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Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

diabetes is…

A

elevation of blood-glucose above diagnostic threshold

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2
Q

c-ppetide is a good measure of ____

A

endogenous insulin secretion- pro-insulin cleaved into insulin and c-peptide so c-peptide used

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3
Q

2 pathophysiology mechanisms for diabetes are

A

disorder of b-cells, impaired insulin secretion

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4
Q

s/s of diabetes

A

polydipsia, polyuria, fatigue, wt loss

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5
Q

ix for diabetes

A

random blood glucose: >11mmol/l
fasting blood glucose: >7mmol/L
2hr post glucose: >11mmol/L

HbA1c: >48mmol/L

Auto antibodies for T1: GAD

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6
Q

what is a ketosis reading for blood-ketones

A

> 5mmol/L

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7
Q

which 2 tests form the glucose tolerance test

A

fasting plasma glucose, 2hr plasma glucose post 75g solution

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8
Q

tx for diabetes

A

MONITOR: HbA1c, capillary blood-glucose, continuous blood glucose monitoring

Rx: insulin, metaphotmin, sulphonylureas, TDZ. SGLT2i (mono, combo, combo + insulin)

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9
Q

what are 2 surgical options for diabetes

A

pancreatic-kidney transplant, islet transplant

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10
Q

what actually is HbA1c?

A

how much glucose is attached to haemoglobin molecule

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11
Q

main complications of T1 diabetes

A

microvascular: retinopathy, nephropathy, neuropathy

hypoglycaemia, DKA

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12
Q

Type 1 diabetes mellitus is…

A

T cell mediated AI destruction of pancreatic b-cells (can’t produce insulin)

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13
Q

aetiology of T1

A

genetic (HLA gene), idiopathic

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14
Q

classic triad of T1 in kids

A

polyuria. polydipsia, wt loss/ not gaining wt

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15
Q

if pt is symptomatic…

A

tes random glucose. Dx = >11mmol/L

asymptomatic- do glucose tolerance test

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16
Q

c-peptide +ve test

A

<0.2mmol/L

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17
Q

classic insulin regimen for T1

A

Background + long acting + short acting (30mins pre-meal)

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18
Q

why must you inject insulin in different locations

A

to avoid lipodystrophy

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19
Q

how does microvascular injury occur

A

chronic hyperglycaemia causes inc vessel wall thickness but it hence becomes weaker and most susceptible to leakage and bursting

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20
Q

50% of T1 diabetics will develop ______

A

nephropahty

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21
Q

T2 diabetes is…

A

mix of insulin resistance and insulin deficiency

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22
Q

pathophysiology of T2

A

obesity > exceeding fat storage threshold > deposited in other sites > lipotoxicity > insulin resistance

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23
Q

s/s of T2

A

fits risks (overweight, older etc), dx of exclusion- polydipsia, polyuria

24
Q

mx for T2

A

lifestyle

Rx- metformin, MF + another drug, MF + another drug + insulin

25
Q

what are tx aims for new T2 diabetic

A

HbA1c 48mmol/L

others 53mmol/L

26
Q

comps for T2

A

HT, HL, hyperglycaemia, microvascular disease

27
Q

what is hypoglycaemia and causes

A

low blood-sugar levels, T1 diabetes, t2 diabetes with insulin therapy, missed meal/lots of exercise

28
Q

s/s of hypo

A

ANS- trembling, anxious, palpitations, tingling fingertips, irritable, hungry

neuroglycopenic: weakness, concentration, coordination, slurred speech, seizures

29
Q

dx reading of a hypo

A

glucose <4mmol/L

30
Q

tx for hypo

A

if swallowing- rapid sugar (lucozade) + slow acting (biscuit)

drowsy- glucose gel

severe- IV dextrose (glucose), IM glucagon

31
Q

hyperglycaemia is…

A

too much glucose, tx is to alter urine which may result in hypo

32
Q

what is DKA

A

production of ketones due to insufficient levels of insulin

33
Q

how does DKA happen

A

no insulin to use up glucose > ketones produced > ketones use up HCO3-= acidosis so ketoacidosis

34
Q

aetiology of DKA

A

insulin deficiency- new dx of diabetes, malcompliance

inc insulin demand: infection. inflammation, intoxication, infarcion

35
Q

s/s of DKA

A

hyperglycaemia, polydipsia/ polyuria

ketone body related: vomiting, flushed, abd pain, kussmaul’s resp, acetonic breath, hypotension

36
Q

dx of DKA

A

hyperglycaemia >11mmol/L
ketosis >3mmol/L
acidosis <7.35pH and HCO3- low
potassium >5.5mmol/L

37
Q

tx for DKA acronym

A

FIG PICK
Fluids
Insulin
Glucose

Potassium
Infection (check)
Chart fluid balance
Ketones

38
Q

what is hyperglycaemia hyperosmolar syndrome

A

hyperglycaemia + hyperosmolarity

39
Q

why does HHS occur

A

in T2 diabetics usually due to new dx of DM or infection

40
Q

ix for diagnosis of HSS

A

hyperglycaemia (usually >30mmol/L), osmolarity >320mosmol/kg

41
Q

how to measure osmolarity

A

2x Na + urea + glucose

42
Q

mx of HSS

A

monitor and chart plasma osmolarity, blood-glucose and Na

fluids*

43
Q

why else can ketoacidosis occur (other than insulin lack)

A

alcohol or starvation

44
Q

lactic acidosis is…

A

lactate is end-product of anaerobic respiration

45
Q

causes of lactic acidosis

A

fasting

46
Q

what are 2 types of lactic acidosis

A

typeA: tissue hypoxaemia, sepsis, haemorrhage

type B: liver disease, leukaemic states, diabetes

47
Q

s/s of lactic acidosis

A

hypervent, confusion, stupor, coma

48
Q

ix for lactic acidosis

A

hypolactataemia (<0.6mmol/L)

reduced bicarbonate, raised anion gap, raised phosphate, no ketonaemia

49
Q

what is monogenic diabetes

A

diabetes caused by mutation in a single gene usually affecting b-cell function

50
Q

types of monogenic diabetes

A

subcategories are- defects in insulin secretion and defects in insulin action

secretion: MODY (GCK MODY and TNF a MODY), neonatal diabetes

51
Q

epi of MODY

A

occurs before 25yo

52
Q

MODY run down

A

onset <25yo, non-insulin dependent diabetes

  • GCK mutation: b-cel glucose sensor muttaion
  • TF mutation: HNF-1a most common
53
Q

what are the most common mutations that cause neonatal diabetes

A

KCNJ11, ABCC8 genes

block Katp channel so membrane doesn’t polarise

54
Q

s/s of MODY

A

acanthosis nigricans, lipodystrophy
GCK: stable hyperglycaemia
TF: progressive

55
Q

how to differentiate between the 2 MODYs

A

oral glucose test, c-peptide

56
Q

tx for MODY

A

GCK: mainly diet

HNF-1a TF MOFY: 1/3rd diet, 1/3rd sulphonylureas, 1/3rd insulin

57
Q

tx for neonatal diabetes

A

insulin then sulphonylureas

Endocrine (14 decks)

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