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Year 3 Medicine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is Diabetes Insipidus?

A

Reduced ADH secretion/kidney response to ADH causes passage of large volumes of dilute urine

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2
Q

Give 3 symptoms of Diabetes Insipidus

A

Polyuria
Polydipsia
Dehydration

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3
Q

Give 3 causes of Cranial DI

A

Congenital (ADH genetic defects)
Tumour
Trauma

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4
Q

Give 3 causes of Nephrogenic DI

A

Inherited
Chronic Renal Disease
Drugs (Lithium, Demeclocycline)

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5
Q

What 4 investigations could you do if you suspected DI?

A

Us and Es
Glucose (rule out DM)
Urine Osmolality (rule out primary polydipsia)
8hr Deprivation Test

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6
Q

How would you treat Cranial DI?

A

Desmopressin

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7
Q

How would you treat Nephrogenic DI?

A

Treat underlying causes
NSAIDs (Prostaglandins locally inhibit ADH)
Bendroflumethiazide (inducing hypovolaemia may kickstart RAAS)

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8
Q

Describe the pathophysiology of Type 1 DM

A

Onset in childhood
Autoimmune destruction of pancreatic B cells
HLA association

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9
Q

Describe the pathophysiology of Type 2 DM

A

Decreased insulin secretion/increased insulin resistance
Associated with obesity/sedentary lifestyle
No HLA association
There is an autosomal dominant form affecting young people

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10
Q

Give 4 other causes of DM

A

Steroids
Pancreatitis
Cushings Disease
Glycogen Storage Disease

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11
Q

What is the triad of DM symptoms

A

Polyuria
Polydipsia
Weight Loss

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12
Q

What are the parameters for diagnosing DM in terms of Venous Glucose?

A

Fasting >7mmol/l

Random >11.1mmol/l

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13
Q

What is the parameter for diagnosing DM using the OGTT?

A

> 11.1mmol/l

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14
Q

What is the parameter for diagnosing DM using HbA1c?

A

> 48mmol/l

>6.5%

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15
Q

What are the parameters for ‘Pre-Diabetes’?

A

Fasting glucose of 5.5-6.9mmol/l

HbA1c of 42-47mmol/l (6-6.4%)

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16
Q

What is required for a Diabetes diagnosis?

A

Either
Symptoms and ONE positive blood result
Or
Positive bloods on two separate occasions

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17
Q

What advice would you give patients who are diagnosed with Type 1 DM? Give 4 points.

A

Review and research diet
Try to limit other things contributing to CVS risk
Ensure foot care
Avoid binge drinking (delayed hypoglycaemia)

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18
Q

Name one ultrafast, one medium and one long acting insulin

A

Ultrafast - Novorapid
Medium - Isophane Insulin
Long - Insulin Glargine

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19
Q

Name a premixed insulin

A

Novomix (30% short, 70%long)

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20
Q

Describe 2 different regimens to manage T1DM

A
  • BD biphasic regimen - Twice Novomix daily

- QDS - Ultrafast at meals, long acting at night (more flexible - can adjust dose with meal size and exercise)

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21
Q

What could you give patients if they struggle with the insulin regime?

A

Insulin Pump

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22
Q

Give three important pieces of advice for T1DM regarding insulin

A

Vary injection site
Change needles
Continue insulin if ill (and replace lost calories with milk)

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23
Q

Describe the 4 step (up) therapy for T2DM

A

1) Lifestyle and Diet
2) Metformin
3) Dual Therapy (Metformin + another)
4) Triple Therapy or Insulin Therapy

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24
Q

What is Metformin’s action?

A

Biguanide reduce hepatic glucose output and increases insulin sensitivity
do not stimulate insulin = do not cause hypoglycaemia

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25
Q

Give 4 SE of Metformin

A

Nausea
Abdo Pain
Lactic Acidosis (in renal impairment)
modest weight loss

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26
Q

Name a DPP4 Inhibitor. What is it’s action?

A

Sitagliptin
DPP4 destroys incretins which enhance insulin release so by inhibiting this = lower blood glucose by preventing incretin degradation
incretin action is glucose dependent so do not stimulate inuslin secretion at normal glucose concentrations = unlikely to cause hypoglycaemia

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27
Q

Name a Glitazone (thiazolidinediones). What is it’s action?

A

Pioglitazone
Increases insulin sensitivity in muscle and adipose tissue
decrease insulin resistance and decrease hepatic glucose

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28
Q

When are Glitazones contraindicated? What are their side effects?

A

CI - Osteoporosis, CCF

SE - Hypoglycaemia, Fractures

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29
Q

Name a Sulphonylurea? What is it’s action?

A

Gliclazide

Increases insulin secretion by binding to ATP sensitive potassium channels, closing them

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30
Q

Name an SGLT2 inhibitor. What is it’s action?

A

Dapaglifozin

Blocks glucose reabsorption in the PCT = decrease blood glucose by passing urine

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31
Q

Name a GLP1 analogue. What is it’s action?

A

Exenatide

Incretin mimics

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32
Q

Name four complications of Diabetes

A

Vascular disease
Nephropathy
Retinopathy
Neuropathy

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33
Q

Give two eye diseases associated with Diabetes

A

Diabetic Retinopathy

Cataracts

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34
Q

Describe the pathophysiology of Diabetic Retinopathy

A

capillary basement membrane thickening leading to leaky vessels, occluded vessels and macular oedema

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35
Q

Describe 3 characteristic features of Diabetic Retinopathy

A

Microaneurysms - physical weakening of vascular walls
Haemorrhages - when weakened vessels rupture, can be small or large (AKA Flame - track along nerve-fibre bundles in superficial retinal layers)
Cotton Wool Spots - Build up of axonal debris

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36
Q

How would Diabetic Retinopathy present?

A

Often gradual painless visual deterioration

If haemorrhages - sudden onset of dark, painless floaters which may resolve over several days.

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37
Q

Most Diabetic Retinopathies are not treated, however if they are, give 2 treatment options

A

Laser Treatment - aim is to induce regression of new blood vessels and reduce central macular thickening

Intravitreal Steroids

38
Q

Give 4 possible features of foot neuropathy

A

Reduced sensation in stocking distribution
Absent ankle jerks
Charcot Joint
Claw Toes

39
Q

How would a diabetic ulcer present?

A

Punched out ulcer in area of thick callus

40
Q

Describe 3 non surgical managements of ‘Diabetic Foot’

A

Regular Chiropody
Bisphophonates
Antibiotics

41
Q

Hypoglycaemia is classified as <3mmol/l glucose. Majority of times it’s a diabetic cause, but using the mnemonic EXPLAIN, state 7 non diabetic causes.

A 
Exogenous Drugs (ACEI, B Blockers)
Pituitary Insufficiency
Liver Failure
Addisons
Insulinoma
Non pancreatic Neoplasms
42
Q

Give 3 autonomic and 3 neuroglycopenic symptoms of Hypoglycaemia.

A

Autonomic - Sweating, Anxiety, Hunger

Neuroglycopenic - Confusion, Drowsiness, Coma

43
Q

What is Whipple’s Triad?

A

Symptoms + Hypoglycaemia + Resolution as plasma glucose rises

44
Q

Describe the pathophyiology of DKA

A

Without insulin to drive glucose into the cells, the body is forced into starvation state, using ketones for energy and causing acidosis

45
Q

Name causes/ triggers of DKA

A 
Infection
Non Compliance
Surgery/trauma 
undiagnosed T1D
drugs affecting carbohydrate metabolism 
Chemo
46
Q

Name 5 symptoms of DKA

A

Drowsiness
Abdo Pain, N&V
Dehydration
Polydipsia, Polyuria

47
Q

Describe 3 diagnostic classifications of DKA

A

Acidaemia - pH<7.3
hyperglycaemia - >11.1mmol/l
Ketonaemia (>3mmol/l) or Ketonuria (>2+)

48
Q

Describe a four step initial management plan of DKA

A

A-E and IV access - 2 large bore
1. 1L 0.9% saline bolus
2. 50 units act rapid in 50ml fluid at 0.1 unit/kg/hr (fixed rate insulin infusion)
3. add potassium to second bag
4. once glucose <14 mmol/L start dextrose infusion
Ref ITU input

49
Q

Give 3 complications of DKA

A

Cerebral Oedema
Hypokalaemia
Aspirational Pneumonia

50
Q

Describe the different between Dry and Wet Gangrene

A

Dry Gangrene - Black ‘mummified’ toes that often autoamputate
Wet Gangrene - indicates infection

51
Q

Describe four features indicating Necrotising Fasciitis from Diabetic Foot

A

Spreading Cellulitis
Black Spots
Dishwater Fluid Appearance
Crepitus (tissue paper sound when pressing - gas gangrene)

52
Q

Describe two features you are looking for on an X-Ray of a diabetic foot

A

Osteomyelitis

Gas Gangrene

53
Q

Why is ABPI generally done on right arm?

A

Steal Syndrome is more common on the left

You generally stand to the right of the patient

54
Q

Explain the ABPI value indicating Diabetic Foot

A

> 1.2
Due to calcification of the peripheral arteries increasing the pressure (NOT because they have superior blood flow to PAD)

55
Q

Describe the Doppler Sounds of vessels

A

Monophasic
Biphasic
Triphasic

Monophasic is diseased, and triphasic is healthy (you can hear the elastic recoil in competent vessels)

56
Q

Using the mnemonic SWOMPD, how would you manage a diabetic foot?

A 
Sepsis
Wound Management
Offloading (Orthotics)
Mechanical (Orthopaedics input)
Perfusion (Lifestyle, Meds, Surgical)
Diabetic Control
57
Q

What antimicrobials would you use for MILD Diabetic Foot?

A

Flucloxacillin

58
Q

What antimicrobials would you use for MODERATE Diabetic Foot?

A

Flucloxacillin, Ciprofloxacin and Metronidazole

59
Q

What antimicrobials would you use for SEVERE Diabetic Foot?

A

Piperacillin, Tazobactam and Vancomycin

60
Q

name 4 short acting insulins - Rapid acting and soluble

A

rapid acting - novorapid & humalog

soluble - humulin S & actrapid

61
Q

name 4 intermediate acting insulins

A

Isophane
Insulatard
Humulin 1
Insuman basal

62
Q

name 4 long acting insulins

A

insulin glargine - lantus
insulin detemir - levemir
insulin degludec - tresiba

63
Q

name 4 symptoms of hyperglycaemia

A

polyuria
polydipsia
blurring of vision
urogenital infections - thrush

64
Q

name 4 symptoms of inadequate energy utilisation

A

tiredness
weakness
lethargy
weight loss

65
Q

what insulin regimen is good to use when switching from tablets to insulin in T2DM?

A

once-daily before-bed long-acting

66
Q

why is insulin given SC?

A

insulin is inactivated by GI enzymes

67
Q

where is best to inject insulin and why?

A

plenty of SC fat - abdomen

quick absorption

68
Q

why is it important to rotate injection sites?

A

prevent lipohypertrophy

which causes erratic absorption leading to poor glycaemic control

69
Q

what do you have to check injection sites for?

A

swelling
bruising
infection
lipohypertrophy

70
Q

what advice should you give someone taking insulin regarding sickness?

A

do not stop taking insulin
maintain calorie intake with milk
check blood glucose at least 4 times a day
monitor for ketonuria
increase insulin if blood glucose increases

71
Q

what are some dangers of taking insulin

A 
hypoglycaemia 
allergy
hypokalaemia
painful injections 
heart failure 
lipohypertrophy
72
Q

what are the 2 functions of insulin?

A

Cause cells to absorb glucose from blood and use it as fuel

Cause muscle and liver cells to absorb glucose and store it as glycogen

73
Q

side effects of DPP4 inhibitor - sitagliptin

A

GI upset

headache

74
Q

side effects of sulphonylureas - glicazide

A

hypoglycaemia - stimulation of insulin secretion
weight gain
gi upset

75
Q

side effects of SGLT2 inhibitors - dapagliflozin

A

increased risk of UTI and genital tract infections

76
Q

what are the microvascular complications of diabetes?

A

diabetic retinopathy
nephropathy
neuropathy

77
Q

what are the macrovascular complications of diabetes?

A

PVD, stroke, MI, intermittent claudication

78
Q

how does diabetic neuropathy come about?

A

multiple mechanisms - including damage to small blood vessels nourishing the peripheral nerves and abnormal sugar metabolism

79
Q

what are the manifestations of diabetic neuropathy?

A

peripheral sensory neuropathy - progresses from loss of vibration to glove and stocking sensory loss
mononeuropathies
amyotrophy - painful wasting of thigh muscle
autonomic neuropathy

80
Q

what is autonomic neuropathy

A

damage to the autonomic nerves from high levels of blood glucose leading to postural hypotension, bladder dysfunction, sweating, temperature regulation issues, and other orthostatic symptoms like nausea, palpitations, light-headedness, tinnitus, SOB

81
Q

what is nephropathy?

A

hypoglycaemia leads to increased glomerular capillary pressure, podocyte damage.
albuminuria is first sign

82
Q

how is nephropathy diagnosed?

A

microalbuminuria = A:Cr 3-30mg/mmol

not detected on urine dip stick at this stage

83
Q

how is nephropathy treated?

A 
good DM control 
BP <130/80
ACEi - reduce proteinuria 
sodium restriction 
statin
84
Q

what medications should be used with caution in CKD?

A

sulfonylureas
Biguanides
SGLT2i
Exenatide

85
Q

signs of DKA

A 
volume depletion
- dry mucous membranes 
- poor skin turgor 
- sunken eyes 
- tachycardia 
- hypotension 
kussmaul respiration - rapid and deep respiration due to acidosis 
acetone breath
86
Q

further management of DKA - not initial steps

A

monitor blood ketone levels and blood glucose levels
consider catheter
check VBG at 2 4 8 12 and 24 hours

87
Q

What is a Hyperosmolar Hyperglycaemic State?

A

Seen in unwell patients with T2DM
Hx of a weeks dehydration with glucose>30mmol/l
NO KETONE METABOLISM as insulin levels are sufficient to prevent this

88
Q

How would you manage Hyperglycaemic Hyperosmolar State?

A

A-E + access
Rehydrate slowly - 0.9% NaCl
Replace K+ when urine starts to flow
Only use insulin if glucose is falling at rate < 5 mmol/L/hr despite adequate fluid replacement - start low 0.05units/kg/hr

89
Q

what causes HHS?

A

poor diabetic control
infection - sepsis
dehydration

90
Q

features of HHS

A

hypovolaemia - volume depletion
hyperglycaemia - >30mmol/L without ++ ketones
hyperosmolarity - >320mosmol/kg
much longer hx than DKA

Year 3 Medicine (15 decks)

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