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Y3 Conditions > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

T1 T2 MODY Mitochondrial diabetes

1
Q

What is Type 1 DM characterised by?

A

insulin deficiency and a tendency to develop ketosis

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2
Q

At what age to people start to develop T1DM?

A

child, teens, young adult

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3
Q

What can we see in the histopathology of early type 1 DM. After a long time?

A

early: - lots of dense dots in islets
- immune cells

long duration: - immune system switches off infiltration
- red: lost shape + dead

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4
Q

What allele is associated with an increased rise level for T1DM?

A

HLA-DR
- DR3, DR4 in particular

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5
Q

What does HLA-DR stand for?

A

human leukocyte antigen

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6
Q

DM

What is a classic presentation of hyperglycaemia in T1DM?

4

A
  • Polyuria / Nocturia
  • Polydipsia
  • Polyphagia
  • Weight loss
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7
Q

DM

What are some non-specific features of hyperglycaemia in T1DM?

5

A
  • Fatigue
  • Visual disturbances
  • Calf cramps
  • Poor wound healing
  • Pruritus
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8
Q

DM

What is the diagnostic criteria for DM (WHO)?

for those who are SYMPTOMATIC

A
  • Symptoms of hyperglycaemia
    AND
  • raised** venous glucose** detected ONCE

raised venous glucose:** fasting >7mmol/l** or random >11.1mmol/l

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9
Q

DM

What is the diagnostic criteria for DM (WHO)?

for those who are ASYMPTOMATIC

A

Raised venous glucose TWICE
OR
high OGTT
OR
high HbA1C (glycated haemoglobin)

venous glucose:
- diabetes: fasting >7mmol/l
- impaired fasting glucose 5.6-6.9mmol/l
- healthy <5.6mmol/l)

OGTT:
- diabetes: 2-hour value >11.1mmol/l
- impaired glucose tolerance 7.8-11.0mmol/l
- healthy <7.8mmolmol)

HbA1c:
- diabetes: >48mmol/mol or 6.5%
- prediabetes 39-46mmol/mol 5.7-6.4%
- healthy <39mmol/mol <5.7%)

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10
Q

DM

What are the parameters for venous blood glucose?
- diabetic
- impaired glucose tolerance
- healthy

A
  • diabetes: fasting >7mmol/l
  • impaired fasting glucose 5.6-6.9mmol/l
  • healthy <5.6mmol/l)
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11
Q

DM

What are the parameters for OGGT?
- diabetic
- impaired glucose tolerance
- healthy

oral glucose tolerance teast

A
  • diabetes: 2-hour value >11.1mmol/l
  • impaired glucose tolerance 7.8-11.0mmol/l
  • healthy <7.8mmolmol)
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12
Q

DM

What are the parameters for HbA1c?
- diabetic
- pre-diabetic
- healthy

A
  • diabetes: >48mmol/mol or 6.5%
  • prediabetes 39-46mmol/mol 5.7-6.4%
  • healthy <39mmol/mol <5.7%)
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13
Q

DM

Although not required for diagnosis, apart from venous blood glucose, OGGT and HbA1c, what other tests might we consider doing?

A
  • autoantibodies
  • c-peptide
  • urine analysis
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14
Q

DM

What are some specific autoantibodies for T1DM?

3

A
  • Anti-GAD (glutamic acid decarboxylase) antibodies
  • Anti-tyrosine phosphatase-related islet antigen (IA-2)
  • Islet cell surface antibody (ICSA; against ganglioside)
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15
Q

DM

What blood test can we use to differentiate between T1DM and T2DM?

A

c-peptide

low: T1
high: T2

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16
Q

DM

What might be seen in the urinalysis on someone with T1DM?

A
  • Microalbuminuria: an early sign of diabetic nephropathy
  • Glucosuria
  • Ketone bodies: present in acute metabolic decompensation in T1DM (DKA)
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17
Q

DM

Insulin deficiency in an (anabolic/catabolic) state.

A

catabolic

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18
Q

DM

What is the treatment for T1DM?

A
  • insulin
  • transplantation
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19
Q

DM

What can be transplanted together with pancreas graft to increase chance of pancreas graft?

A

kidneys

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20
Q

DM

What are some insulin treatment options?

A
  • basal-bolus
  • pump
  • closed-loop / artificial pancreas
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21
Q

DM

How are islet cells transplanted?

A
  • Isolate human islets from pancreas of deceased donor
  • Transplant into hepatic portal vein
  • Requires life-long immunosuppression
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22
Q

DM

What are the aims of T1DM management?

A
  • maintain glucose levels w/out excessive hypos
  • get as close to physiological insulin profile as possible
  • prevent micro and macrovascular complications
  • present metabolic decompensation
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23
Q

DM

Name 3 acute and a chronic complication of T1DM?

A
  • acute
    • DKA
    • uncontrolled hyperglycaemia
    • hypoglycaemia from treatment
  • chronic
    • micro/macrovascular complications
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24
Q

DM

T1DM is associated with two main emergencies:

A

diabetic ketoacidosis (DKA) and hypoglycaemia

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25
Q

DM

How does DKA occur?

A
  1. no insulin
  2. glucose cant enter cells
  3. body feels like there is no sugar = starvation mode
  4. body starts breaking down breaking down adipose tissue to create ketone bodies (ketoacidosis)
  5. ketones build up in body = hyperketonaemia
  6. this causes metabolic acidosis
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26
Q

DM

What are 4 triggers for DKA?

A

Triggers are the 4 ‘I’s
- infection
- infarct (e.g. Myocardial ischemia, cerebrovascular accident)
- inflammation (e.g. Pancreatitis)
- incorrect or non-compliance to insulin dosing.

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27
Q

DM

How do DKA pts present?

A
  • Gradual drowsiness
  • Vomiting and dehydration
  • Abdominal pain
  • Polyuria
  • Polydipsia
  • Lethargy
  • Anorexia
  • Ketotic breath (fruity-scented)
  • Coma
  • Kussmaul hyperventilation*respiratory compensation for metabolic acidosis *
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28
Q

DM

How do we diagnose DKA?
Name the values too.

A
  • Acidaemia – venous blood pH <7.3 or HCO3- <15.0mmol/l
  • Hyperglycaemia – blood glucose >11.0mmol/l or known DM
  • Ketonaemia – >3.0mmol/l or significant ketonuria >2+ on dipstick
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29
Q

DM

What are some severe complications for DKA?

6

A
  • cerebral oedema
  • aspiration pneumonia
  • hypokalaemia
  • hypomagnesaemia
  • hypophosphataemia
  • thromboembolism.
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30
Q

DM

Name some signs of severe DKA.

9

A
  • Blood ketones >6mmol/l
  • Venous bicarbonate <5mmol/l
  • Venous/arterial pH <7.0
  • K⁺ <3.5mmol/l on admission
  • GCS <12
  • O₂ sats <92% on air; assuming no pre-existing respiratory illness
  • Systolic blood pressure <90mm Hg
  • Pulse >100 or <60bpm
  • Anion gap above 16
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31
Q

DM

What is the overall idea of DKA management?

3

A
  • resuscitate (ABCDE)
  • replace volume (IV drip)
  • correct metabolic defects
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32
Q

DM

How to decrease blood glucose in DKA?

A

IV insulin

when glucose reaches <14, administed insulin with 10% glucose

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33
Q

DM

What is them main cause of hypoglycaemia in T1DM pts? (4)

A
  • insulin treatment with increased activity
  • missed meals
  • alcohol binge without prior carbohydrate consumption
  • insulin overdose (accidental or non-accidental).
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34
Q

DM

What are dome autonomic symptoms of hypos?

6

A
  • Sweating
  • anxiety
  • hunger
  • tremor
  • palpitations
  • dizziness
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35
Q

DM

What are some neuroglycopaenic symptoms of hypos?

A
  • Confusion
  • drowsiness
  • visual problems
  • seizures
  • coma
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36
Q

DM

What is an example of a focal symptom of hypos?

this is very rare

A

Transient hemiplegia

37
Q

DM

How to manage a pt in a hypo? (conscious)

A

15-20g of quick-acting carbohydrates should be consumed, and blood glucose rechecked after 10-15min, repeat up to 3 times

38
Q

DM

How to manage a pt in a hypo? (conscious, unable to swallow)

A

patient’s family members/ housemates/ partner can help to abort hypoglycaemia by having sugary drinks, GlucoGel or IM glucagon on hand.

39
Q

DM

How to manage a pt in a hypo? (unconscious )

A

IV glucose
or
IV/IM 1g glucagon

40
Q

DM

What are the aims for blood glucose levels for pt with T1DM?

A

5-7mmol/l on waking for fasting plasma glucose
4-7mmol/l before meals

41
Q

DM

Why should injection sights be varied?

A

to avoid lipodystrophy

42
Q

DM

What type of insulin is used pre-meal to help match carbohydrates consumed?

A

Ultra-fast acting (Humalog, Novorapid)

43
Q

DM

What insulin is used used at bedtime as a basal insulin

A

Long-acting recombinant human insulin analogues (insulin glargine, insulin detemir)

44
Q

DM

What kind of pt would be more fitted for a BD biphasic regimen? What does this regime consist of?

A

pt with regular lifestyle

twice-daily premixed insulin by pen

45
Q

DM

What kind of pt would be more fitted for a QDS regimen? What does this regime consist of?

A

pts with a more varied lifestyle

ultra-fast insulin before meals + long-acting insulin at bedtime

46
Q

DM

What kind of pt would be more fitted for a Insulin pump? What does this consist of?

A

continuous subcutaneous insulin

pts who have poor glycaemic control with above regimens or are unable to achieve target HbA1C despite close management

47
Q

DM

In what circumstances/conditions would a pt require a reduced insulin dose?

A
  • Physical activity
  • vomitting / diarrhoea
  • surgery
48
Q

DM

Why might a pt require an increased insulin dose due to acute stress/illness?

A

many illnesses result in an acute stress reaction and elevated blood glucose levels due to the action of cortisol

49
Q

DM

Which annual screening check-ups do T1DM pts have to check for microvascular complications.

A
  • Eye exams after 5 years with T1DM or from 12 years old to monitor for diabetic retinopathy
  • Urine testing for microalbuminuria (ACR 3-30mg/mmol) from 12 years old, suggesting diabetic nephropathy
  • Foot exams for peripheral neuropathy and diabetic ulcers; advise on wearing appropriate footwear and avoid injury
50
Q

DM

What psychosocial conditions should T1DM pt be checked up for?

A

depression, as T1DM is a chronic lifelong condition

51
Q

DM

Why are pts with T1DM advised to have pneumococcal vaccinations?

A

they are in an immunocompromised state

52
Q

DM

Under what circumstances are T1DM pts not allowed to drive?

A

if they have hypoglycaemic unawareness

53
Q

DM

What is the recommendations regarding alcohol consumption for T1DM pts?

A
  • patients should be advised to consume carbohydrates beforehand in order to avoid hypoglycaemia
  • binge drinking should be avoided due to the danger of delayed hypoglycaemia.
54
Q

DM

T1DM pts:

Blood pressure targets are ____
if there is albuminuria or two or more features of metabolic syndrome in T1DM, the target is ____.

A
  • <135/85mm Hg
  • 130/80mm Hg
55
Q

DM

What are the different methods how we can monitor blood glucose?

A
  • capillary blood glucose monitoring
  • continuous glucose monitoring
  • HbA1c
56
Q

DM

What is Type 2 Diabetes and what is it characterised by?

A

a heterogeneous group of disorders characterized by variable degrees of insulin resistance, impaired insulin secretion, and excessive hepatic glucose production

57
Q

DM

What are some risk factors for T2 DM?

A
  • age
  • high BMI
  • ethnicity
    • Black African
    • African Caribbean
    • South Asian
  • PCOS
  • family history
  • inactivity
58
Q

DM

What is the presentation of T2DM and how may it it differ to T1?

A
  • Hyperglycaemia
  • Overweight
  • Dyslipidaemia
  • osmotic symptoms
    • fewer than T1
  • micro/macrovascular complications
  • insulin resistance -> deficiency
59
Q

DM

How does T2DM present?

A
  • Polyuria
  • Polydipsia
  • Increased appetite
  • Fatigue
  • Recurrent infections (urinary or genitourinary)
  • Asymptomatic or late-stage complications (*skin infections, foot ulcers/neuropathic pain, diabetic retinopathy, MI/stroke *)
60
Q

DM

T2DM is associated with metabolic syndrome. What is that?

A
  • having central obesity (BMI>30)

and having 2 of the following:
- high triglyceride levels
- high blood pressure
- low HDL levels
- high glucose levels

61
Q

DM

How can we use HbA1c to diagnse T2DM?

A
  • 1x HbA1c ≥ 48mmol/L with symptoms
    or
  • 2x HbA1c ≥ 48 mmol/mol (asymptomatic)
62
Q

DM

How is T2DM managed?

A
  1. lifestyle
  2. oral medication / BP + lipid management
  3. structured education

?remission/reversal
- gastric bypass
- very low calorie diet

63
Q

DM

What is HHS? What is it aka?

A

Hyperglycemic Hyperosmolar State

hyperglycaemia hyperosmolar non-ketotic coma (HONK)

a medical emergency related to T2DM

64
Q

DM

How do pts with HHS typically present?

A

severe dehydration and generally feeling unwell in the past few days.

65
Q

DM

Why does Hyperglycemic Hyperosmolar State occur?

A

Insufficient insulin for prevention of unchecked hyperglycemia, but sufficient insulin for suppression of gluconeogenesis lipolysis and ketogenesis

  • Absence of significant acidosis
  • Osmotic diuresis
    • dehydration
66
Q

DM

What do we need to be careful of when treating a pt with HHS?

A

these patients have v. high sodium levels
cannot give fluids too fast
- risk of central pontine demyelinolysis

67
Q

DM

Compare DKA and HHS in regards to these parameters.

A
68
Q

DM

What does HHS typically present together with?

A

renal failure

69
Q

DM

Name 2 types of diabetes caused by genetic defects.

A

MODY
mitochontrial diabetes

70
Q

DM

What is MODY?

A

Maturity-onset diabetes of the young (MODY)

71
Q

DM

What do we call the sudden rise in insulin levels after eating? What happens to this in people with T2DM?

A

1st phase insulin release

this rise is lost and there is just a tiny bit of 2nd phase

72
Q

DM

What is the gastrointestinal incretin effect?

A

greater rise of insulin with oral glucose

73
Q

DM

What do we call the effect where oral glucose causes a greater rise in insulin compared to IV?

A

incretin effect

74
Q

DM

How do we adjust insulin dosage?

A

based on self-monitoring and HbA1c every 3-4 months

75
Q

DM

What are the different types of insulin?

A

short/quick acting
- human insulin
- insulin analogue

long-lasting / basal
- bound to zinc/protamine
- insulin analogue

76
Q

DM

What does basal bolus mean regarding insulin administration?

A

TDS short acting
OD long-acting

or

TDS short-acting
Twice daily intermediate acting

77
Q

DM

How does a pump administer insulin?

A
  • Continuous delivery of short-acting insulin analogue
    • e.g. novorapid via pump
  • Delivery of insulin into subcutaneous space
  • Programme the device to deliver fixed units / hour throughout the day (basal)
  • Actively bolus for meals
78
Q

DM

What is a closed loop / artificial pancreas?

A
79
Q

DM

What is the 1st line drug for T2DM if lifestyle changes doesn’t help?

A

metformin

80
Q

DM

What class of drugs in metformin in?
How does it work?
What is the common side effect?
What are the contraindications?

A

Class
Biguanides

Mechanism
- Increases glucose uptake thus increases insulin sensitivity
- Decreases hepatic gluconeogenesis

**Side effects **
GI side effects

Contraindications
severe liver, severe cardiac or moderate renal failure
(eGFR < 35 ml/min)

81
Q

DM

Give an example of a sulfonylurea.
How does it work?
What is the common side effect?

A

Example
- Gliclazide

Mechanism
- Increases pancreatic insulin secretion

Side effects
- Weight gain
- Hypoglycaemia

82
Q

DM

Give an example of a Thiazolidinediones / Glitazones.
How does it work?
What is the common side effect?
What are the contraindications?

A

Example
* Pioglitazone

Mechanism
* PPARγ agonist which then stimulates glucose transporter molecules

Side effects
* Weight gain
* Oedema
* Post-menopausal fractures
* Hepatotoxicity

Contraindications
* Heart failure (as it causes oedema)

83
Q

DM

Give an example of a Gliptin.
How does it work?
What is the common side effect?

A

Example
- Sitagliptin

Mechanism
- DPP4 inhibitors hence increases GLP-1

Side effects
- Pancreatitis

Dipeptidyl peptidase 4 (DPP-4) inhibitors

84
Q

DM

Give an example of a GLP-1 Analogue.
How does it work?
What is the common side effect?

A

Example:
- Exenatide

Mechanism
- Stimulate insulin release
- Decreases appetite

Side effects
- GI side effects
- Exenatide - injection site reactions

85
Q

DM

Give an example of a SGLT-2.
How does it work?
What is the common side effect?

A

Example:
- dapagliflozin

Mechanism:
- increase glucose excretion in urine

Side effects:
- UTIs
- polyuria

86
Q

DM

How do Alpha-Glucosidase Inhibitors work?
What is the common side effect?

A

Mechanism
- Reduces glucose absorption (inhibits the digestive enzyme)

Side effects
- GI side effects

87
Q

DM

Name some other benefits of SGLT-2 inhibitor apart from increasing glucose excretion.

A
  • lowers HbA1c
  • 32% lower all cause mortality
  • 35% lower risk heart failure
  • Improve CKD
88
Q

DM

empagliflozin
dapagliflozin
canagliflozin

What are these medications?

A

SGLT-2 inhibitors

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