Brainscape's Knowledge GenomeTM

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


See full index

endocrine > diabetes > Flashcards

diabetes Flashcards

1
Q

how does alcohol intake increase the risk of hypoglycaemia?

A

alcohol inhibits gluconeogenesis

may impair hypo awareness and can impact on self care behaviours

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

auto antibodies associated with type 1 diabetes

A

GAD
IA-2
Znt8

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

what is the risk of children getting T1DM if their parents have it?

A

both - 30%

father - 8%
mother - 5%

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

what genes represent 50% of familial risk in T1DM?

A

HLA genes

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

cause of T!DM

A

cause unclear - may be genetic, can be triggered by certin viruses (coxsackie B virus, enterovirus)

pancreas stops veing able to produce insulin
T-cell mediated autoimmune disease

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

is T1DM more common in males or females?

A

males (post puberty)

can present at any age - peak around 10 to 14yrs

afriian, asian decent more at risk

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

T1DM presentation

A

hyperglycaemia, ketones
low insulin, beta cells and ketones

U18 = polyuria, polydipsia, weight loss, excessive tired

adults = rapid weight loss, ketosis, low BMI, fam autoimmune history, blurred vision

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

pathophysio of T1DM

A

no insulin being produced means cells can’t take glucose from blood + use it for fuel –> cells think body is being fasted + has no glucose supply

level of glucose keeps rising causing hyperglycaemia

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

T1DM diagnosis

A
  • symptoms + random glucose >11.1 mmol/l
  • asymptomatic + fasting >7 + 2hr post glucose load >11.1
  • antibodies - GAD, IA-2, Znt8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can blood glucose be monitored?

A

HbA1c - average over RBC lifespan, requires blood sent to lab
capillary glucose
flash glucose monitoring - lag of 5 mins, do cap glucose if hypo suspected

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

what does chronic exposure to hypergycaemia cause?

A

damage to endothelial cells of blood vessels - leads to leaky, malfunctioning vessels that are unable to regenerate

high levels of sugar in blood also causes suppression of the immune system + provides optimal environment for infectious organisms to thrive

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

long term complications of T1DM

A

macrovascular complications - CAD, peripheral ischaemia, stroke, hypertension

microvascular complications - peripheral neuropathy, retinopathy, nephropathy

infection related - UTIs, pneumonia, fungal infections (oral+vaginal candidiasis), foot infections

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

T2DM risk factors

A

older age
ethnicity - black, chinese, south asian
family history

obesity
sendentary lifestyles
high carb diet - esp refind carbs

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

T2DM presentation

A 
fatigue
usually obese
no ketone
polydispsia, polyuria
opportunistic infections
signs of complications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HbA1c + glucose levels in diabetes

A

HbA1c = >48

random glucose = >11
fasting glucose = >7
OGTT 2hr result = >11

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

What receptors are being over stimulated by the enhanced catecholamine effects in hyperthyroidism to cause her palpitations?

A

beta-1 receptors

Thyroid hormones increase the bodies sensitivity to catecholamines. The heart contains β1 receptors, which when activated by catecholamines results in an increase in heart rate.

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

Which test is most likely to be of clinical use in screening for medullary carcinoma recurrence?

A

serum calcitonin levels

Medullary thyroid cancers often secrete calcitonin and monitoring the serum levels of this hormone is useful in detecting sub clinical recurrence.

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

what are psammoma bodies?

A

clusters of calcification

Psammoma bodies consist of clusters of microcalcification. They are most commonly seen in papillary carcinomas.

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

drug treatment for T2DM

A
  1. metformin
  2. add one of: sulfonylurea, pioglitazone, DPP-4 inhibitor, SGLT-2 inhibitor
  3. triple therapy with metformin + 2 of above OR metformin + insulin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what drug treatment is preffered in T2DM patients with cardiovascular disease?

A

SGLT-2 inhibitors

GLP-mimetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

who does hyperosmolar hyperglycaemic state (HHS) commonly affect?

A

older people with T2DM who experience hyperglycaemia
–> can develop over weeks through a combo of illness + dehydration

high mortality (compared to DKA)

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

cause of HHS

A

high refined CHO intake pre-presentation (fizzy drinks)
diuretics and/or steroids

inadequate insulin or oral therapy, stopping medication during illness (swallowing difficulties/nausea)

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

pathophysio of hyperosmolar hyperglycaemic state (HHS)

A

hyperglycaemia results in osmotic diuresis with associated loss of sodium + potassium

severe volume depletion results in a significant raised serum osmolarity –> results in hyperviscosity of blood

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

HHS presentation

A

severe dehydration + electrolyte disturbances
dry mucous membranes
polyuria + thirst
nausea + vomiting
disorientation, gradual loss of consciousness

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

diagnosis of HHS (3 things)

A

hypovolaemia (lack of fluid)

hyperglycaemia (>30) WITHOUT ketonaemia or acidosis

raised serum osmolarity (>320)

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

complications of HHS

A

cardiovascular disease - MI, stroke (due to thickened blood)

sepsis - from underlying infection

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

management of HHS

A

correct fluid deficit + electrolyte abnormalities
monitor
IV insulin ONLY if ketones or blood glucose falling too slowly

treat underlying cause
prevent thromboembolism - LMWH unless contraindicated

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

which medication is lactic acidosis a key side effect of?

A

metformin

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

diabetic ketoacidosis (DKA)

A

T1DM (usually young) who is no producing/injecting adequate insulin

increase in counter-regulatory hormones - glucagon, cortisol, growth hormone

life threatening medi emergency

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

precipitants of DKA

A

insulin deficiency

increase insulin demand (infections, intoxication, infarction, surgery, steroids)

starvation

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

pathophysio of DKA

A

cellls have no fuel + think they are starving so iniate ketogenesis
–> overtime glucose + ketone levels both increase

initially kidneys produce bicarbonate to counteract the ketone acids in the blood + maintain normal pH
–> overtime bicarbonate is used up + blood starts to become acidic = ketoacidosis

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

DKA presentation

A 
abdo pain + tenderness
acetone breath
nausea + vomiting
polyuria + polydipsia/dehydration
altered consciousness
33
Q

diagnosis of DKA

A

hyperglycaemia = blood glucose >11

ketosis = blood ketone >3 or >2 on urine dipstick

acidosis = pH < 7.3

34
Q

priorities in management of DKA

A

dehydration, potassium imbalance, acidosis = what will kill patient

priority = fluid resuscitation
then insulin infusion

35
Q

treatment of DKA

A

FIG-PICK

Fluids - IV saline
Insulin
Glucose - monitor, add dextrose infusion if below certain level

Potassium - monitor
Infection - treat, possible trigger
Chart fluid balance
Ketones - monitor

-> slow infusions

36
Q

how are patients restarted on an insulin regime post DKA?

A

patients must be established on a normal insulin regime prior to stopping the insuline + fluid infusion (part of DKA treatment)

37
Q

complications of DKA

A

cardiac arrest/arrhmyias secondary to hypokalaemia

adult respiratory distress syndrome

cerebral oedema - esp in kids

gastric dilatation/stasis - risk of aspiration pneumonia

38
Q

key complication of DKA in kids

A

cerebral oedema

  • rapid correction with fluids + insulin causes rapid shift in water from extracellular space to intracellular space in brain cells
  • causes brain to swell + oedematous - brain cell destruction + death

*monitor for headaches, altered behaviour, SLOWLY give fluids

39
Q

conditions associated with hypoglycaemia

A 
coeliac disease
addisons/hypopituitarism
hypothyroidism
renal failure
gastroparesis
40
Q

risk factors for hypoglycaemia

A

previous severe hypo
longer duration diabetes
high risk indivdual - old, young, unaware of hypos

T1DM who have been on treatment a while

41
Q

common causes of hypoglycaemia

A 
missed/delayed meal
not enough carbs at last meal
increased physical activity
too much insulin
alcohol - esp. on empty stomach
tight control - little reserves for unexpected events
42
Q

hypoglycaemia presentation

A

tremor, irritability, anxious
hunger, weakness, fatigue
sweating
pallor, dizziness

43
Q

hypoglycaemia glucose level

A

glucose <4 mmol/L

severe hypo can lead to reduced consciousness, coma + death unless treated

44
Q

ways to reduce hypos

A

carry emergency supply of carb dense foods + diabetic ID
check blood glucose frequently - esp before bed

never consume alcohol on an empty stomach
be aware stress, illness, exercise effects blood glucose levels

45
Q

management of hypoglycaemia

A

rapid acting glucose (lucozade) + slow acting carbs (biscuit + toast) for when rapid is used up
–> 15-20g rapidly absorbed carbohydrate

severe = IV dextrose + intramuscular glucagon

46
Q

what is monogenic diabetes?

A

diabetes caused by a mutation in a single gene (mendelian disease)
->results in defects in insulin secretion or insulin action

commonest = MODY

47
Q

types of monogenic diabetes

A

defects in insulin secretion
> MODY
> neonatal diabetes

defects in insulin action
>insulin signalling - AKT, INSR
> fat storage - CIDEC

48
Q

Maturity Onset Diabetes of the Young (MODY)

A

autosomal dominant
non-insulin dependent diabetes

rare 1-2% of people with diabetes
90% misdiagnosed

49
Q

what is the typical age of onset of MODY?

A

usually before 25yrs

50
Q

types of MODY

A

transcription factor mutations
> HNF1-alpha (commonest)
> HNF1-beta
> HNF4-alpha

glucokinase

51
Q

MODY (HNF1-alpha)

A

commonest transcription factor mutation
lowers amount of insulin made by pancreas
autosomal dominant
adolescence onset

treatment = low dose sulphonylureas
risk of long term complications

52
Q

MODY (glucokinase)

A

helps recognise high glucose level in body
onset at birth
usually only slightly higher glucose than normal

no treatment - dietary only
no follow up, complications rare

53
Q

treatment of neonatal diabetes mellitus

A

high dose sulphonylureas

54
Q

treatment for diabetes related nephropathy

A

ACEi / ARB

55
Q

pathophysio of diabetes complications

A

excessive glucose, mitochondria can’t keep up so alternative pathways used
these preciptate -

> polyol pathway - osmotic damage
increased ROS
inflammation
fibrosis

56
Q

nephropathy in diabetes patients

A

caused by damage to capillaries in kidneys glomeruli, microvascular changes - angiopathy of capillaries

characterised by proteinuria + diffuse scarring of glomeruli

microalbuminuria is a marker of high risk

57
Q

types of neuropathy

A

peripheral - charcot foot, numb
proximal - bum leading to weakness in legs
autonomic - changes in bowel, heart/vessels (fainting)

focal - sudden weakness in one or a group - carpal tunnel, bells palsy

58
Q

management of diabetes during pregnancy?

A

Pre-pregnancy counselling
o Good sugar control preconception, limit risk of congenital malformation

Folic acid 5mg – more than in normal pregnancy
Consider change from tablets to insulin (T2DM)
Monitoring everything – HbA1c, BP, blood sugar

59
Q

preferred blood pressure medication in pregnancy?

A

labetalol
nifedipine
methydopa

ACEi = tetragenic

60
Q

types of weight loss surgery?

A

restrictive

  • gastric balloon
  • gastric band
  • sleeve gastrectomy

malapsorptive

  • gastric bypass (roux en y) = gold standard
  • bilio-pancreatic diversion
61
Q

when is orlistat recommended?

A

BMI >= 30 or >=28 with comorbidities

62
Q

guidelines for continuation of orlistat

A

lost >=5% of body weight in first 3 months

lost >=10% of bodyweight in first 6 months

63
Q

what is orlistat? when is it used?

A

non-systemic lipase inhibitor - used for weight loss

blocks 30% dietary fat

64
Q

diet when on orlistat

A

hypocaloric / low fat diet is essential

150/250 kcal deficit/day

65
Q

side effects of orlistat

A

stearrhoea
abdo pain
weird stools

66
Q

management of pre-existing diabetes in pregnancy

A

folic acid 5mg (pre-conception-12weeks)
regular eye checks - accelerated retinopathy
consider change from tablets to insulin in T2DM
monitor - HbA1c, BP

high risk - start aspirin at 12 weeks
avoid ACEi + statins - tetratogenic

67
Q

management of diabetes during labour

A

maintain good blood glucose

may require IV insulin + IV dextrose

68
Q

postnatal care of pregnant diabetics

A

lower insulin dose + be wary of hypoglycaemia, insulin sensitivity will increase after birth + with breast feeding

monitor baby for hypoglycaemia - feed frquently + maintain glood glucose above 2

69
Q

what are babies of mothers with diabetes at risk of?

A

neonatal hypoglycaemia
macrosomia (big babies)

polycythaemia (raised haemoglobin)
jaundice (raised bilirubin)
cangenital heart disease
cardiomyopathy

70
Q

gestational diabetes

A

diabetes triggered by pregnancy - resolves after birth

caused by reduced insulin sensitivity during pregnancy

71
Q

gestational diabetes risk factors

A

previos gestational diabetes
previous macrosomia baby (>= 4.5kg)
BMI >30
black caribbean, middle eastern, south Asian
family history of diabetes - first degree relative

(if RF = OGTT at 24-28weeks)

72
Q

clinical features of gestational diabetes

A

large for dates foetus
polyhydramnios (increased amniotic fluid)
glucose on urine dipstick

73
Q

gestational diabetes management

A

educate - monitoring, diet+exercise
4 weekly US scans to monitor foetal growth + amniotic fluid - from 28-36weeks
metformin then insulin - glibenclamide if cant tolerate

prevention of DM post preg
6 week postnatal OGTT to ensure resolution

74
Q

gestational DM management post pregnancy

A

prevention of DM post preg

6 week postnatal OGTT to ensure resolution

75
Q

which type of lactic acidosis is diabetes associated to?

A

Type B
- can also occur in liver disease / leukaemia

Type A is associated with tissue hypoxaemia, infarcted tissue, hypovolaemic shock

76
Q

when is lactate lowest?

A

fasted state - rises in exercise

77
Q

lactic acidosis presentation

A

hyperventilation
confusion

reduced bicarbonate
raised anion gap (acidosis)

absence of ketone

78
Q

how is an oral glucose tolerance test carried out?

A

performed in the morning after a fast
patient drinks a 75g glucose drink at the start of the test
blood sugar is measured before and then 2hrs fter taking drink

endocrine (15 decks)

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