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diabetes Flashcards

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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

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2
Q

auto antibodies associated with type 1 diabetes

A

GAD
IA-2
Znt8

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3
Q

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

A

both - 30%

father - 8%
mother - 5%

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4
Q

what genes represent 50% of familial risk in T1DM?

A

HLA genes

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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

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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

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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

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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

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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
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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

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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

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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

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13
Q

T2DM risk factors

A

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

obesity
sendentary lifestyles
high carb diet - esp refind carbs

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14
Q

T2DM presentation

A 
fatigue
usually obese
no ketone
polydispsia, polyuria
opportunistic infections
signs of complications
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15
Q

HbA1c + glucose levels in diabetes

A

HbA1c = >48

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

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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.

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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.

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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.

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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
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20
Q

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

A

SGLT-2 inhibitors

GLP-mimetics

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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)

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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)

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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

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24
Q

HHS presentation

A

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

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25
diagnosis of HHS (3 things)
hypovolaemia (lack of fluid) hyperglycaemia (>30) WITHOUT ketonaemia or acidosis raised serum osmolarity (>320)
26
complications of HHS
cardiovascular disease - MI, stroke (due to thickened blood) sepsis - from underlying infection
27
management of HHS
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
28
which medication is lactic acidosis a key side effect of?
metformin
29
diabetic ketoacidosis (DKA)
T1DM (usually young) who is no producing/injecting adequate insulin increase in counter-regulatory hormones - glucagon, cortisol, growth hormone life threatening medi emergency
30
precipitants of DKA
insulin deficiency increase insulin demand (infections, intoxication, infarction, surgery, steroids) starvation
31
pathophysio of DKA
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
32
DKA presentation
``` abdo pain + tenderness acetone breath nausea + vomiting polyuria + polydipsia/dehydration altered consciousness ```
33
diagnosis of DKA
hyperglycaemia = blood glucose >11 ketosis = blood ketone >3 or >2 on urine dipstick acidosis = pH < 7.3
34
priorities in management of DKA
dehydration, potassium imbalance, acidosis = what will kill patient priority = fluid resuscitation then insulin infusion
35
treatment of DKA
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
how are patients restarted on an insulin regime post DKA?
patients must be established on a normal insulin regime prior to stopping the insuline + fluid infusion (part of DKA treatment)
37
complications of DKA
cardiac arrest/arrhmyias secondary to hypokalaemia adult respiratory distress syndrome cerebral oedema - esp in kids gastric dilatation/stasis - risk of aspiration pneumonia
38
key complication of DKA in kids
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
conditions associated with hypoglycaemia
``` coeliac disease addisons/hypopituitarism hypothyroidism renal failure gastroparesis ```
40
risk factors for hypoglycaemia
previous severe hypo longer duration diabetes high risk indivdual - old, young, unaware of hypos T1DM who have been on treatment a while
41
common causes of hypoglycaemia
``` 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
hypoglycaemia presentation
tremor, irritability, anxious hunger, weakness, fatigue sweating pallor, dizziness
43
hypoglycaemia glucose level
glucose <4 mmol/L severe hypo can lead to reduced consciousness, coma + death unless treated
44
ways to reduce hypos
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
management of hypoglycaemia
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
what is monogenic diabetes?
diabetes caused by a mutation in a single gene (mendelian disease) ->results in defects in insulin secretion or insulin action commonest = MODY
47
types of monogenic diabetes
defects in insulin secretion > MODY > neonatal diabetes defects in insulin action >insulin signalling - AKT, INSR > fat storage - CIDEC
48
Maturity Onset Diabetes of the Young (MODY)
autosomal dominant non-insulin dependent diabetes rare 1-2% of people with diabetes 90% misdiagnosed
49
what is the typical age of onset of MODY?
usually before 25yrs
50
types of MODY
transcription factor mutations > HNF1-alpha (commonest) > HNF1-beta > HNF4-alpha glucokinase
51
MODY (HNF1-alpha)
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
MODY (glucokinase)
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
treatment of neonatal diabetes mellitus
high dose sulphonylureas
54
treatment for diabetes related nephropathy
ACEi / ARB
55
pathophysio of diabetes complications
excessive glucose, mitochondria can't keep up so alternative pathways used these preciptate - >polyol pathway - osmotic damage >increased ROS >inflammation >fibrosis
56
nephropathy in diabetes patients
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
types of neuropathy
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
management of diabetes during pregnancy?
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
preferred blood pressure medication in pregnancy?
labetalol nifedipine methydopa ACEi = tetragenic
60
types of weight loss surgery?
restrictive - gastric balloon - gastric band - sleeve gastrectomy malapsorptive - gastric bypass (roux en y) = gold standard - bilio-pancreatic diversion
61
when is orlistat recommended?
BMI >= 30 or >=28 with comorbidities
62
guidelines for continuation of orlistat
lost >=5% of body weight in first 3 months lost >=10% of bodyweight in first 6 months
63
what is orlistat? when is it used?
non-systemic lipase inhibitor - used for weight loss | blocks 30% dietary fat
64
diet when on orlistat
hypocaloric / low fat diet is essential 150/250 kcal deficit/day
65
side effects of orlistat
stearrhoea abdo pain weird stools
66
management of pre-existing diabetes in pregnancy
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
management of diabetes during labour
maintain good blood glucose may require IV insulin + IV dextrose
68
postnatal care of pregnant diabetics
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
what are babies of mothers with diabetes at risk of?
neonatal hypoglycaemia macrosomia (big babies) polycythaemia (raised haemoglobin) jaundice (raised bilirubin) cangenital heart disease cardiomyopathy
70
gestational diabetes
diabetes triggered by pregnancy - resolves after birth | caused by reduced insulin sensitivity during pregnancy
71
gestational diabetes risk factors
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
clinical features of gestational diabetes
large for dates foetus polyhydramnios (increased amniotic fluid) glucose on urine dipstick
73
gestational diabetes management
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
gestational DM management post pregnancy
prevention of DM post preg | 6 week postnatal OGTT to ensure resolution
75
which type of lactic acidosis is diabetes associated to?
Type B - can also occur in liver disease / leukaemia Type A is associated with tissue hypoxaemia, infarcted tissue, hypovolaemic shock
76
when is lactate lowest?
fasted state - rises in exercise
77
lactic acidosis presentation
hyperventilation confusion reduced bicarbonate raised anion gap (acidosis) absence of ketone
78
how is an oral glucose tolerance test carried out?
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)

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