria, macrovascular and microvascular disease

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12
Q

type 2 drugs

A

Metformin, Thiazolidinediones, incretins, SGLT2 inhibitors, Sulfonylureas

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13
Q

metformin MOA

A

reduces glucose production by the liver and sensitizes target tissues to insulin

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14
Q

Sulfonylureas MOA

A

promote insulin secretion

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15
Q

common Sulfonylureas

A

Gliclazide and glipizide

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16
Q

common side effects of Sulfonylureas

A

hypoglycaemia and weight gain

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17
Q

only oral agent shown to reduce cardiovascular risk in diabetes

A

metformin

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18
Q

Thiazolidinediones other name

A

glitazones

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19
Q

what do Thiazolidinediones activate

A

peroxisome proliferator-activated receptor-gamma (PPAR-γ)

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20
Q

what is peroxisome proliferator-activated receptor-gamma (PPAR-γ)

A

a nuclear receptor which regulates genes involved in lipid metabolism and insulin action

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21
Q

Thiazolidinediones MOA

A

educe hepatic glucose production and enhance peripheral glucose uptake

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22
Q

Thiazolidinediones side effects

A

weight gain, fluid retention and heart failure, anaemia and osteoporosis

23
Q

who is Thiazolidinediones contraindicated in

A

patients with heart failure

24
Q

Incretins mimic

A

glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1)

25
Q

where are (GIP) and (GLP-1) released from

A

intestine

26
Q

when are (GIP) and (GLP-1) released

A

after eating

27
Q

what does GLP1 do

A

promote insulin release, inhibit glucagon release, prolong gastric emptying and a reduce in hunger mediated by receptors in the brain

28
Q

SGLT2 inhibitors block

A

sodium/glucose transporter 2 (SGLT2)

29
Q

purpose of SGLT2

A

re-absorb glucose from the renal filtrate and restore it to the circulation

30
Q

type 2 investigations

A

Fasting plasma glucose
Random plasma glucose
HbA1c

31
Q

circumstances which people get diabetic ketoacidosis

A

Previously undiagnosed diabetes
Interruption of insulin therapy
The stress of intercurrent illness

32
Q

when might insulin be stopped

A

when a patient is not eating or vomitting - should not be stopped

33
Q

in type 1 when should insulin be stopped

A

never

34
Q

what is ketoacidosis

A

uncontrolled catabolism

35
Q

what happens when insulin is stopped - DKA

A

increase in hepatic gluconeogenesis

36
Q

in DKA there is peripheral lipolysis which leads to

A

increase in circulating free fatty acids

37
Q

in DKA what happens to the circulating free fatty acids

A

converted within the liver to acidic ketones

38
Q

what does production of acidic ketones in the liver result in

A

metabolic acidosis

39
Q

why is there dehydration in DKA

A

water and electrolyte loss from the kidney and exacerbated by vomiting

40
Q

what breathing do you get in DKA

A

Kussmaul’s respiration

41
Q

why are urea and creatine raised in DKA

A

as a result of dehydration

42
Q

management of DKA

A

Replace fluid and electrolyte loss, restore insulin and acid base balance

43
Q

HHS stands for

A

Hyperosmolar hyperglycemic state

44
Q

who gets HHS

A

uncontrolled type 2

45
Q

most common precipitating cause of HHS

A

infection

46
Q

how does HHS patient present

A

profound dehydration and a decreased level of consciousness

47
Q

management of HHS

A

Replace fluid and electrolyte loss, restore insulin and acid base balance

48
Q

drugs that can cause hypoglycaemia

A

insulin therapy and sulfonylurea therapy

49
Q

symptoms of hypoglycaemia

A

hunger, sweating, pallor and tachycardia

50
Q

treatment of hypoglycaemia

A

rapidly absorbed carbohydrate
intravenous dextrose followed by a flush of normal saline
Intramuscular glucagon
Oral glucose

51
Q

why give saline after dextrose

A

its highly irritant

52
Q

Intramuscular glucagon action

A

acts rapidly by mobilizing hepatic glycogen and is particularly useful where intravenous access is difficult

53
Q

when is oral glucose given

A

replenish glycogen reserves once the patient revives.

metabolic diseases (11 decks)

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