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Endo > Diabetes > Flashcards

Diabetes Flashcards

1
Q

List the insulin dependent vs insulin independent glucose transporters

A

i. Insulin independent
1. Brain = GLUT1
2. B islet cells, liver, kidney + small intestine (basolateral) = GLUT2
3. Neurons = GLUT3
4. GI tract (apical – fructose transport) + spermatocytes = GLUT5

ii. Insulin dependent
1. Skeletal muscle + adipocytes = GLUT4

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2
Q

What is the pattern of insulin secretion? Loss of this =?

A

i. Pulsatile (periodicity of 9-14 minutes)

ii. Loss of pulsatility = one of the earliest signs of basal cell dysfunction

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3
Q

Physiology of insulin secretion in pancreatic beta cells

A

i. Glucose enters B cell of pancreas via GLUT-2 transporter
ii. Glucose is phosphorylated to glucose-6-phosphate by glucokinase
iii. Glucose-6-phosphate can then be metabolised to generate ATP
iv. ↑ ATP leads to closure of ATP-sensitive K channel (K-ATP)
1. K-ATP is made up of two subunits:
a. SUR gene – chromosome 11 p
b. KIR 6.2 gene – chromosome 11 p
v. Closure of channel = intracellular accumulation of potassium = depolarisation of membrane
vi. Calcium channels open
vii. Influx of calcium leads to secretion of insulin

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4
Q

Pathophysiology of neonatal diabetes

A

Activating mutation = ↑ number of open KATP channels at the plasma cell
Hyperpolarization of the beta cells
Decreased release of insulin

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5
Q

Pathophysiology of hyperinsulinism of infancy

A

Inactivating mutations in either gene reduce the number of KATP channels
Depolarisation of beta cells
Increased/hypersecretion of insulin

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6
Q

which hormones counteract insulin (4)?

A

glucagon, GH, adrenaline, cortisol

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7
Q

which is the only organ glucagon clinically acts on?

A

liver

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8
Q
  1. sources of blood glucose (hormones, timing, and how we get the glucose)
  2. what is the order in which these hormones are released?
A

Glucose Diet 2-4 hours
Glycogenolysis Glucagon 10-12 hours
Gluconeogenesis Cortisol 12-24 hours
Lipolysis GH 17-36 hours

adrenaline > glucagon > cortisol > GH

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9
Q

name the three ketone types

A

B-hydroxybutyrate, acetoacetic acid, acetone

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10
Q

3 processes we get glucose from

A
  1. glycolysis
  2. glycogenolysis
  3. gluconeogenesis
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11
Q

physiology of glycolysis (aerobic vs anaerobic)

A

Anaerobic fermentation
glycogen -> x2pyruvate and 2ATP
pyruvate -> lactic acid -> to liver
usually just muscle

AAerobic respiratory
pyruvate oxidation -> acetyl coA
-> krebs -> ETC -> CO2 + H2O + 38ATP
in mitochondria

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12
Q

What infections can induce diabetes (name 3)

A

CMV, HUS, rubella

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13
Q

how many % of new T1DM have FHx?

A

85% have no FHx

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14
Q

what is peak age of t1dm dx?

A

bimodal peak at 4-6 years of age, and another at 10-14 years of age

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15
Q

what genes are associated with t1dm (most common)?

A

HLADR3/DR4

DQ2/8

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16
Q

how much of beta cell is destroyed before you get clinical signs in t1dm

A

90%

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17
Q

dawn phenomenon and t1dm:

  • what is it
  • what causes it
  • when
  • how to fix
A

i. Early morning (2-8am) hyperglycaemia due to overnight GH secretion + ↑ insulin clearance
ii. Occurs in peri-pubertal + pubertal years
iii. Manage with ↑ evening protophane dose

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18
Q

somogyi phenomenon and t1dm

  • what
  • why
A
  • Rebound hyperglycaemia from late night/ early AM hypoglycaemia,
  • Due to exaggerated counter regulatory response-
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19
Q

classic t1dm triad of symptoms

A
  1. polydipsia - from inc serum osm
  2. polyuria - glycosuria + osmotic diuresis
  3. weight loss - hypovolaemia + inc catabolism, insulin def
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20
Q

diagnostic criteria t1dm

A

one of:

  1. Fasting (>8 hours) BSL >7 mmol/L on more than one occasion
  2. Random BSL >11.1 mmol/L on more than one occasion in a patient with symptoms of hyperglycaemia
  3. BSL >11.1 two hours after oral glucose load of 1.75 g/kg (max 75g) in OGTT (rarely done)

nb HbA1c >6.5 – not established as diagnostic for diabetes in children

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21
Q

the 5 t1dm autoantibodies - which is best predictor, and which is most present at dx? progression of autoabs?

A

Insular at first, GAD its mentioned most, but NOMA is the best. Issa Zingga!:

Anti-insulin antibodies (IAA) - first
Anti-glutamic acid decarboxylase (anti-GAD) - second, best
Anti-insulinoma protein 2 (anti-IA2) - third, best
Islet cell cytoplasmic antibodies (ICA) - 70%
Anti-zinc transporter (anti-ZNT8)

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22
Q

which t1dm-associated gene is more associated with AI conditions?

A

HLA DR3 - note longer dm dormancy period, a/w ICA autoabs.

Note HLADR4 - a/w anti-IAA

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23
Q

what % of t1dm will developed coeliac within first 6 yrs of dx?

A

7-15% of children with T1DM develop celiac disease within the first 6 years of diagnosis

24
Q

what % of t1dm will develop hyper vs hypothyroidism?

A

2-5% develop hypothyroidism

1% develop hyperthyroidism (much rarer, but more common than general population)

25
Q

name 5 autoimmune conditiions associated with t1dm

A
  1. thyroid disorder
  2. coeliac disease
  3. AI adrenalitis - 1 %
  4. Gastric autoimmunity - anti-parietal cells, anti-IF
  5. vitiligo - 6%
26
Q

name two autoimmune syndromes associated with t1dm

A

APS-2

IPEX

27
Q

recommended diet stuff for t1dm

A

CHO 50% and low GI, fat 30% with saturated <10%, protein 20%

28
Q

t1dm: target bsl, hba1c, what bsl to treat for hypo, and what ketones to treat

A

Target BSL = 4-8
Target HbA1C = <7.5%

Treat:
Hypoglycaemia = <4
Ketosis = >1

29
Q

6 side effects of insulin Rx

A
  1. Hypoglycaemia
  2. Lipohypertophy at injection sites
  3. insulin resistance
  4. Insulin antibodies - nearly all develop antibodies after several moths
  5. weight gain
  6. local allergy
30
Q

BD vs basal-bolus insulin regimens:

  • TDD
  • distribution
A

both TDD = 1UKD

basal bolus:
- usually nocte levemir (0.4UKD) + tds novo (each 0.2UKD)

BD: usually levemir and novo BD
- mane 2/3 TDD, evenine 1/3 TDD

31
Q

2 molecules to assess mid-long term diabetes control

A

hba1c (2-3 month control)

fructosamine (glycated serum proteins) - 1-2 week control, useful in haemoglobinopathies (HbA1c spuriously ↓/↑)

32
Q

pathogenesis of most of the macro/microvascular complications of t1dm

A
  • Polyol pathway – metabolisms excess glucose to sorbitol then fructose = tissue damage
  • Glycosylation of proteins – glucose binds to proteins irreversibly and alteration leads to loss of function
33
Q

types of diabetic retinopathy

A
  • background - dilated vessels
  • non-proliferative - microinfarcts, cotton wool spots / soft exudate
  • proliferative - hard shit: ischaemia, haemorrhage, scarring, RD!
34
Q

what is the earliest sign of diabetic nephropathy? define it.

A

albuminuria: albumin excretion between 30-300 mg/day (20-200 mcg/min)

35
Q

what is necrobiosis lipoidica

A

inflammatory, granulomatous condition - oval/round plaques on shins. initially red/dusky -> yellow, central atrophy

36
Q

mauriac syndrome:
pathophys
a/w
signs

A

rare complication t1dm
glycogen laden liver -> hepatomegaly + cushingoid facies
a/w delayed puberty and DWARFISM
catch up growth if diabetes fixed

37
Q

what are normal ketone levels

A

<0.6

38
Q

glucagon dosing in severe hypoglycaemia

A
  1. 0.5ml = children <25 kg

2. 1ml = children >25kg

39
Q

definition of DKA

A

hyperglycaemia + metabolic acidosis + ketonaemia

venous gas <7.3 + blood or urinary ketones

40
Q

hypo and hyperkalaemia on ECG

A
  1. Hyperkalaemia = peaked T waves, widened QRS

2. Hypokalaemia = flattened or inverted T waves, ST depression, widened PR interval

41
Q

outline steps in DKA Mx

A
  1. ABC
  2. fluids
  3. insulin infusion (0.1MKH if new Dx)
  4. potassium - total body K deficit but apparent hyperK, risk of hypoK with insulin
42
Q

when to switch to SC insulin from continuous in DKA? When to stop the infusion?

A

start SC just before meal.

stop continuous 30 mins after SC (for overlap)

43
Q

when to give bicarb in DKA?

A

not recommended - causes paradoxical cerebral acidosis

44
Q

what to do if still hypoglycaemic with DKA Mx?

A

inc to 10% dex - dont reduce insulin until 10% dex really not working

45
Q

what is the rule for Na correcting during DKA?

A

Na should improve as glucose falls - hypoNa is dilutional effect of glucose

46
Q

complications of DKA - and which is responsible for highest mortality

A
  1. hypoNa
  2. hypoglycaemia
  3. cerebral oedema - causes 60% deaths
  4. hypo/hyperK
  5. renal failure
  6. pancreatitis
47
Q

cerebral oedema:

  • 3 at risk groups
  • warning signs related to Mx
  • how to treat
A
  • first presentation, long history of poor control, young age (< 5 yr)
  • No sodium rise as glucose falls, hyponatraemia during therapy, initial adjusted hypernatraemia
  • mannitol
48
Q

which other endocrine condition is a risk factor for DKA

A

hyPERthyroidism

49
Q

best T2DM test for Dx?

A

fasting GTT

50
Q

clinical signs of insulin resistance in T2DM, and which is the most common?

A
  • cutaneous: acanthosis nigricans (best!), alopecia, skin tags
  • reproductive: amenorrhoea, hirsutism, virilisation
  • fat
51
Q

treatment regimen of chocie in T2DM

A

metformin monotherapy

52
Q

what is worse than DKA for T2DM?

A

hyperosmolar non-ketotic acidosis

  • insulin deficiency
  • extreme hyperglycaemia
  • extreme dehydration in cells
  • GNG without ketones bc there’s still insulin
  • fluid resus +++
53
Q

MODY inheritance pattern

A

AD

54
Q

MODY 2

  • pathogenesis + gene
  • frequency
  • key clinical feature
  • risk of microvascular disease
  • optimal treatment
A
  • Glucokinase gene GCK (glucose sensor)
  • Defective glucokinase -> increased plasma levels of glucose to elicit normal levels of insulin secretion
  • 15-30%
  • Mild, stable, fasting hyperglycemia, often diagnosed during routine screening. Not progressive.
  • generally no risk of microvascular disease
  • diet Mx
55
Q

MODY 3

  • pathogenesis + gene
  • frequency
  • key clinical feature
  • risk of microvascular disease
  • optimal treatment
A
  • Hepatocyte nuclear factor-1-alpha HNF1alpha
  • Mechanism unclear, ?reduced insulin secretory response to glucose, low renal threshold for glucose (decreased renal absorption of glucose)
  • glycosuria key feature
  • yes to microvascular disease
  • sulfonylureas

Endo (8 decks)

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