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Endocrine SB > Diabetes > Flashcards

Diabetes Flashcards

1
Q

pathogenesis of Type 1 diabetes

A

b-cell failure = absolute insulin deficiency

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2
Q

pathogenesis of Type 2 diabetes

A

Hyperinsulinaemia + insulin resistance

Beta Cell dysfunction

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3
Q

T1DM presentation

A 
pre-school/pre-puberty
severe weight loss
ketonuria ± metabolic acidosis
Tired
polydipsia + polyuria
i.e. very thirsty + peeing a lot
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4
Q

T2DM presentation

A

middle-aged/elderly
usually obese
insidious onset over weeks to years

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5
Q

risk factors for T2DM

A

central obesity
FH
Age
Phx of MI/stroke

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6
Q

symptoms of DM

A 
Thirst 
Polyuria
Thrush
Weakness Fatigue
Blurred Vision
Infections
Weight Loss
T2DM- Signs of complications- neuropathy, retinopathy
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7
Q

useful discriminatory tests for type 1 and type 2

A

GAD/ Anti-Islet Cell antibodies
Ketones
C-peptide (plasma)

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8
Q

what is LADA

A

late-onset type 1 diabetes

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9
Q

what causes Type 3 diabetes

A

Pancreatic disease
Endocrine disease
Drug-induced
Abnormalities of insulin and its receptor i.e. Genetic diseases

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10
Q

what pancreatic diseases can cause diabetes

A

Chronic or recurrent pancreatitis
Haemochromatosis
Cystic Fibrosis


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11
Q

what endocrine diseases can cause diabetes

A

Cushing’s syndrome
Acromegaly
Phaechromocytoma
glucagonoma

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12
Q

what drugs can cause diabetes

A

Glucocorticoids
Diuretics
B-blockers

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13
Q

what genetic diseases are related to diabetes

A

Cystic fibrosis
Myotonic dystrophy
Turner’s syndrome

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14
Q

what is Type 4 diabetes

A

Gestational diabetes:


i.e. Any degree of glucose intolerance arising or diagnosed during pregnancy

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15
Q

what is HbA1c and why do we measure it

A

glycated hemoglobin

provides a measure of glucose control over past 2-3 months

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16
Q

what are complications of diabetes

A

Micro-vascular: Retinopathy, Nephropathy, Neuropathy

Macro-vascular: Heart disease and stroke

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17
Q

what Ix findings are suggestive of diabetes

A

Diagnose diabetes
Fasting glucose ≥ 7.0mmol/l
Random ≥ 11.1mmol/l
and symptoms, OR repeat test

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18
Q

how can the type of diabetes be differentiated

A

Often Type 1 diabetes is diagnosed on the history and presentation (e.g. DKA) alone

GAD/IA2 antibodies [and C-peptide] may help

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19
Q

what antibodies are related to Type 1 DM

A

GAD
IA2 antibodies
IAA
ZnT8Ab

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20
Q

what can be seen on a histology slide of type 1 diabetes

A

lymphocytes attacking the islet

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21
Q

what gene is associated with T1DM

A

HLA genes

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22
Q

why can C-peptide be a diagnostic test

A

C-peptide is produced when insulin is made

if there is a low volume of C-peptide suggests that insulin is not being made

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23
Q

what is the classic triad of DM

A

Polyuria
- Enuresis in children
Polydipsia
Weight loss

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24
Q

what is enuresis

A

involuntary urination, especially by children at night.

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25
Q

Mx of newly diagnosed Type 1 DM

A

Blood glucose and ketone monitoring
Insulin: usually basal [once daily] bolus [with meals] regimen
Carbohydrate estimation
Regular check of prevailing glycaemic control

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26
Q

what is the ideal range of glucose control in T1DM

A

HbA1c 48 to 58 mmol/mol

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27
Q

insulin therapy in Type 1; for adults

A

either regular human or rapid-acting insulin analogues

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28
Q

insulin therapy in Type 1; for children/teens

A

either insulin analogues (rapid-acting or basal), regular human insulin and NPH preparations or an appropriate combination

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29
Q

where is insulin secreted to

A

portal vein

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30
Q

neonatal diabetes - Children diagnosed under the age of six months are more likely to have what

A

Monogenic

rather than T1DM

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31
Q

when should LADA be suspected

A 
age 25-40
male more often 
non-obese
auto-antibody positive
associated auto-immune conditions
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32
Q

CF and diabetes relationship

A

found in ‘severe’ mutations, i.e. ∆508
prone to complications
insulin therapy preferred

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33
Q

what is Wolfram syndrome also known as and why

A

DIDMOAD

Diabetes Insipidus
Diabetes Mellitus
Optic Atrophy
Deafness
Neurological anomalies
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34
Q

presentation of Bardet-Biedl Syndrome

A 
Often very obese
Polydactyly
Hypogonadal
Visual impairment
Hearing impairment
Mental retardation
Diabetes
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35
Q

what are the associated auto-immune conditions of diabetes

A 
Thyroid disease
Coeliac disease
Pernicious Anaemia
Addison’s disease
IgA deficiency
Auto-immune polyglandular syndromes [Type 1 and Type 2]
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36
Q

what is Pernicious Anaemia

A

a deficiency in the production of red blood cells through a lack of vitamin B12

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37
Q

which type of Polyglandular Endocrinopathy is associated w/ T1DM

A

Type 2

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38
Q

what else is type 2 Polyglandular Endocrinopathy associated with

A 
T1DM
Addison’s disease
Vitiligo
Primary hypogonadism
Primary hypothyroidism
Coeliac disease
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39
Q

what is type 1 Polyglandular Endocrinopathy associated with

A

Primary hypoparathyroidism/Pernicious anaemia/alopecia

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40
Q

what is insulin resistance

A

receptor is not as responsive to the insulin molecule and therefore less glucose enters the cell. This results in a build up of glucose in the blood

41
Q

what causes Insulin Resistance

A

Ectopic Fat Accumulation and increase FFA circulation
+ increase inflammatory mediators

> > > Inhibition of insulin via serine kinases responsible for phosphorylation of Insulin Receptor Substrate-1 (IRS-1)

> > > Reduction in insulin-stimulated glycogen synthesis due to reduced glucose transport

42
Q

what is insulin resistance a pre-cursor for

A

Type 2 diabetes

43
Q

how does the beta cells initially compensate for increasing insulin resistance

A

body tries to compensate by producing more insulin as insulin resistance increases

44
Q

when do blood glucose levels increase

A

when the beta cells burn out

45
Q

what cause declining beta cell function

A

Glucotoxicity - hyperglycaemia

Lipotoxicity - elevated FFA, TG

46
Q

what is the Metabolic Syndrome

A

at least three of five of the following:

  • abdominal (central) obesity,
  • elevated blood pressure,
  • insulin resistance
  • high serum triglycerides
  • low HDL levels.
47
Q

what is the therapy staircase for Type 2 diabetes

A

1 - diet and exercise
2 - oral mono therapy
3 - oral combination
4 - injectable and oral therapy

48
Q

what are the risks with alcohol consumption in diabetes

A

Hypoglycaemia, esp. if no food (alcohol activity of insulin) - more prone if using insulin or sulphonylureas
‘Confusing’ hypo symptoms

49
Q

what is MODY

A

Maturity onset diabetes of the young
Autosomal dominant inheritance
Non-insulin dependent diabetes
Age of onset usually before age 25

50
Q

what are the 2 phenotypes of MODY

A 
transcription factor (HNF-1alpha)
glucokinase (GCK)
51
Q

what are HNF1A sensitive to

A

SU

52
Q

what is the treatment of GCK MODY

A

does not require treatment

53
Q

what can cause neonatal diabetes

A

potassium channel mutation

54
Q

what are the two types of neonatal diabetes

A

Transient neonatal diabetes
(TNDM)

Permanent neonatal diabetes
(PNDM)

55
Q

what is PNDM treated with

A

SU’s

56
Q

what are symptoms of hypoglycaemia

A 
shaking
sweating
anxious, irritable 
dizziness
tachycardia
blurred vision
weakness
fatigue
headache 
hunger
57
Q

what can hypoglycaemia cause

A

seizures, unconsciousness

58
Q

Tx of mild hypoglycaemia

A

Consume 15-20 grams of glucose or simple carbohydrates

Recheck your blood glucose after 15 minutes

59
Q

examples of 15grams of simple carbohydrates

A

glucose tablets
gel tube
coke/lucazade

60
Q

Tx of severe hypoglycaemia

A

Glucagon 1 mg

  • Inject into buttock / arm or thigh
  • May cause nausea + vomiting
61
Q

what is impaired hypoglycemia awareness

A

When hypoglycaemia occurs (4.0-3.5 mmol/l) and individuals feel no or a change symptoms.

62
Q

what are common precipitant of DKA

A

infection - Gastroenteritis
illicit drugs and alcohol
non-adherence w/ treatment
newly diagnosed diabetes

63
Q

symptoms/signs of DKA

A 
Thirst/Polyuria/Dehydration
Flushed
Vomiting
Abdo pain and tenderness
Breathless - Kussmaul's respiration
64
Q

classic biochemistry of DKA at presentation

A

Glucose: Median level around 40 mmol/L [Normal 5

65
Q

Complications of DKA

A

Cerebral oedema
ARDS
Hypokalemia&raquo_space; Cardiac dysrhythmia

66
Q

Mx of DKA

A

IV fluids
- Potassium replace
- IV insulin
Supportive care

67
Q

what do urine ketone testing machines measure

A

acetoacetate levels

68
Q

when should a T1DM be admitted into hospital

A 
Unable to tolerate oral fluids
Persistent vomiting
Persistent hyperglycaemia
Persistent positive/increasing levels of ketones
Abdominal pain / breathlessness
69
Q

what is Hyperglycaemic Hypersomolar Syndrome (HHS)

A

complication of T2DM - severe hyperglycaemia, hyperosmolality, and volume depletion, in the absence of severe ketoacidosis.

70
Q

features of HHS

A

Diabetes may be known, often not
If known, then often treatment is ‘diet alone’
Usually older individuals
Associated risks - MI, stroke, sepsis, Glucocorticoids and thiazides

71
Q

symptoms/signs of HHS

A

altered mental state
thirsty/polyuria/weight loss
weakness
poor skin turgor

72
Q

Tx of HHS

A

IV fluids
Supportive
Insulin
Treat underlying cause

73
Q

what is lactic acidosis

A

when lactic acid builds up in the bloodstream faster than it can be removed

74
Q

clinical features of lactic acidosis

A

Hyperventilation
Mental confusion
Stupor or coma if severe

75
Q

lab findings of lactic acidosis

A

reduced bicarbonate
raised anion gap
raised phosphate
absent of ketonaemia

76
Q

what is the target of type 2 diabetics glucose control

A

HbA1c 48mmol/mol

77
Q

complications of diabetes

A

Macrovascular:
IHD
Stroke

Microvascular:
Neuropathy
Nephropathy
Retinopathy

Erectile Dysfunction

78
Q

how does diabetes cause microvascular problems

A

reduced blood flow

79
Q

precipitating factors of neuropathy

A

poor glycemic control
T1DM > T2DM
Smoking + Alcohol
increased length of diabetes

80
Q

what are symptoms of Peripheral nerve damage (PND)

A 
Numbness/ insensitivity
Tingling/ burning
Sharp pains or cramps
Sensitivity to touch
Loss of balance and coordination
81
Q

complications of PND

A

infections/ulcers
deformities (hammertoes)
amputations

82
Q

Tx of PND

A

Analgesia

Stronger opiods

83
Q

symptoms of Autonomic neuropathy

A

Constipation/Diarrhoea
Gastroparesis - nausea, vomiting, bloating
Oesophagus nerve damage - swallowing difficulty

84
Q

what is Charcot foot

A

Fractures and dislocations of bones and joints that occur with minimal or no known trauma. Occurs in patients with neuropathy.

85
Q

what is diabetic nephropathy

A

damage of capillaries in glomeruli

86
Q

consequences of diabetic nephropathy

A

Development of hypertension
Relentless decline in renal function - can lead to Kidney failure
Accelerated vascular disease

87
Q

what can be a sign of impending trouble

A

microalbuminuria

88
Q

risk factors of nephropathy profession

A

hypertension
high cholesterol
smoking
albuminuria

89
Q

what can be very useful in Tx of diabetic nephropathy

A

ACE inhibitors

90
Q

what pathology of the eyes do diabetics get

A

diabetic retinopathy
cataract
glaucoma
visual blurring due to acute hyperglycamia

91
Q

what are the stages of retinopathy

A

Mild non-proliferative
Moderate non-proliferative
Severe non-proliferative
Proliferative

92
Q

what is seen in pre-proliferative retinopathy

A

Micro aneurysms, hard exudates, haemorrages

93
Q

what is seen in Severe Non-proliferative Retinopathy

A


(IRMA, venous beading, haemorrages)

94
Q

what is seen in severe proliferative retinopathy

A

new vessel formation

95
Q

complications of diabetic retinopathy

A

bleeding - sudden change in vision
floaters
secondary glaucoma
retinal detachment

96
Q

Tx of diabetic retinopathy

A

Laser
Vitrectomy
Anti-VEGF injections

97
Q

what are guidelines in place to reduce chance of CHD in diabetics

A

Lipid lowering therapy in diabetes over age 40 regardless of baseline cholesterol

BP

98
Q

what are psychiatric complications

A

Depression
Eating Disorders
Bi-polar
Schizophrenia

Endocrine SB (15 decks)

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