Week 2 Flashcards
(190 cards)
1
Q
At what blood glucose level is considered as hypoglycaemia
A
<4 mM
2
Q
At what blood glucose level is considered as serious hypoglycaemia
A
<3mM
3
Q
Which type of diabetic is most commonly affected by hypoglycaemia
A
Diabetics, especially type 1
4
Q
What can cause hypoglycaemia in diabetics
A
Incorrect dosage of medications for diabetes
Changes in medications
Hypoglycaemic drugs
Dietary or activity changes
5
Q
What are the hypoglycaemic drugs
A
Sulphonylureas
Insulin
6
Q
Why is severe hypoglycaemia most common in diabetics
A
Because they have hypoglycaemia unawareness and defective glucose counter-regulatory response
7
Q
What causes hypoglycaemia unawareness in diabetics
A
Reduced neurogenic response
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
9
Q
Which group of patients is likely to experience recurrent hypoglycaemia
A
Type 1 diabetics
10
Q
Is hypoglycaemia always symptomatic?
A
No, it can be asymptomatic in diabetics who have reduced neurogenic response
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
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
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
14
Q
What is insulinoma
A
Hyperinsulinaemia condition; a benign tumour of beta cells that causes excess secretion of insulin
15
Q
How may cancer cause hypoglycaemia
A
Release insulin-like growth factor
16
Q
What is Whipple’s triad used for
A
for diagnosis of hypoglycaemia
17
Q
What is included in Whipple’s triad
A
- Identify symptoms of hypoglycaemia
- Evidence of low blood sugar level
- 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
18
Q
Symptoms of mild hypoglycaemia
A
Tremor
Hunger
Anxiety
Sweating
19
Q
Symptoms of severe hypoglycaemia
A
Cognitive impairment
Seizure
Dizziness
Drowsiness
20
Q
What heart conditions can be caused by hypoglycaemia
A
Prolonged QT interval (arrhythmia)
Heart block
Heart failure
Myocardial infarction
21
Q
Seizures due to hypoglycaemia is common in which group of people
A
Children
22
Q
Investigations for hypoglycaemia
A
Blood glucose level
23
Q
Further investigations for severe hypoglycaemia
A
GCS level
C peptide level
(Insulin level)
24
Q
What would the C peptide be if the patient has hypoglycaemia secondary to hyperinsulinaemia
A
High
25
What would the 72 hour fast test result be in normal people and why
No hypoglycaemia due to normal glucose counter-regulatory mechanisms
26
Management of mild hypoglycaemia
Oral glucose
27
Management of severe hypoglycaemia (low GCS level)
IV glucose
IV/IM/SC glucagon
Assess patient again - should see rapid improvement if the low GCS score is due to hypoglycaemia
28
Why may IV/IM/SC glucagon be ineffective for hypoglycaemia
It may be ineffective if used on patients with low glycogen store - such as those that are malnourished / with hepatic disease
29
Describe the structure of adrenal gland and its location
Located on top of each kidney
Has 2 layers: Outer cortex and inner medulla
30
What are the 3 layers of outer cortex of adrenal gland
Zona fasciculata
Zona Reticularis
Zona glomerulosa
31
What is the function of zona fasciculata
Release glucocorticoids such as cortisol
32
What is the function of zona reticularis
Release mineralocorticoids such as aldosterone
33
What is the function of zone glomerulosa
Release androgrens (sex hormones)
34
What is the function of cortisol relating to insulin
It is a counter-regulatory hormone for insulin
35
Effects of cortisol
Stimulates hepatic glucose production
Stimulates lipolysis, proteolysis
Inhibits glucose uptake in peripheral tissue
= increase in blood glucose
36
Which axis controls the release of cortisol
Hypothalamus-Pituitary-Adrenal axis
37
Describe the hypothalamus-pituitary-adrenal axis
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
38
What is hypophyseal portal system
Vascular system that connects hypothalamus and pituitary gland
39
What is the function of inner medulla of adrenal gland
Secrete:
-adrenaline
-noradrenaline
-dopamine
40
What is Addison's disease
Autoimmune destruction of adrenal gland, causing lower levels of certain hormones (androgens, cortisol,aldosterone)
41
What causes Addison's disease
Primary adrenal deficiency caused by
1. autoimmune destruction
2. surgery
3. TB / infections
4. Haemorrhage
5. Infarction
42
What are the infections that can cause Addison's disease
TB
HIV
Meningitis
43
Adrenal insufficiency caused by meningococcal disease is called
Waterhouse-Friderichsen Syndrome
44
What are the typical hormone level findings for Addison's disease
High ACTH
Low cortisol
45
Symptoms of Addison's disease (STEROIDS)
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
46
What may be the blood test findings for addison's disease
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
47
What causes the loss of axillary / pubic hair in addison's disease and it is most commonly seen in which group of people
Due to loss of androgens
Most commonly seen in females
48
What is acute Addisonian crisis
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)
49
How can Addison's disease lead to Addisonian crisis
due to additional stress such as infection causing exacerbation of pre-existing deficiency
50
Signs of Addisonian crisis
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Hypotensive
Confusion
Coma
Pyrexia
51
Management of Addisonian crisis
IV fluid
IV hydrocortisone
52
Management of Addison's disease
If cortisol is low -> Hydrocortisone
If aldosterone is low -> Fludrocortisone
Usually give both
53
What is Type 1 diabetes
Inability to produce / secrete insulin due to autoimmune destruction of beta cells
54
To what extent should the destruction of beta cells be to cause type 1 diabetes
90% of beta cells destroyed so no longer can maintain normal blood glucose -> hyperglycaemia
55
Which autoantibody is found in 85% of T1 diabetics
Anti-GAD (glutamic acid decarboxylase)
56
Risk factors of T1 diabetes
Genetics
Presence of other autoimmune conditions such as
-Grave's
-Addison's
57
What is LADA
Latent onset autoimmune diabetes in adults; it is a form of T1D but slower destruction by autoimmunity
58
When should you suspect latent onset diabetes in adults
If the person
-experienced weight loss
-low BMI
-has family history of autoimmune conditions
59
What are the consequences of reduced insulin level
High glucagon levels
Increase in hepatic glucose production
Increase in lipolysis
Increase in proteolysis
Decrease in uptake of glucose into peripheral tissues
60
Why will there be high glucagon levels in T1 diabetics
Because the presence of insulin was supposed to inhibit glucagon secretion
So without insulin, glucagon secretion not inhibited
61
What occurs in patients with T1 diabetes that leads to dehydration
Low insulin -> hyperglycaemia -> glycosuria -> osmotic diuresis -> polyuria -> dehydration and derangement of electrolytes
62
What is an emergency complication most commonly seen in T1 diabetics
Diabetic ketoacidosis
63
What causes diabetic ketoacidosis in T1 diabetics
lack of insulin means that glucose cannot be moved into cells for energy -> need to use another source of energy: ketones
64
What factor in diabetes allow ketogenesis to occur
Lack of insulin allow increase in lipolysis -> increase in FFA -> FFA can be oxidized into ketones in liver
65
Signs of T1 diabetes
Glucosuria
Weight loss
Low BMI
Polyuria
Polydipsia
Dehydration
66
First line treatment for T1D
Basal bolus insulin regime
67
Signs of DKA
Vomiting / diarrhea
Nausea
Reduced GCS level
Kussmaul Breathing
Acidic breath
Arrhythmia
Tachycardia
Abdominal pain
68
What is the severe complication of DKA
Cerebral Oedema
69
Signs of cerebral oedema
headache
Reduced conscious level
Hypertensive
Decreased pulse
seizures
70
Cerebral oedema is most commonly seen in
Children with DKA
71
What is Kussmaul breathing
Fast and deep breaths to breathe out more CO2 to compensate metabolic acidosis
72
Complications of diabetes
Nephropathy
Neuropathy
Retinopathy
CVD
Diabetic foot
73
How does diabetes cause retinopathy
Persistent microvascular damage of the retina causing areas of ischaemia and angiogenesis (formation of weak vessels)
This increases risk of haemorrhage and retinal detachment
74
What education should be given to patients with T1 diabetes
Sick day rules
DAFNE
75
What is DAFNE
Dose adjustment for normal eating
Allows T1 diabetic patients to adjust their insulin dose according to the amount of carbs in their meal
76
What are the sick day rules for
To help patients understand what to do to prevent recurrence of DKA / occurrence of dehydration..etc
77
What are the sick day rules
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
What can cause euglycaemic DKA
SGLT2i (rare)
Inadequate dose of insulin
Alcohol euglycaemic DKA
79
What causes DKA in general relating to insulin deficiency and demand for insulin
Absolute insulin deficiency
or
Relative insulin deficiency + stress that increases insulin demand
80
Why may T1 diabetics who were given insulin prescriptions still develop DKA
Non-compliancy - Insulin omission
81
What are the additional stresses that cause an increase in insulin demand
Infections
Intoxication
Inflammation
Infarction
Iatrogenic
82
What infections can cause increase in insulin demand
Cellulitis
Pneumnonia
UTI
83
How do infections cause an increase in insulin demand
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
Intoxication of what chemicals can lead to an increase in insulin deman d
Alcohol
Cocaine
Methanol
Salicylate
85
What are the iatrogenic causes for increase in insulin demand
Steroids
Surgery
86
How does steroids cause an increase in insulin demand
Steroids
- increase blood glucose
- increase hepatic glucose production
- inhibit glucose uptake
= higher blood glucose = more demand for insulin
87
How does an increase in ketone bodies cause nausea and vomiting
Triggers the chemo-trigger zone in medulla
88
What happens to the level of H+ in DKA
Increase in H+
89
What are the consequences of increase in H+ in DKA
HAGMA
Hyperkalaemia
Kussmaul breathing
90
What is HAGMA
High anion gap metabolic acidosis
91
How does increase in H+ cause hyperkalaemia
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
What ECG abnormalities can be caused by hyperkalaemia
-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
How does an increase in H+ cause Kussmaul breathing
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
What causes abdominal pain in DKA
Hyperkalaemia
95
Why may hypokalaemia occur in DKA
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
What arrhythmia can be caused by hypokalaemia
QT prolongation
97
Management of DKA
IV fluid
IV insulin
Consistent monitoring of blood glucose, ketone level, electrolytes
98
Which one should be administered first in managing DKA
IV fluid first then IV insulin
99
What needs to be stopped when giving patient IV insulin
Short acting insulin
100
Which ketone body is measured in ketone meters
B-hydroxybutyrate
101
Which type of diabetes often has relative insulin deficiency
Type 2
102
What is relative insulin deficiency
Insulin deficient patient who still has a little bit of insulin sensitivity left
103
Difference between hyperosmolar hyperglycemic state (HHS) and DKA
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
Why may patients with HHS not have elevated ketone bodies, assuming that HHS and DKA did not overlap
Because the patients often still have enough insulin to prevent activation of ketogenesis
105
How does HHS occur
Hyperglycaemia -> glucosuria -> osmotic diuresis -> polysuria -> dehydration
Dehydration causes blood to be very concentrated = hyperosmolar
106
Symptoms of HHS
Polyuria
Polydipsia
Dry skin
Drowsiness
Loss of consciousness
107
Biochemical findings in HHS
Higher glucose than DKA
High normal / raised sodium
Raised osmolarity
less / not ketoacidotic
108
How to calculate osmolarity
2 x Sodium + Urea + glucose
109
What is the normal range of osmolarity
275-295
110
T2 diabetes is a polygenic disease. What does polygenic mean
Multiple genes contributing to risk of T2 diabetes. Each of them poses a small risk bu in combination they become a large risk
111
What are the 2 main risk factors for T2 diabetes
Obesity
Genetics
112
Why are obese people more at risk of insulin resistance
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
Why may some obese people not develop insulin resistance
They have higher fat storage threshold so can safely store more fat without spilling it
114
Why may some slim people develop T2 diabetes
no where to store fat = Low fat storage threshold = fat spill and cause lipotoxicity
115
Risks associated with insulin resistance
PCOS
Hypertension
Hyperlipidaemia
CVD
Stroke
CHD
116
Do all T2 diabetics have insulin resistance
No, only 90% have insulin resistance. The rest developed T2 diabetes due to impaired insulin secretion
117
Difference between T1 and T2 diabetes
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
What should you also treat when treating a T2 diabetic
Blood pressure and lipids
Because insulin resistance / obese patients are at increased risk of CVD, CHD
119
What is monogenic diabetes
Diabetes caused by a mutation in a single gene
120
Which 2 defects can be caused by monogenic diabetes
Defect in insulin secretion
Defect in insulin action - signalling pathway or fat storage
121
Examples of monogenic diabetes with defect in insulin secretion
MODY (maturity onset diabetes of the young)
Neonatal diabetes
KCNJ11 mutation
122
What is CGL (congenital generalised lipodystrophy)
A type of monogenic diabetes due to defect in fat storage
123
Characteristic of CGL
The patient is slim, muscular due to lack of adipose tissue
124
Why do CGL patients develop into diabetes
Because they cannot store fat hence has low fat storage threshold -> fat spill -> insulin resistance
125
What is MODY
Maturity onset diabetes in the young
T2 diabetes found in young people
126
Inheritance pattern of MODY
Autosomal dominant
127
Age of onset of MODY
before 25 years old
128
Mutations in what structures can cause MODY (types of MODY)
Glucokinase
Transcription factors
129
Why is mutation in glucokinase less concerning than mutation in transcription factors
Because in glucokinase mutation, the rest of the beta cell is still functional so still respond well to glucose levels
130
Effect of MODY caused by glucokinase mutation
Higher fasting glucose level but still secretes insulin in response to decrease in glucose level after meal
= stable hyperglycaemia
131
Management of MODY due to glucokinase mutation
Diet management
No need insulin
132
Difference between glucokinase MODY and transcription factor MODY
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
What is the most common cause of MODY
Transcription factor MODY, especially HNF1a MODY
134
Management of HNF1A MODY
low dose Sulphonylurea
If the patient was previously misdiagnosed with T1 diabetes, stop insulin treatment and start SU
135
Where does KCNJ11 mutation affect
Kir 6.2, a subunit of K+ channel in beta cells
136
Effect of KCNJ11 mutation
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
Onset of KCNJ11 monogenic diabetes
Before 6-12 months of age
138
Why is T1 diabetes unlikely to be the diagnosis of a patient presenting with diabetes at 6 weeks of age
T1 diabetes unlikely to occur before the age of 1 because autoimmunity should not have developed that early on (immature immune system)
139
When is T1 diabetes usually diagnosed at
13-14 years old
140
Management of KCNJ11 monogenic diabetes
high dose SU
141
Hypoglycaemic risk in patients with KCNJ11 monogenic diabetes taking SU
Very low risk of hypoglycaemia. Lower than those that have T2 diabetes
142
How does diabetes cause nephropathy
Damage to the capillaries in the glomeruli
143
Signs of nephropathy
Proteinuria, microalbuminuria
Nodular glomerulosclerosis
144
Consequences of diabetic nephropathy
Hypertension
Decline in renal function 1/min/month if untreated
Increase in risk of death
145
When should ACR and PCR be measured in diabetics
At diagnosis then at regular intervals (annually)
146
Normal level of ACR (albumin:creatine) in female
<3.5 mg/mmol
147
Microalbuminuria threshold
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
Proteinuria (macroalbuminuria) threshold
ACR >30 mg/mmol
PCR >45 mg/mmol
149
How many times should you test ACR before making a diagnosis of microalbuminuria
2 or 3 times
Diagnosis established if positive for 2 or 3 times
150
How many times should you test PCR before making a diagnosis of proteinuria
2 or 3 times
151
What is insipient nephropathy and what is the level of it
Presence of low but abnormal albumin level in urine
ACR = above 2.5 (3.5 Females) - 30
152
What is overt nephropathy
Persistent macroalbuminuria for 24 hours or more
153
Why do you need to repeat the ACR and PCR tests for 2 to 3 times before establishing a diagnosis
Because it varies a lot- it can vary due to exercise / fluid load / protein load / day or night / day to day
154
What do you need to screen for if a diabetic patient developed microalbuminuria
Screen for vascular diseases
Screen for retinopathy
155
Management of nephropathy due to diabetes
Start ACEi or ARB (angiotensin receptor blocker) immediately after diagnosis of microalbuminuria / proteinuria
Tighten blood pressure control
Tighten glycemic control
Discourage smoking
156
What level should the blood pressure for patients with nephropathy be controlled at
<130/80 mmHg
157
How does ACEi help prevent nephropathy from developing into end stage renal failure
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
What happens to GFR when the patient starts taking ACEi
Decrease
Allow up to 20% decrease in eGFR due to decrease in filtration pressure
159
Contraindication for ACEi
Pregnancy
160
Which drug for diabetes provides renal protection
SGLT2i
161
What happens to the effect of SGLT2i when the eGFR is <45ml/min
Reduces glucose lowering effects but still provides renal protection
162
Why does the glucose lowering effect of SGLT2i reduce if eGFR <45ml/min
Because the glucose lowering effect is dependent on renal glucose filtration. If renal function is impaired = less SGLT2i effect
163
Risk factors for neuropathy as a complication of diabetes
Prolonged length of diabetes
Poor glycemic control
Smoking
High cholesterol
High lipids
Alcohol
Genetics
164
Long / short nerves are more likely to be affected by neuropathy in diabetes
Long nerves
165
What is the glove and stocking distribution describing
Describes the areas which are commonly affected by peripheral neuropathy
- feet and hands
166
Symptoms of peripheral neuropathy
Burning, tingling sensation
Pain
Hypersensitivity
Loss of balance / coordination
Numbness / loss of sensation (late stage of neuropathy)
167
Consequences of peripheral neuropathy
Damaging the feet without realizing due to neuropathy can lead to ulcers, infection and potentially amputation
Increased risk of Charcot foot
168
What is Charcot foot
A destructive inflammatory process in foot which damages the bones, causing deformity
169
Presentation of Charcot foot
Hot, swollen foot in someone with neuropathy
170
How to distinguish between Charcot foot and infection
use MRI
171
Treatment of Charcot foot
Taking weight off the foot
Total contact cast
Aircast boot
172
Moderate foot risk criteria
Impaired sensation
Absent foot pulses
No skin calluses/deformity
patient cannot take care of their foot
173
High foot risk criteria
Impaired sensation
Absent foot pulses
presence of skin calluses / deformity
Previous amputation or foot ulcers
174
When should you urgently refer a patient with foot disease to specialist team
During active foot ulcers / infections / ischaemia / gangrene / swelling..etc
175
How often should diabetic patients go to their podiatrist
Annually if they are considered at moderate or high risk of foot diseases
176
How often should patients screen for foot disease even if they don't have any
Annually by healthcare professionals (not podiatrist)
177
Treatment of pain in neuropathy
First line:
Amitriptyline
Duloxetine
Gabapentin
topical Capsaicin cream (used in combination with others)
178
What is diabetic amyotrophy
Proximal neuropathy with episodic, asymmetrical pain on one side of hip / thigh / buttock and muscle wasting and weakness
179
What is autonomic neuropathy
Neuropathy affecting the autonomic nervous system
180
What are the GI consequences of autonomic neuropathy
Slow gastric emptying
Gastric slowing
Oesophageal nerve damage causing difficulty in swallowing
181
Symptoms of slow gastric emptying
Unable to control blood glucose level
Nausea
Vomiting
Bloating
Loss of appetite
182
Symptoms of gastric slowing
Constipation / diarrhea
183
Why do patients with autonomic neuropathy find it hard to control their blood glucose levels
Because they can't predict when is the food going to go down and be digested
184
Management of gastroparesis due to autonomic neuropathy
Advise patients to have regular smaller portions of food
Promotility drugs
Anti-nausea drugs
NSAID / tricyclic antidepressants for pain management
Gastric pacemaker
185
What are the promotility drugs used for gastroparesis
Metoclopramide
Domperidone
Erythromycin
186
Example of a tricyclic antidepressant drug
Amitriptyline
187
Example of antiemetic
Serotonin Antagonist (5HT3 antagonist)
188
What is the CV consequence of autonomic neuropathy
Unable to adjust blood pressure and heart rate
189
What happens if you can't adjust your blood pressure and heart rate
Postural hypotension - faint / light-headed when standing up after sitting
Heart rate remaining high instead of rising then falling in response to activities
190
Which hand neuropathy are diabetics at an increased risk of
Carpal tunnel syndrome - median nerve neuropathy
