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Year 2 - Endocrinology (DP) > Clinical (Weeks 1 + 2 - Diabetes) > Flashcards

Clinical (Weeks 1 + 2 - Diabetes) Flashcards

1
Q

What antibodies might be present in T1DM?

A

Anti-GAD

Anti-islet cell

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2
Q

When is a person though to have T2DM?

A

When they don’t have:

 - T1DM
 - Monogenic DM
 - Other condition/Treatment causing secondary DM
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3
Q

What are some risk factors for T2DM?

A 
Central obesity
FHx
Gestational DM
Age
Ethnicity:
     - Asian
     - African
     - Afro-Caribbean
PMHx of MI/CVA
Medications
IGT/IFG
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4
Q

What are some symptoms of DM?

A 
Thirst
Polyuria
Thrush
Weakness
Blurred vision
Infections
Weight loss
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5
Q

What pancreatic diseases can cause secondary DM?

A

Chronic/Recurrent pancreatitis
Haemochromatosis
CF

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6
Q

What endocrine diseases can cause secondary DM?

A

Cushing’s
Acromegaly
Phaeochromocytoma
Glucogonoma

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7
Q

What drugs can induce DM?

A

Glucocorticoids
Diuretics
β-blockers

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8
Q

What genetic disorders can result in DM?

A

CF
Monogenic dystrophy
Turner’s

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9
Q

What are the principles of T2DM treatment?

A 
Alleviate hyperglycaemia symptoms
Improve glycaemic control
Minimise:
     - Hypoglycaemia
     - Weight gain
Reduce complications
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10
Q

What do biguanides do?

A

Increase insulin sensitivty

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11
Q

What dose of biguanide do we usually start with?

A

500mg once/twice daily

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12
Q

Give an example of a biguanide

A

Metformin

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13
Q

Does metformin cause weight loss/no change/weight gain?

A

No change

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14
Q

How much can metformin reduce a patient’s HbA1c?

A

15-20 mmol/L

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15
Q

Does metformin cause hypoglycaemia?

A

Not if used as monotherapy

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16
Q

What effect does metformin have on a patient’s lipid status?

A

Decreased triglycerides and LDL

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17
Q

Is metformin safe in pregnancy?

A

Yes

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18
Q

What are some side effects of metformin?

A 
Anorexia
Nausea/Vomiting/Diarrhoea/Abdo. pain
Anaemia
Lactic acidosis:
     - If in renal failure
     - If in cardiac/liver failure
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19
Q

In what patient’s should metformin be stopped?

A 
Renal failure:
     - If eGFR  150 micromol/L
Liver:
     - Advanced cirrhosis
     - Liver failure
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20
Q

When might metformin be beneficial?

A

NAFLD

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21
Q

In what patient’s should metformin be used with caution due to the increased risk of lactic acidosis?

A 
Acute CHF
Sepsis
Acute MI
Respiratory failure
Hypotension
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22
Q

How do sulphonylureas work?

A

Insulin secretagogues

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23
Q

Give examples of SUs

A

Glicazide
Glipizide
Glimeparide

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24
Q

What complications can metformin prevent?

A

Microvascular

Macrovascular

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25
Q

What complications can SUs prevent?

A

Microvascular

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26
Q

How do SUs manage hyperglycaemia?

A

Decrease HbA1c by 15-20 mmol/mol
Increased insulin secretion
More rapid action than metformin

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27
Q

When are SUs used?

A

1st line in underweight T2DM

2nd line as add-on to metformin/intolerant to metformin

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28
Q

What are some side effects of SUs?

A

Hypoglycaemia:
- Caution in elderly/alcoholics/liver disease
GI upset
Headache

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29
Q

What is the only available thiazolidinedione?

A

Pioglitazone

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30
Q

How do TZDs work?

A

They are PPARγ agonists - Increase insulin sensitivity

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31
Q

What effect do TZDs have on weight?

A

Increase is common:

- Due to increased S/C fat and fluid retention

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32
Q

Why can TZDs increase the risk of CHF?

A

Fluid retention

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33
Q

What other effects do TZDs have?

A

Improve microalbuminaemia
Prevent macrovascular complications
Increase hip fracture risk

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34
Q

How dies Dapaglifozin work?

A

Act on the incretin pathway:

- SGLT2 inhibitor

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35
Q

What are the incretins?

A

Stimulate intestinal secretion of insulin:

 - GIP from K cells
 - GLP-1 from L cells
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36
Q

What type of drug is exenatide?

A

GLP-1 receptor agonist

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37
Q

How does exenatide work?

A 
Increased insulin secretion (no hypos)
Suppress glucagon
Decrease gastric emptying -> Early satiety
Reduce appetite
Weight loss
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38
Q

What are some side effects of exenatide?

A

Nausea

Pancreatitis

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39
Q

Give some examples of DPP-IV inhibitors

A

Vildagliptin
Sitagliptin
Saxagliptin
Linagliptin

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40
Q

What drugs are less potent; GLP-1 receptor agonist, DPP-IV inhibitors?

A

DPP-IV inhibitors:

 - Only work on what's present
 - DLP-1 decreased in T2DM
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41
Q

What are some benefits of DPP-IV inhibitors?

A

Increase insulin secretion (no hypos)
Decrease glucagon
Weight neutral

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42
Q

How do SGLT2 inhibitors work?

A

Decrease sugar uptake by ~25%:

 - Glycosuria (~80g/day)
 - ~1lb decrease in weight/week
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43
Q

What side effects are common with SGLT2 use?

A

Sugar in urine:

 - Thrush
 - UTIs
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44
Q

What type of insulin is used in T2DM?

A

Basal insulin

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45
Q

When is bariatric surgery considered?

A

When 30

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46
Q

What is acanthosis nigricans?

A 
Skin becomes:
     - Hyperpigmented
     - Velvety
Found at:
     - Axilla
     - Neck
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47
Q

What is acanthosis nigricans a sign of?

A

Insulin resistance ie T2DM

48
Q

What are some microvascular complications of T2DM?

A 
Retinopathy
Nephropathy
Neuropathy:
     - Impotence
     - Digestion/Urination problems
Amputation
49
Q

What are some macrovascular complications of T2DM?

A

CVS disease:

 - MI
 - CHD
 - CVA
 - PAD
 - Angina
50
Q

How can alcohol result in hypoglycaemia?

A

Increases insulin activity

51
Q

How long do rapid-acting insulin analogues last and give examples?

A 
~5 hours
Examples:
     - Humalog
     - Novorapid
     - Apidra
52
Q

How long do short-acting insulin analogues last and give examples?

A 
~8 hours
Examples:
     - Humulin S (human insulin)
     - Actrapid
     - Insuman rapid
53
Q

How long do intermediate-acting insulin analogues last and give examples?

A 
~20 hours
Examples:
     - Insulatard
     - Humulin I
     - Insuman basal
54
Q

How long do long-acting insulin analogues last and give examples?

A

~24 hours:

 - Lantus (Levels remain high at end of day)
 - Levemir (Levels reduced at end of day)
55
Q

How can we evaluate glucose control?

A 
Home blood glucose monitoring
Urine testing:
     - Glucose
     - Ketones
HbA1c
56
Q

What does glycated Hb give us an idea of?

A

Measure of blood glucose over 6-8 weeks

57
Q

What is the ideal HbA1c target?

A

48 mmol/mol

58
Q

What are the downsides to injectable insulin?

A

It’s into the S/C tissue (instead of portal blood)
Peaks too slow -> Can’t prevent post-meal hyperglycaemia
Slow clearance

59
Q

What factors affect the absorption of injectable insulin?

A 
Pen accuracy
Leakage
Temperature
Injection site
Exercise
60
Q

When is IV insulin prescribed?

A

DKA
HSS
Acute illness
Fasting patients who cannot tolerate PO intake

61
Q

What monitoring is important during the delivery of IV insulin?

A 
Hourly BG (5-12 mmol/L)
Free of hypos
Ketones if BG > 12 mmol/L
U+Es daily
Transition from IV to S/C
62
Q

What are some indications for a pancreas transplant?

A

Imminent/ERSD with kidney transplant
Severe hypos
Incapacitating problems

63
Q

What are the four mains steps in islet transplantation?

A
  1. Donation and retrieval
  2. Islet isolation
    • Sterility
    • Pancreas digestion
    • Islet purification
  3. Islet culture (24 hours)
  4. Transplantation
64
Q

What are some signs and symptoms of hypoglycaemia?

A 
Shaking
Sweating
Anxious
Dizzy
Hungry
Tachycardia
Decreased vision
Weakness + fatigue
65
Q

What can severe hypoglycaemia lead to?

A

Seizures

Unconsciousness

66
Q

What is the immediate treatment of hypoglycaemia?

A
  1. 15-20g of glucose/simple carbohydrates
  2. Recheck BG after 15 minutes
  3. If still hypo -> Repeat
  4. Once BG normal -> Small snack if next meal >1hr away
67
Q

Treatment of severe hypoglycaemia?

A

1mg glucagon injection:

 - Buttock
 - Arm
 - Thigh
68
Q

What is the definition of impaired hypoglycaemia awareness?

A

When BG

69
Q

During DKA what hormones increase in levels?

A

Counter-regulatory:

 - Glucagon
 - Adrenaline
 - Cortisol
 - GH
70
Q

What does the activation of certain hormones in DKA cause?

A 
Increased lipolysis
Decreased glucose utilization:
     -> Hyperglycaemia
Increased proteolysis:
     -> Hyperglycaemia
Increased gluconeogenesis:
     -> Hyperglycaemia
71
Q

What does hyperglycaemia result in?

A

Glycosuria

 - > Electrolyte loss
           - > Dehydration
                      - > Dehydration and Hyperosmolar state
72
Q

What is the biochemical diagnosis of DKA?

A
  1. Ketonaemia > 3mmol/L OR Ketonuria > ++
  2. BG > 11.0mmol/L OR Known DM
  3. Bicarbonate <15mmol/L OR venous pH <7.3
73
Q

What can commonly precipitate DKA?

A

Infection
Drugs/Alcohol
Non-adherence to therapy
Newly diagnosed DM

74
Q

What signs and symptoms are caused by the following in DKA:

  • Osmotic changes
  • Ketone body related
A 
Osmotic:
     - Thirst
     - Polyuria -> Dehydration
Ketone bodies:
     - Flushing
     - Vomiting
     - Abdominal pain
     - Kussmaul's respiration
     - +/- Ketone breath
75
Q

What other biochemical changes can be seen in DKA?

A 
Potassim is often raise (> 5.5mmol/L)
Creatinine is often raised
Sodium is often decreased
Increased lactate
Ketones increased:
     - β-hydroxybutarate in blood
     - Acetoacetate in urine
76
Q

What causes death in DKA?

A 
Adults:
     - Hypokalaemia
     - Aspiration pneumonia
     - ARDS
Kids:
     - Cerebral oedema
77
Q

How is DKA managed?

A

Replace losses:

 - Fluid -> 0.9% NaCl
            - > Dextrose when glucose
78
Q

What HbA1c levels indicate the following:

  1. Normal
  2. Pre-diabetes
  3. Diabetes
A

Normal:

 - 48mmol/L
 - >6.5%
79
Q

What fasting glucose levels indicate the following:

  1. Normal
  2. Pre-diabetes
  3. Diabetes
A

Normal:

- 7.0mmol/L

80
Q

What 2hr OGTT levels indicate the following:

  1. Normal
  2. Pre-diabetes
  3. Diabetes
A

Normal:

- 11.1mmol/L

81
Q

What is the normal blood ketone level?

A
82
Q

What is the typical biochemistry in Hyperglycaemia Hyperosmolar Syndrome?

A 
Higher glucose than DKA
Significant renal impairment
Increased sodium
Increased osmolarity (~400)
Less acidotic
83
Q

Where does lactate originate from?

A

Erythrocytes
Skeletal muscle
Brain
Renal medulla

84
Q

How is lactate cleared?

A

Hepatic uptake

Aerobic conversion -> Pyruvate -> Glucose

85
Q

What is the normal range for lactate?

A

0.6-1.2mmol/L

86
Q

How do we calculate the anion gap?

A

[Na+ + K+] - [HCO3- + Cl-]

87
Q

What is the normal ion gap?

A

10-18mmol/L

88
Q

What causes of acidosis present with a normal ion gap?

A 
Diarrhoea
RTA
Addison's
Reason:
     - Bicarbonate is reduced
     - Cl- is raised
89
Q

What causes of acidosis present with a high ion gap?

A 
MUDPILES
Reason:
     - Bicarbonate reduced
     - Replaced by sulfate, phosphate
     - Cannot be replaced sufficiently
90
Q

What is Type A lactic acidosis?

A 
Associated with tissue hypoxia:
     - Infarct
     - Cardiogenic shock
     - Hypovolaemic shock
               > Sepsis
               > Haemorrhage
91
Q

What is Type B lactic acidosis?

A

Liver disease
Leukaemia
Associated with DM:
- Metformin in illness/renal failure

92
Q

What are the targets for each of the following in DM?

  • BMI
  • HbA1c
  • BP
  • Total cholesterol
  • LDL
  • Triglycerides
A

BMI -> 25
HbA1c -> 7% (75mmol/mol)
BP ->

93
Q

How do we treat T2DM in the following situations:

  • BMI >25
  • BMI
A

BMI >25:
- Metformin up to 1g tds
BMI

94
Q

What anti-lipid therapies are recommended in diabetes?

A 
Statins:
     - Increase dose to lower cholesterol
Fibrates
Ezetimibe
Cholestyramine:
     - Unpleasant
95
Q

What is peripheral neuropathy?

A

Pain/Loss of feeling in:

 - Hands
 - Feet
96
Q

What is autonomic neuropathy?

A 
Changes in bowel habit
Bladder function
Sexual response
Sweating
HR/BP/Hypoglycaemic unawareness
97
Q

What is proximal neuropathy?

A

Pain in thigh/hips/buttocks:

- Leg weakness (Amyotrophy)

98
Q

What factors precipitate neuropathy?

A 
Increased length of DM
Poor glycaemic control
T1DM > T2DM
Increased cholesterol
Smoking/Alcohol/Genetics
99
Q

A diabetic patient presents with numbness, tingling and sharp pains in their foot. It is very sensitive to touch and they have lost their balance.

A

Peripheral nerve damage

100
Q

What complications can peripheral neuropathy result in?

A

Infections/Ulcers
Charcot foot
Deformities
Amputations

101
Q

What is the step up treatment for painful neuropathy?

A
  1. Simple analgesia
  2. TCAs (amitryptiline at night)
  3. Gabapentin
  4. Oxycodone/Tramadol
102
Q

A patient presents with constipation, nausea, bloating and a loss of appetite. He has difficulty swallowing and has known, poorly controlled DM.

A

Autonomic neuropathy

103
Q

How can gastroparesis be treated?

A

Metoclopramide
Domperidone
Erythromycin
Gastric pacemaker

104
Q

What is diabetic nepropathy also known as?

A

Kimmelsteil-Wilson Syndrome

Nodular Glomerulosclerosis

105
Q

What can result in diabetic nepropathy?

A

Hypertension
Decreased renal function:
- GFR down by 1ml/min/month
Accelerated vascular disease

106
Q

How is diabetic nephropathy screened for?

A

Urinary albumin creatinine ratio (ACR)
Confirm with EMU
Dipstick
U+Es -> eGFR

107
Q

What is a normal ACR?

A

Male:

-

108
Q

What is defined as microalbuminuria?

A

30-300mg/L of urine

109
Q

What is macroalbuminuria?

A

> 300mg/L of urine

110
Q

What can cause a false positive urinary albumin excretion rate? (UAER)

A 
Menstruation
Vaginal discharge
UTI
Pregnancy
Illness
Renal discharge
111
Q

What are cotton wool spots a sign of in diabetic retinopathy?

A

Ischaemia

112
Q

What are hard exudates a sign of in diabetic retinopathy?

A

Lipid break down products

113
Q

Which of the following drugs doesn’t cause erectile dysfunction:

  • Thiazides
  • Beta blcoerks
  • Antidepressants
  • Analgesics
  • NSAIDs
A

NSAIDs

114
Q

Put the following steps in atheroslcersosis development in order:

  • Macrophages ingest LDL to become foam cells
  • Fibrous cap forms from smooth muscle migration
  • Cap rupture
  • Monocytes migrate into epithelium
  • Smooth muscle degenerated by activated macrophages
  • Cytokines produced result in smooth muscle migration
  • Platelets aggregate at site of rupture and thrombus forms
A
  1. Monocytes migrate into epithelium (become macrophages)
  2. Macrophages ingest LDL to become foam cells
  3. Cytokines produced result in smooth muscle migration
  4. Fibrous cap forms from smooth muscle migration
  5. Smooth muscle degenerated by activated macrophages
  6. Cap rupture
  7. Platelets aggregate at site of rupture and thrombus forms
115
Q

How do we diagnose diabetes?

A
  1. Symptomatic and:
    • One-time fasting glucose >7.0mmol/L OR
    • One-time random glucose >11.1mmol/L
      OR
  2. Two time results of:
    • Fasting glucose >7.0mmol/L OR
    • OGTT >11.1mmol/L OR
    • Random glucose >11.1mmol/L

OR

  1. HbA1c >48mmol/L (>6.5%)

Year 2 - Endocrinology (DP) (15 decks)

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