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Y2 Endocrine > Week 2 > Flashcards

Week 2 Flashcards

1
Q

At what blood glucose level is considered as hypoglycaemia

A

<4 mM

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2
Q

At what blood glucose level is considered as serious hypoglycaemia

A

<3mM

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3
Q

Which type of diabetic is most commonly affected by hypoglycaemia

A

Diabetics, especially type 1

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4
Q

What can cause hypoglycaemia in diabetics

A

Incorrect dosage of medications for diabetes
Changes in medications
Hypoglycaemic drugs
Dietary or activity changes

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5
Q

What are the hypoglycaemic drugs

A

Sulphonylureas
Insulin

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6
Q

Why is severe hypoglycaemia most common in diabetics

A

Because they have hypoglycaemia unawareness and defective glucose counter-regulatory response

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7
Q

What causes hypoglycaemia unawareness in diabetics

A

Reduced neurogenic response

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8
Q

What does defective glucose counter-regulatory response mean

A

The patients will not produce glucagon in response to low blood glucose level, leading to hypoglycaemia

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9
Q

Which group of patients is likely to experience recurrent hypoglycaemia

A

Type 1 diabetics

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10
Q

Is hypoglycaemia always symptomatic?

A

No, it can be asymptomatic in diabetics who have reduced neurogenic response

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11
Q

Why is asymptomatic hypoglycaemia dangerous

A

Because their blood glucose level may be very low and they won’t experience symptoms till blood sugar level drops to the point where cognitive impairment occurs

If they experience symptoms, we can intervene earlier to prevent that

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12
Q

Risk factors for hypoglycaemia

A

Diabetic
Hyperinsulinaemia conditions
Alcohol consumption
Cancer
Preschool age / adolescents
low socioeconomic status (malnourishment)
Previous hypoglycaemia episodes
Addison’s disease

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13
Q

How does alcohol consumption cause hypoglycaemia

A

Ethanol inhibits gluconeogenesis but not glycogenolysis

It will take days of increased alcohol consumption to deplete glycogen store and cause hypoglycaemia

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14
Q

What is insulinoma

A

Hyperinsulinaemia condition; a benign tumour of beta cells that causes excess secretion of insulin

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15
Q

How may cancer cause hypoglycaemia

A

Release insulin-like growth factor

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16
Q

What is Whipple’s triad used for

A

for diagnosis of hypoglycaemia

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17
Q

What is included in Whipple’s triad

A
  1. Identify symptoms of hypoglycaemia
  2. Evidence of low blood sugar level
  3. Test if symptoms can be relieved when blood glucose concentration is restored to normal
    If yes = symptoms are due to hypoglycaemia
    If no = symptoms due to other reasons
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18
Q

Symptoms of mild hypoglycaemia

A

Tremor
Hunger
Anxiety
Sweating

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19
Q

Symptoms of severe hypoglycaemia

A

Cognitive impairment
Seizure
Dizziness
Drowsiness

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20
Q

What heart conditions can be caused by hypoglycaemia

A

Prolonged QT interval (arrhythmia)
Heart block
Heart failure
Myocardial infarction

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21
Q

Seizures due to hypoglycaemia is common in which group of people

A

Children

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22
Q

Investigations for hypoglycaemia

A

Blood glucose level

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23
Q

Further investigations for severe hypoglycaemia

A

GCS level
C peptide level
(Insulin level)

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24
Q

What would the C peptide be if the patient has hypoglycaemia secondary to hyperinsulinaemia

A

High

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25
Q

What would the 72 hour fast test result be in normal people and why

A

No hypoglycaemia due to normal glucose counter-regulatory mechanisms

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26
Q

Management of mild hypoglycaemia

A

Oral glucose

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27
Q

Management of severe hypoglycaemia (low GCS level)

A

IV glucose
IV/IM/SC glucagon
Assess patient again - should see rapid improvement if the low GCS score is due to hypoglycaemia

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28
Q

Why may IV/IM/SC glucagon be ineffective for hypoglycaemia

A

It may be ineffective if used on patients with low glycogen store - such as those that are malnourished / with hepatic disease

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29
Q

Describe the structure of adrenal gland and its location

A

Located on top of each kidney

Has 2 layers: Outer cortex and inner medulla

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30
Q

What are the 3 layers of outer cortex of adrenal gland

A

Zona fasciculata
Zona Reticularis
Zona glomerulosa

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31
Q

What is the function of zona fasciculata

A

Release glucocorticoids such as cortisol

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32
Q

What is the function of zona reticularis

A

Release mineralocorticoids such as aldosterone

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33
Q

What is the function of zone glomerulosa

A

Release androgrens (sex hormones)

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34
Q

What is the function of cortisol relating to insulin

A

It is a counter-regulatory hormone for insulin

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35
Q

Effects of cortisol

A

Stimulates hepatic glucose production
Stimulates lipolysis, proteolysis
Inhibits glucose uptake in peripheral tissue

= increase in blood glucose

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36
Q

Which axis controls the release of cortisol

A

Hypothalamus-Pituitary-Adrenal axis

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37
Q

Describe the hypothalamus-pituitary-adrenal axis

A

1) Paraventricular nucleus of hypothalamus secretes CRH into hypophyseal portal system
2) CRH travels to pituitary gland
3) Anterior pituitary gland secretes ACTH into the blood in response to CRH
4) ACTH travels to adrenal gland and stimulates the release of cortisol
5) Cortisol exhibits negative feedback effect on CRH and ACTH; decreasing both hormones

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38
Q

What is hypophyseal portal system

A

Vascular system that connects hypothalamus and pituitary gland

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39
Q

What is the function of inner medulla of adrenal gland

A

Secrete:
-adrenaline
-noradrenaline
-dopamine

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40
Q

What is Addison’s disease

A

Autoimmune destruction of adrenal gland, causing lower levels of certain hormones (androgens, cortisol,aldosterone)

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41
Q

What causes Addison’s disease

A

Primary adrenal deficiency caused by
1. autoimmune destruction
2. surgery
3. TB / infections
4. Haemorrhage
5. Infarction

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42
Q

What are the infections that can cause Addison’s disease

A

TB
HIV
Meningitis

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43
Q

Adrenal insufficiency caused by meningococcal disease is called

A

Waterhouse-Friderichsen Syndrome

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44
Q

What are the typical hormone level findings for Addison’s disease

A

High ACTH
Low cortisol

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45
Q

Symptoms of Addison’s disease (STEROIDS)

A

Sugar and sodium low
Tiredness
Electrolyte imbalance (high K low Na)
Reproductive changes (loss of sex drive / loss of pubic or axillary hair)
hypOtension
Increased pigmentation of skin
Depression, dehydration

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46
Q

What may be the blood test findings for addison’s disease

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia

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47
Q

What causes the loss of axillary / pubic hair in addison’s disease and it is most commonly seen in which group of people

A

Due to loss of androgens

Most commonly seen in females

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48
Q

What is acute Addisonian crisis

A

Exacerbation of adrenal insufficiency due to increase in demand for glucocorticoids / mineralocorticoids (e.g. surgery / illness puts lots of stress -> increase in demand for cortisol but supply doesn’t meet)

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49
Q

How can Addison’s disease lead to Addisonian crisis

A

due to additional stress such as infection causing exacerbation of pre-existing deficiency

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50
Q

Signs of Addisonian crisis

A

Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Hypotensive
Confusion
Coma
Pyrexia

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51
Q

Management of Addisonian crisis

A

IV fluid
IV hydrocortisone

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52
Q

Management of Addison’s disease

A

If cortisol is low -> Hydrocortisone

If aldosterone is low -> Fludrocortisone

Usually give both

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53
Q

What is Type 1 diabetes

A

Inability to produce / secrete insulin due to autoimmune destruction of beta cells

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54
Q

To what extent should the destruction of beta cells be to cause type 1 diabetes

A

90% of beta cells destroyed so no longer can maintain normal blood glucose -> hyperglycaemia

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55
Q

Which autoantibody is found in 85% of T1 diabetics

A

Anti-GAD (glutamic acid decarboxylase)

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56
Q

Risk factors of T1 diabetes

A

Genetics
Presence of other autoimmune conditions such as
-Grave’s
-Addison’s

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57
Q

What is LADA

A

Latent onset autoimmune diabetes in adults; it is a form of T1D but slower destruction by autoimmunity

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58
Q

When should you suspect latent onset diabetes in adults

A

If the person
-experienced weight loss
-low BMI
-has family history of autoimmune conditions

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59
Q

What are the consequences of reduced insulin level

A

High glucagon levels
Increase in hepatic glucose production
Increase in lipolysis
Increase in proteolysis
Decrease in uptake of glucose into peripheral tissues

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60
Q

Why will there be high glucagon levels in T1 diabetics

A

Because the presence of insulin was supposed to inhibit glucagon secretion

So without insulin, glucagon secretion not inhibited

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61
Q

What occurs in patients with T1 diabetes that leads to dehydration

A

Low insulin -> hyperglycaemia -> glycosuria -> osmotic diuresis -> polyuria -> dehydration and derangement of electrolytes

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62
Q

What is an emergency complication most commonly seen in T1 diabetics

A

Diabetic ketoacidosis

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63
Q

What causes diabetic ketoacidosis in T1 diabetics

A

lack of insulin means that glucose cannot be moved into cells for energy -> need to use another source of energy: ketones

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64
Q

What factor in diabetes allow ketogenesis to occur

A

Lack of insulin allow increase in lipolysis -> increase in FFA -> FFA can be oxidized into ketones in liver

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65
Q

Signs of T1 diabetes

A

Glucosuria
Weight loss
Low BMI
Polyuria
Polydipsia
Dehydration

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66
Q

First line treatment for T1D

A

Basal bolus insulin regime

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67
Q

Signs of DKA

A

Vomiting / diarrhea
Nausea
Reduced GCS level
Kussmaul Breathing
Acidic breath
Arrhythmia
Tachycardia
Abdominal pain

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68
Q

What is the severe complication of DKA

A

Cerebral Oedema

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69
Q

Signs of cerebral oedema

A

headache
Reduced conscious level
Hypertensive
Decreased pulse
seizures

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70
Q

Cerebral oedema is most commonly seen in

A

Children with DKA

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71
Q

What is Kussmaul breathing

A

Fast and deep breaths to breathe out more CO2 to compensate metabolic acidosis

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72
Q

Complications of diabetes

A

Nephropathy
Neuropathy
Retinopathy
CVD
Diabetic foot

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73
Q

How does diabetes cause retinopathy

A

Persistent microvascular damage of the retina causing areas of ischaemia and angiogenesis (formation of weak vessels)
This increases risk of haemorrhage and retinal detachment

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74
Q

What education should be given to patients with T1 diabetes

A

Sick day rules
DAFNE

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75
Q

What is DAFNE

A

Dose adjustment for normal eating

Allows T1 diabetic patients to adjust their insulin dose according to the amount of carbs in their meal

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76
Q

What are the sick day rules for

A

To help patients understand what to do to prevent recurrence of DKA / occurrence of dehydration..etc

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77
Q

What are the sick day rules

A

1) Continue insulin therapy, alterations may be required (e.g. corrective doses)
2) Increase frequency of blood glucose monitoring
3) ketone monitoring
4) Maintain good hydration and when possible a normal meal pattern
5) seek for medical help if there is persistent vomiting /drowsiness

78
Q

What can cause euglycaemic DKA

A

SGLT2i (rare)
Inadequate dose of insulin
Alcohol euglycaemic DKA

79
Q

What causes DKA in general relating to insulin deficiency and demand for insulin

A

Absolute insulin deficiency
or
Relative insulin deficiency + stress that increases insulin demand

80
Q

Why may T1 diabetics who were given insulin prescriptions still develop DKA

A

Non-compliancy - Insulin omission

81
Q

What are the additional stresses that cause an increase in insulin demand

A

Infections
Intoxication
Inflammation
Infarction
Iatrogenic

82
Q

What infections can cause increase in insulin demand

A

Cellulitis
Pneumnonia
UTI

83
Q

How do infections cause an increase in insulin demand

A

1) causes a stress response in the body by increasing the amount of certain hormones such as cortisol and adrenaline
2) those stress hormones increase blood glucose level
3) so insulin demand increases

84
Q

Intoxication of what chemicals can lead to an increase in insulin deman d

A

Alcohol
Cocaine
Methanol
Salicylate

85
Q

What are the iatrogenic causes for increase in insulin demand

A

Steroids
Surgery

86
Q

How does steroids cause an increase in insulin demand

A

Steroids
- increase blood glucose
- increase hepatic glucose production
- inhibit glucose uptake

= higher blood glucose = more demand for insulin

87
Q

How does an increase in ketone bodies cause nausea and vomiting

A

Triggers the chemo-trigger zone in medulla

88
Q

What happens to the level of H+ in DKA

A

Increase in H+

89
Q

What are the consequences of increase in H+ in DKA

A

HAGMA
Hyperkalaemia
Kussmaul breathing

90
Q

What is HAGMA

A

High anion gap metabolic acidosis

91
Q

How does increase in H+ cause hyperkalaemia

A

1) More 3 H+ moved into the cell via H+/K+ pump in exchange for 1 K+ out (3H+ in 1K+ out)
2) K+ is supposed to move back into the cell via Na+/K+ ATP pump but this pump only works in presence of insulin
3) hence accumulation of K+ in blood = hyperkalaemia

92
Q

What ECG abnormalities can be caused by hyperkalaemia

A

-Peaked or ‘tall tented’ T waves
-Prolonged PR interval (> 200 ms)
-Widening of the QRS interval (> 120 ms)
-Small, or absent, P waves
-asystole

93
Q

How does an increase in H+ cause Kussmaul breathing

A

1) Increase in H+ stimulates chemoreceptors in aortic and carotid bodies
2) vagus and glossopharyngeal nerves carry the signal up to the medulla
3) triggers the medulla
4) causes an increase in respiratory rate
5) breath out acetone as a compensatory mechanism

94
Q

What causes abdominal pain in DKA

A

Hyperkalaemia

95
Q

Why may hypokalaemia occur in DKA

A

During treatment.
If not carefully monitoring K+ level while giving insulin, you may give too much insulin and driving too much K+ back into cells

96
Q

What arrhythmia can be caused by hypokalaemia

A

QT prolongation

97
Q

Management of DKA

A

IV fluid
IV insulin
Consistent monitoring of blood glucose, ketone level, electrolytes

98
Q

Which one should be administered first in managing DKA

A

IV fluid first then IV insulin

99
Q

What needs to be stopped when giving patient IV insulin

A

Short acting insulin

100
Q

Which ketone body is measured in ketone meters

A

B-hydroxybutyrate

101
Q

Which type of diabetes often has relative insulin deficiency

A

Type 2

102
Q

What is relative insulin deficiency

A

Insulin deficient patient who still has a little bit of insulin sensitivity left

103
Q

Difference between hyperosmolar hyperglycemic state (HHS) and DKA

A

HHS more common in T2 diabetics with relative insulin deficiency + additional stress (infection) whereas DKA more common in T1

HHS more common in older patients

Primary sign of HHS is not elevated ketones (though HHS and DKA can overlap)

104
Q

Why may patients with HHS not have elevated ketone bodies, assuming that HHS and DKA did not overlap

A

Because the patients often still have enough insulin to prevent activation of ketogenesis

105
Q

How does HHS occur

A

Hyperglycaemia -> glucosuria -> osmotic diuresis -> polysuria -> dehydration

Dehydration causes blood to be very concentrated = hyperosmolar

106
Q

Symptoms of HHS

A

Polyuria
Polydipsia
Dry skin
Drowsiness
Loss of consciousness

107
Q

Biochemical findings in HHS

A

Higher glucose than DKA
High normal / raised sodium
Raised osmolarity
less / not ketoacidotic

108
Q

How to calculate osmolarity

A

2 x Sodium + Urea + glucose

109
Q

What is the normal range of osmolarity

A

275-295

110
Q

T2 diabetes is a polygenic disease. What does polygenic mean

A

Multiple genes contributing to risk of T2 diabetes. Each of them poses a small risk bu in combination they become a large risk

111
Q

What are the 2 main risk factors for T2 diabetes

A

Obesity
Genetics

112
Q

Why are obese people more at risk of insulin resistance

A

1) adiposity exceeding own fat storage threshold
2) Causes FFA to spill over to liver, pancreas and muscle
3) Lipotoxicity
4) Beta cells are damaged hence can no longer respond to glucose and produce more insulin
5) muscle and liver cells become insulin resistant

113
Q

Why may some obese people not develop insulin resistance

A

They have higher fat storage threshold so can safely store more fat without spilling it

114
Q

Why may some slim people develop T2 diabetes

A

no where to store fat = Low fat storage threshold = fat spill and cause lipotoxicity

115
Q

Risks associated with insulin resistance

A

PCOS
Hypertension
Hyperlipidaemia
CVD
Stroke
CHD

116
Q

Do all T2 diabetics have insulin resistance

A

No, only 90% have insulin resistance. The rest developed T2 diabetes due to impaired insulin secretion

117
Q

Difference between T1 and T2 diabetes

A

T1 diabetes is due to autoantibodies attacking beta cells whereas in T2 there is no autoimmunity, it is due to impaired insulin secretion / insulin resistance / both

118
Q

What should you also treat when treating a T2 diabetic

A

Blood pressure and lipids

Because insulin resistance / obese patients are at increased risk of CVD, CHD

119
Q

What is monogenic diabetes

A

Diabetes caused by a mutation in a single gene

120
Q

Which 2 defects can be caused by monogenic diabetes

A

Defect in insulin secretion
Defect in insulin action - signalling pathway or fat storage

121
Q

Examples of monogenic diabetes with defect in insulin secretion

A

MODY (maturity onset diabetes of the young)
Neonatal diabetes
KCNJ11 mutation

122
Q

What is CGL (congenital generalised lipodystrophy)

A

A type of monogenic diabetes due to defect in fat storage

123
Q

Characteristic of CGL

A

The patient is slim, muscular due to lack of adipose tissue

124
Q

Why do CGL patients develop into diabetes

A

Because they cannot store fat hence has low fat storage threshold -> fat spill -> insulin resistance

125
Q

What is MODY

A

Maturity onset diabetes in the young
T2 diabetes found in young people

126
Q

Inheritance pattern of MODY

A

Autosomal dominant

127
Q

Age of onset of MODY

A

before 25 years old

128
Q

Mutations in what structures can cause MODY (types of MODY)

A

Glucokinase
Transcription factors

129
Q

Why is mutation in glucokinase less concerning than mutation in transcription factors

A

Because in glucokinase mutation, the rest of the beta cell is still functional so still respond well to glucose levels

130
Q

Effect of MODY caused by glucokinase mutation

A

Higher fasting glucose level but still secretes insulin in response to decrease in glucose level after meal

= stable hyperglycaemia

131
Q

Management of MODY due to glucokinase mutation

A

Diet management

No need insulin

132
Q

Difference between glucokinase MODY and transcription factor MODY

A

Glucokinase MODY onset at birth whereas TF MODY has adolescent onset

Glucokinase MODY causes stable hyperglycaemia whereas TF MODY has unstable hyperglycaemia

Glucokinase MODY does not need treatment whereas TF MODY requires

Glucokinase MODY does not really cause complications whereas TF MODY does

133
Q

What is the most common cause of MODY

A

Transcription factor MODY, especially HNF1a MODY

134
Q

Management of HNF1A MODY

A

low dose Sulphonylurea

If the patient was previously misdiagnosed with T1 diabetes, stop insulin treatment and start SU

135
Q

Where does KCNJ11 mutation affect

A

Kir 6.2, a subunit of K+ channel in beta cells

136
Q

Effect of KCNJ11 mutation

A

K+ channel always open, so hyperpolarisation cannot occur hence voltage gated Ca2+ channel does not open and insulin will not be secreted
= monogenic diabetes

137
Q

Onset of KCNJ11 monogenic diabetes

A

Before 6-12 months of age

138
Q

Why is T1 diabetes unlikely to be the diagnosis of a patient presenting with diabetes at 6 weeks of age

A

T1 diabetes unlikely to occur before the age of 1 because autoimmunity should not have developed that early on (immature immune system)

139
Q

When is T1 diabetes usually diagnosed at

A

13-14 years old

140
Q

Management of KCNJ11 monogenic diabetes

A

high dose SU

141
Q

Hypoglycaemic risk in patients with KCNJ11 monogenic diabetes taking SU

A

Very low risk of hypoglycaemia. Lower than those that have T2 diabetes

142
Q

How does diabetes cause nephropathy

A

Damage to the capillaries in the glomeruli

143
Q

Signs of nephropathy

A

Proteinuria, microalbuminuria
Nodular glomerulosclerosis

144
Q

Consequences of diabetic nephropathy

A

Hypertension
Decline in renal function 1/min/month if untreated
Increase in risk of death

145
Q

When should ACR and PCR be measured in diabetics

A

At diagnosis then at regular intervals (annually)

146
Q

Normal level of ACR (albumin:creatine) in female

A

<3.5 mg/mmol

147
Q

Microalbuminuria threshold

A

30 > ACR > 3.5 mg/mmol for females for 2-3 ACR tests
30 > ACR > 2.5 mg/mmol for males for 2-3 ACR tests

148
Q

Proteinuria (macroalbuminuria) threshold

A

ACR >30 mg/mmol
PCR >45 mg/mmol

149
Q

How many times should you test ACR before making a diagnosis of microalbuminuria

A

2 or 3 times

Diagnosis established if positive for 2 or 3 times

150
Q

How many times should you test PCR before making a diagnosis of proteinuria

A

2 or 3 times

151
Q

What is insipient nephropathy and what is the level of it

A

Presence of low but abnormal albumin level in urine
ACR = above 2.5 (3.5 Females) - 30

152
Q

What is overt nephropathy

A

Persistent macroalbuminuria for 24 hours or more

153
Q

Why do you need to repeat the ACR and PCR tests for 2 to 3 times before establishing a diagnosis

A

Because it varies a lot- it can vary due to exercise / fluid load / protein load / day or night / day to day

154
Q

What do you need to screen for if a diabetic patient developed microalbuminuria

A

Screen for vascular diseases
Screen for retinopathy

155
Q

Management of nephropathy due to diabetes

A

Start ACEi or ARB (angiotensin receptor blocker) immediately after diagnosis of microalbuminuria / proteinuria
Tighten blood pressure control
Tighten glycemic control
Discourage smoking

156
Q

What level should the blood pressure for patients with nephropathy be controlled at

A

<130/80 mmHg

157
Q

How does ACEi help prevent nephropathy from developing into end stage renal failure

A

Blocks ACE which converts Angiotensin I to angiotensin II hence blocks the subsequent step of angiotensin II to Aldosterone

Angiotensin II is a vasoconstrictor so blocking it causes vasodilation of efferent arterioles -> reduces filtration pressure = renal protection and less protein forced out into urine

158
Q

What happens to GFR when the patient starts taking ACEi

A

Decrease
Allow up to 20% decrease in eGFR due to decrease in filtration pressure

159
Q

Contraindication for ACEi

A

Pregnancy

160
Q

Which drug for diabetes provides renal protection

A

SGLT2i

161
Q

What happens to the effect of SGLT2i when the eGFR is <45ml/min

A

Reduces glucose lowering effects but still provides renal protection

162
Q

Why does the glucose lowering effect of SGLT2i reduce if eGFR <45ml/min

A

Because the glucose lowering effect is dependent on renal glucose filtration. If renal function is impaired = less SGLT2i effect

163
Q

Risk factors for neuropathy as a complication of diabetes

A

Prolonged length of diabetes
Poor glycemic control
Smoking
High cholesterol
High lipids
Alcohol
Genetics

164
Q

Long / short nerves are more likely to be affected by neuropathy in diabetes

A

Long nerves

165
Q

What is the glove and stocking distribution describing

A

Describes the areas which are commonly affected by peripheral neuropathy
- feet and hands

166
Q

Symptoms of peripheral neuropathy

A

Burning, tingling sensation
Pain
Hypersensitivity
Loss of balance / coordination
Numbness / loss of sensation (late stage of neuropathy)

167
Q

Consequences of peripheral neuropathy

A

Damaging the feet without realizing due to neuropathy can lead to ulcers, infection and potentially amputation

Increased risk of Charcot foot

168
Q

What is Charcot foot

A

A destructive inflammatory process in foot which damages the bones, causing deformity

169
Q

Presentation of Charcot foot

A

Hot, swollen foot in someone with neuropathy

170
Q

How to distinguish between Charcot foot and infection

A

use MRI

171
Q

Treatment of Charcot foot

A

Taking weight off the foot
Total contact cast
Aircast boot

172
Q

Moderate foot risk criteria

A

Impaired sensation
Absent foot pulses
No skin calluses/deformity
patient cannot take care of their foot

173
Q

High foot risk criteria

A

Impaired sensation
Absent foot pulses
presence of skin calluses / deformity
Previous amputation or foot ulcers

174
Q

When should you urgently refer a patient with foot disease to specialist team

A

During active foot ulcers / infections / ischaemia / gangrene / swelling..etc

175
Q

How often should diabetic patients go to their podiatrist

A

Annually if they are considered at moderate or high risk of foot diseases

176
Q

How often should patients screen for foot disease even if they don’t have any

A

Annually by healthcare professionals (not podiatrist)

177
Q

Treatment of pain in neuropathy

A

First line:
Amitriptyline
Duloxetine
Gabapentin

topical Capsaicin cream (used in combination with others)

178
Q

What is diabetic amyotrophy

A

Proximal neuropathy with episodic, asymmetrical pain on one side of hip / thigh / buttock and muscle wasting and weakness

179
Q

What is autonomic neuropathy

A

Neuropathy affecting the autonomic nervous system

180
Q

What are the GI consequences of autonomic neuropathy

A

Slow gastric emptying
Gastric slowing
Oesophageal nerve damage causing difficulty in swallowing

181
Q

Symptoms of slow gastric emptying

A

Unable to control blood glucose level
Nausea
Vomiting
Bloating
Loss of appetite

182
Q

Symptoms of gastric slowing

A

Constipation / diarrhea

183
Q

Why do patients with autonomic neuropathy find it hard to control their blood glucose levels

A

Because they can’t predict when is the food going to go down and be digested

184
Q

Management of gastroparesis due to autonomic neuropathy

A

Advise patients to have regular smaller portions of food
Promotility drugs
Anti-nausea drugs
NSAID / tricyclic antidepressants for pain management
Gastric pacemaker

185
Q

What are the promotility drugs used for gastroparesis

A

Metoclopramide
Domperidone
Erythromycin

186
Q

Example of a tricyclic antidepressant drug

A

Amitriptyline

187
Q

Example of antiemetic

A

Serotonin Antagonist (5HT3 antagonist)

188
Q

What is the CV consequence of autonomic neuropathy

A

Unable to adjust blood pressure and heart rate

189
Q

What happens if you can’t adjust your blood pressure and heart rate

A

Postural hypotension - faint / light-headed when standing up after sitting

Heart rate remaining high instead of rising then falling in response to activities

190
Q

Which hand neuropathy are diabetics at an increased risk of

A

Carpal tunnel syndrome - median nerve neuropathy

Y2 Endocrine (6 decks)

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