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phase 2 endo > DM > Flashcards

DM Flashcards

1
Q

What are the 3 major cell types of endocrine pancreas and what do they release?

A
  • β→ insulin
  • α→ glucagon
  • δ→ Somatostatin
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2
Q

What is the sequence of events involved in insulin release

A

↑BM→ ↑ glucose in β cells (GLUT2) → ATP ↑→ATP-sensitive K+ channel closing →depolarisation→ ↑Ca →exocytosis of vesicles

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3
Q

What are the main target tissues of insulin

A

liver, skeletal muscles, adipose tissue

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4
Q

what is the difference between actions of insulin and glucagon

A

insulin is anabolic and glucagon catabolic

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5
Q

what is the aetiology of T1DM

A

autoimmune destruction of β cells

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6
Q

what are the causative factors in T1DM

A

Genetic: concordance of 30% IT
Triggers: Coxsackie B4, vit D deficiency, dietary
HLA DR3/4 (also other autoimmunity)

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7
Q

what s the demographics of T1DM

A

↑ Scandinavian/Caucasian

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8
Q

What is the aetiology of T2DM

A
  • Loss of first phase of insulin response
  • ↑↑↑insulin secretion + ↓↓tissue response
  • Followed by ↓↓ function of β cells (due to glucotoxicity)
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9
Q

what is the prevalence of DM and what age group

A

> 40s 4.45% but undiagnosed

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10
Q

What ethnic groups are more at risk

A

South Asian, African, and African-Caribbean, , Middle-Eastern and American-Indian ancestry.

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11
Q

What is MODY

A

Maturity onset diabetes of the young (MODY) is a rare autosomal dominant form of type 2 DM affecting young people with a +ve family history

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12
Q

What are the RF for T2DM

A
  • ↓exercise ↑ alcohol +calories
  • FH: 80% concordance in IT/2xrisk
  • Ethnicity: South Asian, African, and African-Caribbean, , Middle-Eastern and American-Indian ancestry
  • Gestational diabetes
  • Impaired glucose tolerance and/or fasting glucose
  • Combination of thiazide diuretic + β-blocker
  • Diet: ↓fiber, ↑glucose
  • Metabolic syndrome
  • Polycystic ovarian syndrome
  • Low birth weight
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13
Q

Define IGT

A

Impaired glucose tolerance
it is either
Fasting plasma glucose 6.1- 6.9 mmol/L OR OGTT 7.8-11.1 and it is a RF for DM

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14
Q

Define IFG

A

impaired fasting glucose: fasting plasma glucose between 6.1-6.9 mmol/L

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15
Q

What is the significance if IGT and IFG

A

increased risk of T2Dm i.e. incidence of DM is 25% with upper level of normal IFG and HbA1c

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16
Q

Name 3 other cause + examples of DM

A

Drugs: e.g steroids
pancreatitis/ pancreatic cancer/CF destruction
Endocrine: Cushion’s, acromegaly, pheochromocytoma; hyperthyroidism; pregnancy

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17
Q

What is the prevalence of DM among pregnant women

A

4%

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18
Q

What are the criteria for diagnosis of gestational DM

A

FG 5.6 mmol/litre or above

OGTT 7.8 mmol/litre or above,

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19
Q

What are the risks of gestational DM

A 
o	miscarriage, 
o	pre-term labour, 
o	pre-eclampsia, 
o	congenital malformations, 
o	macrosomia,
o	A worsening of diabetic complications, e.g. retinopathy, nephropathy.
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20
Q

What are the RF for gestational DM

A

Risk factors: >25, FH, PMH, ↑BMI, non-Caucasian, HIV (screen at 16-18 week check if RF

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21
Q

What sort of advice can be offer per-conception in terms of DM

A

↓BMI, discuss risks, folic acid, stop hypoglycemics, metformin ok

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22
Q

What dietary advice could be offered to a t2DM

A
  • 3 meals per day
  • ↓ sugar, fat (35% of intake), salt (6g/24h), alcohol
  • ↑ starchy carbohydrates (40-60%), fibres
  • 2/7 x oily fish, eg mackerel, sardines, salmon and pilchards.
  • Exercise: 30min 5/7
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23
Q

What driving advice should be given to DM patients

A

• Inform DVLA/car insurance if: on insulin/oral hypoglycaemics, diabetic retinopathy
loss of hypoglycaemia awareness may lead to loss of license

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24
Q

What are the common sites for insulin injunctions?

A

buttock, abdomen, upper outer arm and thigh

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25
Q

what are the steps that can betaken to prevent CVS disease in DM patients

A
  • Stop smoking

* BP

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26
Q

What is the oral hypoglycameic regiment for treatment T2DM

A
  • 1st line: Metformin
  • If HbA1c ≥53mmol/L 16wks later, add: Sulfonylurea/gliptins if BMI≥35
  • If at 6mths, HbA1c ≥57mmol/L consider: insulin or glitazone
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27
Q

What sort of short-term and long term montoring is required in DM patients

A

• Fingerpick BM: before and after meals to adjust insulin
• HbA1c→mean glucose level in 8 weeks
o Target 48–57mmol/L
• Hypoglycaemic awareness

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28
Q

How would you instruct someone about use of insulin syringes?

A

• Instruction: dial dose→ insert needle 90° to

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29
Q

what are the 4 insulin types

A
  • Ultra-fats acting (Humalog, Novarapid) → just before meal/meal dependent dose
  • Isophane: peak 4-12h
  • Long acting e.g. Glargine; OD/BD, no peak →good nocturnal control
  • Pre-mixed: short and long acting component e.g. 30 = 30% Short acting and 70% long acting
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30
Q

What is the demand for insulin during acute illness

A

it may increase hence monitor BM and adjust the dose…get help if difficult to control

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31
Q

Why is it important to rotate injunction sites for insulin

A

to prevent lipohypertrophy and poor insulin absorption

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32
Q

Name some effects of automatic neuropathy

A

o Postural BP drop; ↓cerebrovascular autoregulation; loss of respiratory sinus arrhythmia (vagal neuropathy); gastroparesis; urine retention; erectile dysfunction (ED); gustatory sweating; diarrhoea

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33
Q

What is autonomic neuropathy

A

it is damage to autonomic nerves that can have an effect on number of organs, deneravtion of the heart is particularly concerning and leads to sinus arrhythmia

34
Q

what is symmetric sensory polyneuropathy

A

glovs and stocking distribution of loss of sensation, proprioception, pain , numbness tingling

35
Q

What is Sequelae neuropathy?

A

: interosseous wasting due to abnormal nerve supply to small muscles of the feet
o abnormally high arch of the foot and callus formation due to abnormal pressure distribution

36
Q

What is mononeuritis multiplex

A

o Isolated damage to at least two separate nerve areas particularly cranial nerves
o Painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy

37
Q

What is amyotrophy

A

o Asymmetrical motor diabetic neuropathy resulting
o Painful wasting of quadriceps and shoulder muscles
o Particularly older men with DM

38
Q

What are the microvascular complications of DM?

A

o Asymmetrical motor diabetic neuropathy resulting
o Painful wasting of quadriceps and shoulder muscles
o Particularly older men with DM

39
Q

What are the macrovascular complications of DM

A
  • Stroke
  • MI
  • ↓ leg blood supply
40
Q

What is the correlation between DM and vascular disease

A

o Common cause of death
o Stroke 2x as common
o MI 4 x as common and likely silent
o Women at ↑↑risk as removal of sex related advantage

41
Q

what steps can be taken to prevent vascular disease in DM

A

Stop smoking, aspirin and Statins, fibrates, HTN control

42
Q

What is the advice on HTN in DM?

A

15% Antihypertensive; target:

43
Q

What is maculopathy and what are associated sign

A

macular oedema leading to reduced acuity

44
Q

What are the changes in peripheral retina

A

microaneurisms, cotton wool spits,haemorrhages, hard exudate, proliferation of blood vessels, venous beading

45
Q

what is the treatment for maculopathy/

A

laser photocoagulation that stops production of angiogenic factors

46
Q

what is the treatment for changes in peripheral retina

A

o Intravitreal triamcinolone→ steroid injections

47
Q

what is the treatment for macular oedema

A

Prompt laser, intravitreal steroids or anti-angiogenic agents may be needed in macular oedema.

48
Q

What examinations should be carried out when checking DM feet

A
  • Absent ankle jerks

* test sensation with a 10g monofilament fibra applied with just sufficient force to bend it

49
Q

What are the evidence of ischameia and neuropathy in diabetic feet

A 
o	loss of leg pulses 
o	can be examined with Doppler
o	Neuropathy
o	Bone deformity
o	Infection → swabs and check for osteomyelitis with x-ray
50
Q

What are the management options for diabetic foot ischaemia

A

o Surgery → endovascular angioplasty balloons, stents, and subintimal recanalization

51
Q

What sort of steps should patients be taking to prevent foot ulcers when suffering from DM

A

o Daily foot exam →with the mirror to check the soles
o Comfortable shoes
o No barefoot walking
o No corn plasters

52
Q

Who can be involved in diabetic foot care

A

o Regular chiropody → removal of callus (ulcers can develop below it)
consultant diabetologist
o Regular pediatrist checks

53
Q

What are the 3 characteristics of diabetic feet ulcers

A

o Painless
o Pouched out in area of thick callus
o May be infected

54
Q

What are the possible management steps for foot ulcers

A

o Relieve high pressure areas with bed rest

o Surgery → metatarsal head

55
Q

How should cellulitis be treated in DM and what are the common causes

A

o Relieve high pressure areas with bed rest

o Surgery → metatarsal head

56
Q

what are diagnostic criteria for metabolic syndrome

A

o central obesity (BMI >30, or ↑ waist circ),
o plus 2 of
 BP ≥130/85,
 triglycerides ≥1.7mmol/L,
 HDL ≤ 1.03♂/1.29♀mmol/L,
 fasting glucose ≥5.6mmol/L or DM (∼20% are affected)

57
Q

What are the risks related to metabolic syndeome

A 
o	Vascular events i.e. MI
o	DM
o	Neurodegeneration
o	Microalbuminuria
o	Gallstones
o	Cancers i.e. pancreas
o	Fertility problems in M and F
58
Q

What is the management of metabolic syndrome

A 
o	Lifestyle: exercise, weight loss, diet
o	Antihypertensive
o	Hypoglycemics
o	Statins
o	Antidepressants
59
Q

What are the symptoms of hypoglycaemia

A

• Autonomic
o Sweating, anxiety, hunger, tremor, palpitations, dizziness.
• Neuroglycopenic
o Confusion, Drowsiness, Visual trouble, Seizures, Coma.
o Rarely focal symptoms, e.g. transient hemiplegia. Mutism, personality change, restlessness and incoherence → prone to misdiagnosis of alcohol intoxication

60
Q

define hypoglycaemia

A

Plasma glucose ≲3mmol/L. Threshold for symptoms varies.

61
Q

what are the two types of hypoglycaemia

A
  • Fating

* Post-prandial

62
Q

what are the causes of fasting hypoglycaemia

A

o Insulin or sulfonylureas treatment → ↑activity, skipped meals, overdose etc.
o In NON-DM
 Exogenous →
• Insulin, oral hypoglycemics→ body builders
• Alcohol
• aspirin poisoning; ACE-i; β-blockers; pentamidine; quinine sulfate; aminoglutethamide; insulin-like growth factor.
 Pituitary insufficiency
 Liver failure, plus some rare inherited enzyme defects
 Addison’s disease.
 Islet cell tumours (insulinoma) and immune hypoglycaemia
 Non-pancreatic neoplasms, e.g. fibrosarcomas

63
Q

how is hypoglycamia assessed

A

o BM
o Blood glucose, c-peptide, plasma ketones
o Drug history

64
Q

what is o Hypoglycaemic hyperinsulinaemia

A

Low blood glucose due to excessive insulin i.e. insulinoma, sulfonylureas, insulin

65
Q

what causes hypoglycaemia with normal insulin and ketones

A

non-pancreatic neoplasia, anti-insulin receptor antibody

66
Q

What causes hypoglycaemia with Insulin↓, ketones↑.

A

o Insulin↓, ketones↑.

 Causes: Alcohol, pituitary insufficiency, Addison’s disease.

67
Q

what is Post-prandial hypoglycaemia

A

Hypoglycemia occurring few hours post ↑↑↑carbohydrate meal due to excess insulin secretion, common with bariatric surgery

68
Q

how is Post-prandial hypoglycaemia managed

A

o 1st line Oral sugar or long-acting starch
o 2nd line: 25-50ml of 50% glucose +flash to prevent phlebitis
o Small high starch meals if recurrent

69
Q

What is the Whipple’s triad

A

Symptoms due to fasting/exercise→ hypoglycaemia + symptoms →relief of symptoms with serum glucose returning to normal

70
Q

what is insulinoma what are the symptoms and screening test

A

pancreatic endocrine tumour
• Symptoms
o Fasting hypoglycaemia with Whipple’s triad
• Screening test
o Hypoglycaemia + ↑insulin during fasting

71
Q

what is the cositive process in diabetic ketoacidosis

A

o Alternative metabolic pathway in starvation →acetate production → fruity breath
o If ↓↓insulin → glucose not taken in → starvation-like state
o Combination of sever acidosis and hyperglycaemia

72
Q

what are the signs of dehydration

A 
	Dry mucus membranes
	Decreased skin turgor
	Sunken eyes
	Slow capillary refill
	Tachycardia and weak pulse
	Hypotension
73
Q

what are the tiggers for diabetic ketoacidosis

A

o Infection, MI, surgery, pancreatitis
o Chemotherapy, antipsychotic
o Medication problem

74
Q

What criteria can be used for transfer to ITU

A

o Blood ketones >6mmol/L

o Venous bicarbonate 100 or

75
Q

what is the initial management of diabetic ketoacidosis

A 
o	ABCDE
	SATs, ECG, BP, HR, EWS 
	Long-bore peripheral IV access 
	Urinary catheter → urine output 
	? TED stockings/LMWH
	NG tube if vomiting/ ↓GCS
	Fluids → saline → replace with 5% dextrose when BM 5.5 mmol/l => no 
o	3.5-5.5. => 40mmol
o	Insulin:
	Sliding scale insulin or weight based IV infusion
	Infusion even with ↓BM as DKA required to clear (0.1 U/kg) 
	↓ BM by 3mmol/L/h
76
Q

What are the complications of diabetic ketoacidosis

A 
o	Cerebral oedema (get help if sudden CNS decline), 
o	Aspiration pneumonia, 
o	Hypokalaemia, 
o	Hypomagnesaemia, 
o	Hypophosphataemia, 
o	Thromboembolism.
77
Q

How is hypoglycaemic coma managed

A

o Give 20–30g glucose IV, e.g.
 200–300mL of 10% dextrose.
 This is preferable to 50–100mL 50% glucose i.e. phlebitis
o Expect prompt recovery

78
Q

what are the symptoms of hypoglycaemic coma

A

• Usually rapid onset; may be preceded by odd behavior (e.g. aggression), sweating, pulse↑, seizures.

79
Q

what is Hyperosmolar non-ketotic (HONK) coma

A

marked dehydration and glucose >35mmol/L. leads to increased osmolarity

80
Q

what is the management of HONK

A

o DVT—give LMWH prophylaxis to all unless contraindication
o Rehydrate slowly with 0.9% saline IVI over 48h, typical deficits are 110–220mL/kg, i.e. 8–15L for a 70kg adult.
o Replace K+ when urine starts to flow.
o Only use insulin if blood glucose not falling by 5mmol/L/h with rehydration or if ketonaemia—start slowly 0.05u/kg/h.
o Keep blood glucose at least 10–15mmol/L for first 24 hours to avoid cerebral oedema.
o Look for the cause, e.g. MI, drugs, or bowel infarct.

81
Q

what is the high risk HbA1c

A

42-47 mmol/mol

82
Q

What is the HbA1c that is consider to be DM

A

48 mmol/mol

phase 2 endo (4 decks)

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