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A2 ME3031 ENDO DM > 04: Clinical Lectures 3 DIABETES > Flashcards

04: Clinical Lectures 3 DIABETES Flashcards

1
Q

Describe how glucose is controlled in health and disease

A

insulin only hormone which lowers [BG] allowing tight control
= allows uptake at tissues

meanwhile glucagon supports glycogenolysis and gluconeo

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2
Q

Define Diabetes Mellitus and its classification

A

group of metabolic diseases of multiple aetiologies characterised by hyperglycaemia together with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both

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3
Q

State the common presenting symptoms of diabetes mellitus

A

polydipsia, polyuria, blurred vision, weight loss, infections

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4
Q

Describe the common epidemiological features of diabetes mellitus and how this relates locally, nationally and internationally

A

TYPE 1, much less than TYPE 2

DM2 RF: fhx, 30+ Maori & Indian subcontinent & Pacific Island, hx of gestational DM

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5
Q

Compare and contrast types 1 and 2 diabetes mellitus

A

T1DM
+AuAb e.g. anti-GAD
younger
genetic predisp + TRIGGER (?viral)

T2DM
As the Bcells become damaged by lipotoxicity and glucotoxicity as a result of insulin resistance, they can eventually no longer compensate, resulting in hyperglycaemia. a result of underlying insulin resistance and subsequent β-cell dysfunction.
*body requires more insulin to stimulate effective Glc control/uptake

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6
Q

Summarise the factors which may contribute to beta cell damage and the eventual clinical presentation of type 1 diabetes mellitus

A

Beta cell destruction = nil insulin

• INCREASED LIPOLYSIS = Wt loss
• REDUCED Glc UPTAKE = RAISED Glc PROD = HYPERGLYCAEMIA = Vasc. ; Urine+; Dehydr.
• KETONEAEMIA = DKA = N+V, Sweet breath, tired + unconscious

+glycosuria. = infection

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7
Q

Importance of hyperglc

A

Metabolic decompensation: DKA/HHS
Long term complications:
microvascular (retinopathy, neuropathy, nephropathy),
macrovascular (stroke, MI, PVD)

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8
Q

DM diagnosis levels

A

fasting ≥7.0 mmol/l, random ≥ 11.1 mmol/l

OGTT: 2hr after 75g: ≥11.1

HbA1c ≥48mmol/mol

  • ONE diagnostic lab glucose plus symptoms
  • TWO diagnostic lab glucose or HbA1c levels without symptoms.
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9
Q

Intermediate hyperglycaemia

A

Impaired fasting glucose 6.1-7 mmol/l

Impaired glucose tolerance 2h glucose ≥7.8 and <11mmol/l

HbA1c 42-47mmol/mol

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10
Q

When HbA1c cannot be used for diagnosis

A

All children and young people

corticosteroids, antipsychotic drugs (2 months or less). HbA1c can be used in patients taking such medication long term (i.e. over 2 months) who are not clinically unwell.

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11
Q

OTHER TYPES OF DIABETES

A

MODY: maturity onset diabetes in the young

  • AD = single gene defect
  • impaired B function

*glucokinase mut=birth, stable hyperglc.
> diet tx
*TF mut. = YA onset, progressive hyperglc.
>diet, OHA, insulin

GESTATIONAL: Fhx, insulin res. in preg.
*neonatal problems

2º DIABETES: corticosteroids, pancreatic destruction, syndromes,
*endocrine disorders: cushings, acromegaly, pheochromocytoma

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12
Q

Outline the principles of insulin therapy.

A

injected to ensure activated absorption (subcut. or intravenously)

30 mins before eating in order for hexamer insulin to dissociate

  • altering structure of insulin = affect rate of abs.
  • amount of insulin injected for meals should balance the carbohydrate intake consumed
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13
Q

Describe the various methods of administrating insulin therapy; twice daily, basal bolus, insulin pump treatment

A

BASAL BOLUS
SHORT: rapid cover CHO at meals 1unit/10g
LONG: background (twice/once daily)

TWICE DAILY - rapid, intermediate acting
pre-breakkie+pre-eve meal

(3) +intermediate @ bedtime
(4) short acting BB, BL, BT; intermediate BBed

CONT. SUBCUTANEOUS INULIN INFUSION
controls how much insulin injected

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14
Q

Understanding of Home blood glucose monitoring, flash glucose monitoring and targets

A

HOME BLOOD GLC. MONITORING & KETONE TESTING: adjusts insulin dose prior to driving e.g.

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15
Q

Understanding of Blood ketone monitoring HbA1c and glycaemic control

A

Monitoring vital in identifying at risk of DKA (>0.6) and thus knowledge of seeking urgent medical attention

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16
Q

Describe the symptoms, causes and emergency treatment of hypoglycaemia.

A
  • sweating++
  • pale
  • trembling,, shaking
  • anxious
  • tinling lips
  • hunger
  • palpitations

Rebound ketosis
Arrhythmias
Acute brain injury

d/t falling plasma glucose and resulting neuronal cell death via multiple pathways

conscious, oritentated, swallow+
> fast acting CHO
> rpt
> IV glc or IM Glucagon

conscious, swallow+ BUT CONFUSED
> treat as if mild if cooperative
> Glucagon & IV Glc

severe, unconscious, agressive, NBM
> stop insulin
> IV Glc +/- RPTs
> restart insulin once glc >4mmol

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17
Q

Aware of patient education resources

A

a

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18
Q

Describe the management of a patient with a new diagnosis of Type I Diabetes

A

> Levemir twice daily and a rapid acting analogue – be that Novorapid, Humalog or Apidra

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19
Q

Appreciate the importance of patient education and self management in a long term condition

A

TYPE 1 STRUCTURED EDUCATION

TECH. ENABLED DIABETES CARE

CONNECTED BG METERS

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20
Q

Discuss the natural progression of diabetes and the importance of patient centred care

A

Optimal blood glucose control (HbA1c)
to reduce microvascular disease e.g. retinopathy
to improve pregnancy outcome

Optimal blood pressure control
to reduce nephropathy

Manage cardiovascular risk factors
e.g. smoking, cholesterol

Screen for early detection of complications
feet, eyes & kidneys

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21
Q

Discuss the impact life events have on health and the importance of behavioural change and psychological support

A

a

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22
Q

DKA

A

d/t ⇧lipolysis; ⇧FFA to liver = ⇧ketogenesis

Nausea&vomiting
……………………………………….................
Abdominalpain
…………………………………………………..
Sweetsmelling,"ketotic"
Breath
……………………………………………….
Drowsiness
……………………………………………….
Rapid, deep “sighing” respiration
……………………………………………….
Coma

*known T1 or NEW T1; breathless pt d/t metabolic acidosis

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23
Q

DKA pres. mgmt

A

ketones less than <0.6mmol = normal
>rpt after 2 hours

0.6-1.4mmol/l = risk of DKA
1.5-2.9mmol/l
> rehydrate (sugar free), insulin, retest glc and ket

≥3.0mmol/l = DKA
>EMERGENCY
• ABC; IV access; vitals; clinical assess; full exam.
• glc, venous blood gas, urinanlysis/ketones, U+E, FBC, culture blood/urine, ECG+cardiac monitor, CXR

(hr 1) ACTRAPID 6units/hr + 0.9%saline
(hr 2) add dextrose with KCl, reduce insulin to 3U/hr
(hr 3) “”
(hr 4) restart s/c regiment when normal

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24
Q

Describe and explain the effects of acute deficiency of insulin, as in untreated Type I Diabetes

A

KETOACIDOSIS = DKA

HYPERGLC. = DEHYDR. = RENAL IMPAIRMENT

DEHYDR. = HYPEROSMOL.

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25
Q

Show the distinction between Type 1 and Type 2 Diabetes, with reference to insulin availability to and action upon its target cells.

A

In t2DM:
B cell dysf. + Diminished Incretin = ⇩insulin prod

XS Glucagon + Insulin resistance = ⇩insulin action

⇩insulin prod + action => ⇧blood glucose levels

26
Q

Describe the sites of action of insulin, mechanism of action of insulin and the interaction with the counter regulatory hormones (glucagon, adrenaline, cortisol and growth hormone)

A

a

27
Q

Describe the respective roles of diet, lifestyle issues and therapeutic agents eg,oral hypoglycaemic agents, SGLT2 inhibitors, GLP1 agonists and insulin in lowering blood glucose levels.

A

a

28
Q

Explain the causes, prophylaxis and treatment of hypoglycaemia (“hypos”) and hyperglycaemia (diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS))

A
  • restore bloog glc levels and cessating insulin infusions
  • HHS only seen in T2DM, nil ketones, presents w/ urine symptoms, polydipsia => dehydration alongside polyphagia => renal dysfunction as well as neuro dmg
29
Q

Explain the necessity for education of the patient in the management of his/her disease, and the role of a multi-disciplinary diabetic team.

A

a

30
Q

Describe the indications for and aims of treatment of the main groups of drugs used in the treatment of diabetes.

A

(1) METFORMIN (biguanide), addition to Wt loss and life-style mods
(2) SULPHONYLUREAS (Gli-ides) for osmotic symptoms or ⇧HbA1c (home monitoring)
(2) THIAZOLIDINEDIONES (Pioglitazone)

(2) DPP-IV INHIBITORS (…gliptin)
2nd or 3rd line agent

(2/3) GLP-1 ANALOGUES (…tides)
(2nd or) 3rd line agent
BMI >35, stop after 6/12
+oral agents, and stop after 3-6/12 / individual target reached

(2/3) SGLT-2 inhibitors - established CVD

31
Q

Describe their mode of action, and be able to illustrate examples from each group.

A

(1) METFORMIN (biguanide), improve insulin action @ liver, muscle
⇩FFA synth
improve R funct.; inhibit gluconeo.
+improves cvd outcomes in obese T2DM
+preg. safe
!lactic acidosis d/t inhibition of lactic acid uptake by liver
!B12 malabs.

(2) SULPHONYLUREAS (Gli-ides), ⇧insulin release@ PANCREAS binding to SUR-1 R.
-ATP K channels close depolarising B = Calcium influx
=> secretion of insulin
+used w/ metformin, rapid action
!hypoglc., wt gain, renal hepatic disease.
!CI prego.

(2) THIAZOLIDINEDIONES (e.g Glitazone,Pioglitazone),
improve insulin + protects pancreatic cells @ LIVER, ADIPOSE TISSUE, MUSCLE
-stimulates PPAR-gamma and insulin-sens genes
- ⇧expense of insulin-dependent glc.
- ⇩withdrawal of glc from liver
+effective for insulin res., cvd safety
!bladder ca., fluid retention, fractures in females
!wt. gain

(2/3) DPP-IV INHIBITORS (…gliptin)
improve insulin, incretin mimetics (diminished by DPP4)
+renal impairment safe, weight neutral, no hypoglc.
- more minimal glycemic control
!prego and breastfeeding
!nausea and vom
!injection and expensive

(2/3) GLP-1 ANALOGUES (…tides); incretin mimetics and increased insulin release, resistant to enz. breakdown = maintain glc levels
*weight loss
!nausea+vom, early satiety, injection and expensive
*LIRAGLUTIDE = great CVD, PVD reduction in hazard ratio
*exanatide pens

(2/3) SGLT-2 INHIB (…gliflozin e.g. canagliflozin)
= ⇧glucose excretion

32
Q

Discuss professional services and facilities necessary/ available to support education of individuals with diabetes.

A

a

33
Q

Discuss the importance of including family, colleagues, peers, etc. in diabetes education

A

a

34
Q

Main roles and interactions of drugs

A
  • displace sulfonylureas
  • ⇩ sulfonylurea metab.
  • ⇩ urinary excretion
  • intrinsic hypoglycaemic activity
35
Q

METFORMIN: indications & features

A

addition to Wt loss and life-style mods

(1) METFORMIN (biguanide), improve insulin action @ liver, muscle
⇩FFA synth
improve R funct.; inhibit gluconeo.
+improves cvd outcomes in obese T2DM
+preg. safe
!lactic acidosis d/t inhibition of lactic acid uptake by liver
!B12 malabs.

36
Q

SULPHONYLUREAS

A

for osmotic symptoms or ⇧HbA1c (home monitoring)

(2) SULPHONYLUREAS (Gli-ides), ⇧insulin release@ PANCREAS binding to SUR-1 R.
-ATP K channels close depolarising B = Calcium influx
=> secretion of insulin
+used w/ metformin, rapid action
!hypoglc., wt gain, renal hepatic disease.
!CI prego.

37
Q

THIAZOLIDINEDIONES

A

(2) THIAZOLIDINEDIONES (e.g Glitazone,Pioglitazone),
improve insulin + protects pancreatic cells @ LIVER, ADIPOSE TISSUE, MUSCLE
-stimulates PPAR-gamma and insulin-sens genes
- ⇧expense of insulin-dependent glc.
- ⇩withdrawal of glc from liver
+effective for insulin res., cvd safety
!bladder ca., fluid retention, fractures in females
!wt. gain

38
Q

INCRETIN MIMETICS

A

2nd or 3rd line agent

BMI >35, stop after 6/12
+oral agents, and stop after 3-6/12 / individual target reached

(2/3) DPP-IV INHIBITORS (…gliptin)
improve insulin, incretin mimetics (diminished by DPP4)
+renal impairment safe, weight neutral, no hypoglc.
- more minimal glycemic control
!prego and breastfeeding
!nausea and vom
!injection and expensive

(2/3) GLP-1 ANALOGUES (…tides); incretin mimetics and increased insulin release, resistant to enz. breakdown = maintain glc levels
*weight loss
!nausea+vom, early satiety, injection and expensive
*LIRAGLUTIDE = great CVD, PVD reduction in hazard ratio
*exanatide pens

39
Q

SGLT-2 INHIBITORS

A

established cvd risk = benefit

(2/3) SGLT-2 INHIB (…gliflozin e.g. canagliflozin)
= ⇧glucose excretion
- block action of sodium/glc transporter 2, ensuring glc is excreted

  • ⇧glycosuria = osmotic diuresis = dehydr, + hypoT
  • wt loss ~4kg VS DPPIV (2kg)
  • ⇩systolic BP = cessation of antiHT d/t slight Na excretion
!expensive
!UROGENITAL INFECTION
!digital amputation, DKA risk
!prego and breastfeeding
!renal (apart from CANAGLIFLOZIN @ low eGFR)
40
Q

INSULIN in T2DM

A

Insulin replacement as a solution; when other options are exhausted
OR osmotic symptoms and rapid emergency situation for symptom control

*supplementary insulin therapy Vs replacement insulin
= adds 1 injection of long acting insulin in combo of non-insulin meds
*progress to replacement
*low risk of hypoglc.
*ISOPHANE INSULIN, 1/day and at bedtime

=aim to suppress hepatic glc prod and control fasting glc level

41
Q

Alcohol & Diabetes

A

Alcohol reduces glycogenolysis
Alcohol contains calories
results in rise followed by fall in glucose

42
Q

Exercise and DM

A

reduce insulin before and after (upto 24 hours)
Reduction hypo risk
eat more (appropriate carbohydrate)
use different insulin regimen (maximise flexibility)

ideal: 7.0-15 blood glucose

43
Q

Driving and DM

A

Risks of hypos, poor vision, neuropathy

inform insurance, DVLA (if on insulin)

44
Q

Describe the link between obesity and type 2 diabetes and CVD

A

It is understood that people with diabetes are at increased risk of CVD and
the presence of obesity increases that risk.

Dietary intervention is crucial to the management

People with type 2 diabetes are at increased risk of CVD.
• Obesity is a well-established risk factor and is associated with
insulin resistance, hypertension, dyslipidaemia, inflammation and
cardiac dysrhythmia.

45
Q

Describe the presentation, screening and early management of diabetic macro and micro vascular disease.

A

MACROvasc: coronary vasc, cerebrovasc., PVD

MICROvasc: retinopathy, nephropathy, neuropathy

> Good diabetes control
Blood pressure control
Lipid control
Smoking cessation, weight, exercise

FOOT ULCER
>debridement + podiatry
> IV abx
>XR: ?osteomyelitis

46
Q

Outline the main mechanisms and pathological complications of diabetes mellitus.

A

DYSLIPIDAEMIA = ⇧triglyceride, LDLs = atherosclerosis = CVD & PVD

47
Q

RETINOPATHY

A

non-proliferative: CAPILLARY PLATELET AND BLOOD viscocity dysf.

PROLIFERATIVE: ischaemia, neovasc., viterous haemorrhage, retinal detachment

> laser photocoagulation

fundoscope: abdn exudates (white patches); engorged vessels; haemorrhagic spots (dark collections of blood)

48
Q

NEPHROPATHY

A

Microalbuminuria (basement membrane), glomerular HT => end-stage renal disease

screen: Albuminuria
DM control
RAAS block; >ACE inhib etc.
HT control

49
Q

NEUROPATHY

A

objective loss, particularly in feet & lower legs; subjective symptoms, especially paresthesia

lack of sensation can lead to the development of neuropathic ulcers, which, alongside poor macro-vasculature, leads to severe foot infections

AUTONOMIC neuropathy = GI effects (stomach, intestines),; cardiovascular system (tachycardia, blood pressure fluctuations)

50
Q

Other conditions in LT DM

A

Erectile dysfunction/sexual dysfunction

depression

51
Q

Discuss the impact life events have on health and the importance of behavioural change and psychological support

A

CBT and ACT

52
Q

Framework for introducing changes to behaviour

A

COM-B

CAPABILITY; OPPORTUNITY; MOTIVATION = BEHAVIOUR

53
Q

Aware of the importance of Laboratory services in the diagnosis and management of diabetes and endocrine disorders

A

random venous or fasting blood glc (≥11.1 / 7mmol)

2hr plasma glc ≥11.1 in OGTT

HbA1c ≥48mmol/mol (t2DM): glc moves intracellular into rbc

asymptomatic: rpt on another day

54
Q

Knowledge of point of care meters

A

ACUTE:

  • urine
  • glc meter: capillary blood glc
55
Q

Significance of biochemistry

A

HCO3 - low bicarb d/t metabolic acidosis to balance

UREA - marker of dehydration

CREATININE - high; marker of dehydration

Na - low d/t diluted ECF and travelling back

K - high d/t acidotic, moves out of cell to balance electrically

+urine albumin:creat DM renal - microvascular screening

+lipids - macrovascular screening

56
Q

Measurement of insulin

A

⇧insulin but absent C-peptide = FACTITIOUS HYPOGLYCEMIA (d/t exog. insulin)

⇧c-peptide = insulinoma!

57
Q

Significance of haemolytic anaemia

A

normal hba1c but not reflective + accurate diabetic blood glc measurement

+bilirubin can be elevated d/t breakdown product

58
Q

Weight mgmt

A 
NON-SURGICAL
>ORLISTAT: inhibit lipases
!GI sfx
\+in tandem w/ lifestyle changes
≥28BMI

tier 3 - Specialist wt

tier 4 - bariatric sx; gastric bands; specialist follow up
BMI ≥35
several comorb. that will improve upon wt. reduction
evidence of structured programme

59
Q

Which diabetic medication is contraindicated in patient populations at risk or diagnosed w/ angina and/or HFailure

A

THIAZOLIDINEDIONES = insulin sensitising drugs in DM2

In normal or sub=> HF monitoring indicated

60
Q

Significance of BMI and diabetic medication prescribing considerations

A

SFX of Wt. Gain
SULPHONYLUREAS = pancratic insulin stimulation

THIAZOLIDINEDIONES = insulin sensitising drug

On the other hand, 
METFORMIN 
and
GLP-1 = incretin-promoting
=> Wt. Loss SFX

A2 ME3031 ENDO DM (11 decks)

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