Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Type 1 Diabetes and Hypo management > Flashcards

Type 1 Diabetes and Hypo management Flashcards

1
Q

what are the symptoms of T1DM

A

weight loss, excessive thirst, polyuria, fatigue

can also be headache, anxiety, muscle spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are GAD autoantibodies

A

antibody often seen in T1DM, destroys GAD cells (in pancrease) which produce the enzyme glutamate decarboxylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is T1DM

A

autoimmune beta cell destruction leading to absolute insulin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is type two DM

A

progressive sensory defect on the background on insulin resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is gestational DM

A

diabetes diagnosed in 2nd/3rd trimester that is not clearly overt diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the two types of monogenic diabetes

A

neonatal DM and MODY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

give an example of an endocrine pancreas disease that can cause diabetes

A

cystic fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what can induce diabetes

A

drugs (HIV treatment, organ transplant) or chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what cell mediates T1DM

A

T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the onset of T1DM like

A

prolonged, months to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what causes T1DM

A

genetic susceptibility and environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how long before symptoms begin

A

need to have lost 80-90% of beta cells before marked hyperglycaemia occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what other autoimmune conditions is T1DM associated with

A

thyroid, coeliac (1:20 will have T1DM), addisons, pernicious anaemia, vitiligo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is LADA

A

latent autoimmune diabetes of adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is the presentation of LADA

A

slowly progressive disease onset, non obese, no FHx T2DM, age >35 at onset, mild insulin resistance, low C peptide, HLA gene positive (GAD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does a positive GAD mean

A

80% of + will be insulin dependent in 6 years

75-84% of recent onset T1DM will be GAD +

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what does C peptide show

A

how much insulin is being produced, low= low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the incidence of T1DM in scotland

A

1 in 25, 3rd in the world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is polyglandular endocrinopathy type 2

A

autoimmune conditions that causes T1DM along with (any/all of):

  • addisons disease
  • hypothyroidism
  • hypogonadism
  • vitiligo
  • coeliac

(not linked to a gene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is polyglandular endocrinopathy type 1

A 
(autosomal recessive)
mild immune deficiency with T1DM, addisons, hypothyroidism, hypogonadism, vitiligo, coeliac 
PLUS there may also be:
-alopecia
-pernicious anaemia
-hypoparathyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the difference in histology between T1DM and T2DM

A

T1DM- lymphocytic infiltrate attacking islets

T2DM- amyloid deposition in islet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the islet autoantibodies

A

IA-2, IA-2beta, GAD65, ZnT8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how many newly diagnosed cases will have positive antibodies - what can cause them to vary

A

70-80%

age, ethnicity, gender, quality of assay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what autoantibodies are most commonly tested

A

IA-2, GAD, Znt8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what gene is associated with T1DM

A

chromosome 6, HLA DR3, DR4 and DQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does insulin deficiency affect protein metabolism

A

increase protein catabolism =
increased AA in plasma
urinary nitrogen loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how does insulin deficiency affect lipid metabolism

A

increased lipolysis =
increased plasma FFA
ketogenesis
ketonuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the function of insulin

A

released in response to carbohydrate, suppresses glycolysis and stimulate glycogenesis and lipogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

is insulin anabolic or catabolic

A

anabolic- insulin deficiency a catabolic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the features of insulin deficiency

A

accelerated starvation, hyperglycaemia, hepatic gluconeogenesis, lipolysis, protein catabolism, reduced glucose storage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what happens to the alpha and delta cells when beta cells destroyed

A

are dysregulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the symptoms of diabetic ketoacidosis

A

vomiting, abdominal pain, altered consciousness,
acidotic beathing, pH
<7.3, urine ketones +++, dehydrated, coma/death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the classical presentation of T1DM

A

acute onset, presents with DKA or severe symptoms, pre-school and peri-puberty (can present at any age), non obese, insulin dependant, FHx uncommon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the BM diagnosis guidelines

A

a random venous plasma glucose concentration ≥ 11.1 mmol/l or
a fasting plasma glucose concentration ≥ 7.0 mmol/l (whole blood ≥ 6.1 mmol/l) or
two hour plasma glucose concentration ≥ 11.1 mmol/l two hours after 75g anhydrous glucose in an oral glucose tolerance test (OGTT).
An HbA1c of 48mmol/mol (6.5%) is recommended as the cut off point for diagnosing diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the long acting, background insulins

A

glargine and determir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the mealtime insulins

A

aspart, lispro and gulisine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

why do you need more insulin to achieve homeostasis in T2DM

A

as patients will all be hyper insulinaemic (too much insulin compared to glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what can cause glucose variability even with correct insulin dosages

A

injection- failure to mix insulin, accuracy of device, leak from injection site

external factors- exercise and temp will increase absorption

tissue- injection into muscle (will increase absorption), lipohypertrophy, blood supply

carb delivery- meal constituents, gastroparesis (delayed stomach emptying- increased fat in the meal)

39
Q

what is DAFNE

A

dose adjustment for normal eating

40
Q

what does high glucose over time cause

A

micro (retinopathy, nephropathy, neuropathy) and macro (heart, stroke and peripheral limb ischaemia) vascular disease

41
Q

how do you evaluate metabolic control

A

glycated haemoglobin (HbA1c)

42
Q

what is HbA1c

A

formed by non enzymatic glycation of haemoglobin on exposure to glucose- shows how much glucose has been in blood over past 6-8 weeks

43
Q

what can HbA1c vary with

A

haemolytic anaemia, blood loss, pregnancy

44
Q

what are the markers for HbA1C

A

42 and above pre-diabetes
48 and above diabetes
75 and above high risk of complications
goal for diabetics 52

45
Q

how do you monitor blood glucose

A

BM, urine, implanted devices (freestyle libre)

46
Q

what resp condition is made in diabetes

A

cystic fibrosis

47
Q

what is DIDMOAD or wolfram syndrome

A 
Diabetes Insipidus
Diabetes Mellitus
Optic Atrophy
Deafness
Neurological anomalies
48
Q

what is bardet biedl syndrome

A 
Often very obese
Polydactyly
Hypogonadal
Visual impairment
Hearing impairment
Mental retardation
Diabetes

Consanguineous parents

49
Q

what is the treatment foe T1DM

A

insulin, DAFNE

50
Q

what are the prandial insulins

A

insulin analogues- insulin aspart, lispor, gluisine

soluble insulin- actrapid, humulin S

51
Q

what are the basal insulins

A

insulatard, humulin I, glargine, determir

52
Q

what can happen if there is repeated insulin injections at the same site

A

lipohypertrophy, insulin absorption poor, problems with hypo and hyperglycaemia

53
Q

what happens if you inject insulin into subcutaneous oedema

A

delays insulin absorption

54
Q

what happens when you inject insulin into muscle

A

is absorbed too quickly, can cause hypoglycemia

55
Q

what is the concentration of the vast majority of insulin in hospital

A

100 units per millilitre

56
Q

should all insulin be kept in the fridge

A

opened ‘in-use’ insulin devices are stable at room temperature for one month
in use devices should not be kept in the fridge in hospital to avoid cross infection
unopened vials/ devices should be stores in the fridge

57
Q

what is hypoglycaemia

A

a BG less than 4 millimoles per litre

58
Q

what medications can cause hypos

A

sulphonylureas- gliclazide, glipizide, glimepiride, glibenclamide
insulin

59
Q

what hormones are released in the body in response to hypoglycaemia

A

adrenaline, glucagon, cortisol, growth hormone

aimed to release glucose from the liver

60
Q

when in hypglycaemia can glucose release be impaired

A 
if patients are:
malnourished 
have had repeated hypoglycaemia 
have severe liver disease 
excessive alcohol consumption
61
Q

what causes the symptoms of hypos

A

the activation of the autonomic nervous system

62
Q

what are the symptoms of a hypo

A 
trembling
anxiety
palpitations 
numbness and tingling around lips/finger tips 
irritability 
hunger
pale and sweaty 
feel vulnerable or afraid
63
Q

what are the neuroglycopenic symptoms of a hypo

A

when the brain becomes short of glucose (usually at 2mmol/L or lower)

  • weakness
  • concentration and coordination difficulties
  • vision problems
  • slurred speech
  • loss of consciousness
  • seizure
64
Q

what is the treatment for hypos

A

if patient can swallow- 15-20g of fast acting carbohydrates:

  • glucose tablets
  • glucose gel if drowsy but can swallow (squeezed between teeth and gums

unconscious patients:

  • stop insulin IV
  • IV glucose
  • subcutaneous/ IM glucagon
65
Q

in treating hypos who should you avoid giving fruit juice to

A

patients with renal failure

66
Q

when might glucagon be ineffective

A

undernourish patients or those with severe liver disease, repeated hypos
or those who have had an OHA induced hypo

67
Q

how is glucagon stored and administerd

A

in fridge
subcutaneously/ IM/ IV
adult (>25kg) dose 1mg, child 500 micrograms

68
Q

how do you prevent the recurrence of hypos

A

think what caused it
check BG every 15 mins after treatment
if BG still under 4 mmol/L give more glucose

after initial 20 grams of more complex carbs should be given to those who can swallow (bread, biscuits) or IV infusion if they cant swallow

69
Q

what is the target BG range for inpatients

A

6-12mmol/l

70
Q

what must quick acting insulins always be given with

A

carbohydrates- cover snacks, meal times with carbs

71
Q

what are the types of quick acting insulins

A

rapid acting analogue, short acting (soluble) insulin)

72
Q

give examples of rapid acting insulin analogues

A

humalog, novorapid, apidra

73
Q

what is the action of onset and duration of rapid acting analogues

A

immediate onset, peak at 2 hours, last 4 hours

74
Q

what is the action of onset and duration of short acting soluble insulin

A

30 mins before effect, peak at 4 hours, lasts 8 hours

75
Q

give examples of short acting soluble insulin

A

actrapid, humulin S, insuman rapid

76
Q

give examples of intermediate acting insulin- how long do they last

A

insulatard, humulin I, ismuman basal (last 16 hours)

77
Q

give examples of long acting analogue insulin - how long do they last

A

lantus and levemir basal insulin (last 24 hours

78
Q

what is in fix mix insulin

A

rapid acting analgoue intermediate mixture

short acting- intermediate mixture

79
Q

name 5 bolus insulins

A

novorapid, humalog, humulin S, aprida, actrapid

80
Q

what effect does acute kidney injury have on insulin duration

A

reduces insulin secretion- effects will last longer

81
Q

how much change in insulin is recommended to improve BG control

A

+/- 10%
whatever time you measure BG to be high or low, increase the dosage of the previous meal in the next day (high at lunch, increase breakfast dose, low at breakfast reduce basal dose)

82
Q

what insulin at not at standard concentration

A

tresiba, humalog, toujeo, humunlin R

83
Q

what are the indications for IV insulin

A

acute illness
DKA
HHS
unable to take oral/ fasting patients

84
Q

is IV insulin good for people who are eating and drinking

A

not generally suitable

85
Q

how long is IV insulins half life

A

approx 5 mins

86
Q

what can prolonged IV insulin cause

A

cannula related complications (infection), electrolyte abnormalities (hyponatraemia)

87
Q

what separate infusions are given with IV insulin (through same cannula)

A

Iv glucose and potassium
insulin in solution of sodium chloride
different fluids for different clinical needs

88
Q

patients switching to IV insulin should continue what

A

subcutaneous long acting basal insulin if they already take it

89
Q

after how long must all IV insulin solutions be discarded

A

24 hours

90
Q

how often do you monitor BG in IV insulin

A

hourly

91
Q

when can you switch from IV insulin to subcutaneous

A

when patient is stable and 30- 60 mins after short acting (and long acting basal if not already still on that) has been given
queck BG 4 times daily after stopping IV insulin

92
Q

when can you restart oral medication from IV insulin

A

after patient is tolerating food and clinically stable

93
Q

what else should be measured when on IV glucose

A

daily urea and electrolytes

Endocrinology (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions