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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
# DM How does DKA occur?
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
26
# DM What are 4 triggers for DKA?
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.
27
# DM How do DKA pts present?
* Gradual drowsiness * Vomiting and dehydration * Abdominal pain * Polyuria * Polydipsia * Lethargy * Anorexia * Ketotic breath (fruity-scented) * Coma * Kussmaul hyperventilation*respiratory compensation for metabolic acidosis *
28
# DM How do we diagnose DKA? Name the values too.
* **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
29
# DM What are some severe complications for DKA? | 6
- cerebral oedema - aspiration pneumonia - hypokalaemia - hypomagnesaemia - hypophosphataemia - thromboembolism.
30
# DM Name some signs of **severe** DKA. | 9
* 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
31
# DM What is the overall idea of DKA management? | 3
- resuscitate (ABCDE) - replace volume (IV drip) - correct metabolic defects
32
# DM How to decrease blood glucose in DKA?
IV insulin when glucose reaches <14, administed insulin with 10% glucose
33
# DM What is them main cause of hypoglycaemia in T1DM pts? (4)
- insulin treatment with increased activity - missed meals - alcohol binge without prior carbohydrate consumption - insulin overdose (accidental or non-accidental).
34
# DM What are dome autonomic symptoms of hypos? | 6
* Sweating * anxiety * hunger * tremor * palpitations * dizziness
35
# DM What are some neuroglycopaenic symptoms of hypos?
* Confusion * drowsiness * visual problems * seizures * coma
36
# DM What is an example of a focal symptom of hypos? | this is very rare
Transient hemiplegia
37
# DM How to manage a pt in a hypo? (conscious)
15-20g of quick-acting carbohydrates should be consumed, and blood glucose rechecked after 10-15min, repeat up to 3 times
38
# DM How to manage a pt in a hypo? (conscious, unable to swallow)
patient’s family members/ housemates/ partner can help to abort hypoglycaemia by having sugary drinks, GlucoGel or IM glucagon on hand.
39
# DM How to manage a pt in a hypo? (unconscious )
IV glucose or IV/IM 1g glucagon
40
# DM What are the aims for blood glucose levels for pt with T1DM?
5-7mmol/l on waking for fasting plasma glucose 4-7mmol/l before meals
41
# DM Why should injection sights be varied?
to avoid lipodystrophy
42
# DM What type of insulin is used pre-meal to help match carbohydrates consumed?
Ultra-fast acting (Humalog, Novorapid)
43
# DM What insulin is used used at bedtime as a basal insulin
Long-acting recombinant human insulin analogues (insulin glargine, insulin detemir)
44
# DM What kind of pt would be more fitted for a BD biphasic regimen? What does this regime consist of?
pt with regular lifestyle twice-daily premixed insulin by pen
45
# DM What kind of pt would be more fitted for a QDS regimen? What does this regime consist of?
pts with a more varied lifestyle ultra-fast insulin before meals + long-acting insulin at bedtime
46
# DM What kind of pt would be more fitted for a Insulin pump? What does this consist of?
continuous subcutaneous insulin pts who have **poor glycaemic control with above regimens** or are **unable to achieve target HbA1C despite close management**
47
# DM In what circumstances/conditions would a pt require a reduced insulin dose?
- Physical activity - vomitting / diarrhoea - surgery
48
# DM Why might a pt require an increased insulin dose due to acute stress/illness?
many illnesses result in an acute stress reaction and elevated blood glucose levels due to the action of cortisol
49
# DM Which annual screening check-ups do T1DM pts have to check for microvascular complications.
* 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
# DM What psychosocial conditions should T1DM pt be checked up for?
depression, as T1DM is a chronic lifelong condition
51
# DM Why are pts with T1DM advised to have pneumococcal vaccinations?
they are in an immunocompromised state
52
# DM Under what circumstances are T1DM pts not allowed to drive?
if they have hypoglycaemic unawareness
53
# DM What is the recommendations regarding alcohol consumption for T1DM pts?
* 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
# DM T1DM pts: Blood pressure targets are ____ if there is albuminuria or two or more features of metabolic syndrome in T1DM, the target is ____.
- <135/85mm Hg - 130/80mm Hg
55
# DM What are the different methods how we can monitor blood glucose?
- capillary blood glucose monitoring - continuous glucose monitoring - HbA1c
56
# DM What is Type 2 Diabetes and what is it characterised by?
a heterogeneous group of disorders characterized by variable degrees of insulin resistance, impaired insulin secretion, and excessive hepatic glucose production
57
# DM What are some risk factors for T2 DM?
- age - high BMI - ethnicity - *Black African* - *African Caribbean* - *South Asian* - PCOS - family history - inactivity
58
# DM What is the presentation of T2DM and how may it it differ to T1?
- Hyperglycaemia - Overweight - Dyslipidaemia - osmotic symptoms - fewer than T1 - micro/macrovascular complications - insulin resistance -> deficiency
59
# DM How does T2DM present?
* 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
# DM T2DM is associated with metabolic syndrome. What is that?
* having central obesity (BMI>30) and having 2 of the following: - high triglyceride levels - high blood pressure - low HDL levels - high glucose levels
61
# DM How can we use HbA1c to diagnse T2DM?
- 1x HbA1c ≥ 48mmol/L with symptoms or - 2x HbA1c ≥ 48 mmol/mol (asymptomatic)
62
# DM How is T2DM managed?
1. lifestyle 2. oral medication / BP + lipid management 3. structured education ?remission/reversal - gastric bypass - very low calorie diet
63
# DM What is HHS? What is it aka?
Hyperglycemic Hyperosmolar State hyperglycaemia hyperosmolar non-ketotic coma (HONK) | a medical emergency related to T2DM
64
# DM How do pts with HHS typically present?
severe dehydration and generally feeling unwell in the past few days.
65
# DM Why does Hyperglycemic Hyperosmolar State occur?
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
# DM What do we need to be careful of when treating a pt with HHS?
these patients have v. high sodium levels cannot give fluids too fast - risk of central pontine demyelinolysis
67
# DM Compare DKA and HHS in regards to these parameters.
68
# DM What does HHS typically present together with?
renal failure
69
# DM Name 2 types of diabetes caused by genetic defects.
MODY mitochontrial diabetes
70
# DM What is MODY?
Maturity-onset diabetes of the young (MODY)
71
# DM What do we call the sudden rise in insulin levels after eating? What happens to this in people with T2DM?
1st phase insulin release this rise is lost and there is just a tiny bit of 2nd phase
72
# DM What is the gastrointestinal incretin effect?
greater rise of insulin with oral glucose
73
# DM What do we call the effect where oral glucose causes a greater rise in insulin compared to IV?
incretin effect
74
# DM How do we adjust insulin dosage?
based on self-monitoring and HbA1c every 3-4 months
75
# DM What are the different types of insulin?
short/quick acting - human insulin - insulin analogue long-lasting / basal - bound to zinc/protamine - insulin analogue
76
# DM What does basal bolus mean regarding insulin administration?
TDS short acting OD long-acting or TDS short-acting Twice daily intermediate acting
77
# DM How does a pump administer insulin?
- 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
# DM What is a closed loop / artificial pancreas?
79
# DM What is the 1st line drug for T2DM if lifestyle changes doesn't help?
metformin
80
# DM What class of drugs in metformin in? How does it work? What is the common side effect? What are the contraindications?
**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
# DM Give an example of a sulfonylurea. How does it work? What is the common side effect?
**Example** - Gliclazide **Mechanism** - Increases pancreatic insulin secretion **Side effects** - Weight gain - Hypoglycaemia
82
# DM Give an example of a Thiazolidinediones / Glitazones. How does it work? What is the common side effect? What are the contraindications?
**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
# DM Give an example of a Gliptin. How does it work? What is the common side effect?
**Example** - Sitagliptin **Mechanism** - DPP4 inhibitors hence increases GLP-1 **Side effects** - Pancreatitis | Dipeptidyl peptidase 4 (DPP-4) inhibitors
84
# DM Give an example of a GLP-1 Analogue. How does it work? What is the common side effect?
**Example**: - Exenatide **Mechanism** - Stimulate insulin release - Decreases appetite **Side effects** - GI side effects - Exenatide - injection site reactions
85
# DM Give an example of a SGLT-2. How does it work? What is the common side effect?
Example: - dapagliflozin Mechanism: - increase glucose excretion in urine Side effects: - UTIs - polyuria
86
# DM How do Alpha-Glucosidase Inhibitors work? What is the common side effect?
**Mechanism** - Reduces glucose absorption (inhibits the digestive enzyme) **Side effects** - GI side effects
87
# DM Name some other benefits of SGLT-2 inhibitor apart from increasing glucose excretion.
- lowers HbA1c - 32% lower all cause mortality - 35% lower risk heart failure - Improve CKD
88
# DM empagliflozin dapagliflozin canagliflozin What are these medications?
SGLT-2 inhibitors

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