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Year 2 Medicine @ Lancaster Uni > 2.07 - Diabetes and Adrenal disorders > Flashcards

2.07 - Diabetes and Adrenal disorders Flashcards

1
Q

What is the function of the HPA axis?

A
  • Helps to control communication between the hypothalamus, pituitary gland and the adrenal cortex
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2
Q

What is secreted by the hypothalamus?

A
  • CRH - Corticotropin
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3
Q

What is secreted by the anterior pituitary gland in the HPA axis?

A
  • ACTH - Adrenocorticotropic
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4
Q

What is secreted by the adrenal cortex in the HPA axis?

A
  • Cortisol
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5
Q

How does the HPA axis self-regulate?

A
  • Negative feedback systems
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6
Q

What are the adrenal glands found in relation to the peritoneum?

A
  • Retroperitoneal
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7
Q

What are the different parts of the adrenal gland?

A
  • Adrenal cortex
  • Adrenal medulla
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8
Q

What zones make up the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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9
Q

What cell type is found in the adrenal medulla?

A
  • Chromaffin cells
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10
Q

What hormones are released by the chromaffin cells?

A
  • Adrenaline/Noradrenaline
  • Peptides (Somatostatin/Substance P)
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11
Q

What is secreted from the zona glomerulosa?

A
  • Mineralocorticoids
  • Eg. Aldosterone
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12
Q

What is secreted from the zona fasciculata?

A
  • Glucocorticoids
  • Eg. Cortisol/Cortisone
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13
Q

What is secreted from the zona reticularis?

A
  • Androgens
  • Eg. Estrogens/Testosterone
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14
Q

What is the role of steroid hormones in the body?

A
  • Immune functions
  • Controls metabolism
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15
Q

What is the role of cortisol in the body?

A
  • Anti-inflammatory
  • Glucose in the liver
  • Withstand injury/stress
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16
Q

What is role of aldosterone in the body?

A
  • Salt and water balance (BP regulation)
  • RAAS system
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17
Q

What is the role of androgens in the body?

A
  • Sex hormones
  • Development of sexual characteristics
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18
Q

Where are catecholamines derived from?

A
  • From the amino acid tyrosine
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19
Q

What is tyrosine modified by to produce dopamine?

A
  • DOPA decarboxylase
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20
Q

How is dopamine converted into noadrenaline?

A
  • Oxygenation
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21
Q

What is primary adrenal insuffciency also called?

A
  • Addisons disease
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22
Q

What is the cause of primary adrenal insufficiency?

A
  • Destruction/dysfunction of adrenal cortex
  • Reduced cortisol and aldosterone
  • Desensitisation to ACTH
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23
Q

What causes secondary adrenal insufficiency?

A
  • Caused by damage or loss to the pituitary gland
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24
Q

What happens in secondary adrenal insufficiency?

A
  • Insuffcient ACTH release -> lack of stimulation to the adrenal gland
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25
Q

What happens in Sheehan syndrome?

A
  • PPH causes avascular necrosis
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26
Q

What is the most common cause of tertiary adrenal insuffciency?

A
  • Long-term steroid use
  • Causes suppression of the hypothalamus
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27
Q

What happens in tertiary adrenal insuffciency?

A
  • Inadequate release of CRH by the hypothalamus
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28
Q

What is Addison’s disease?

A
  • Primary adrenal insuffciency which is caused by destruction/damage of the adrenal cortex
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29
Q

What happens as a result of Addison’s disease?

A
  • Leads to an decrease in release of glucocorticoids and mineralcorticoids as ACTH is unable to stimulate the adrenal cortex
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30
Q

What are some autoimmune causes of adrentitis?

A
  • Most common cause in the western world
  • Caused by enzyme: 21-hyrdroxylase
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31
Q

What are some causes of infective adrenalitis?

A
  • TB (Most common)
  • HIV
  • Fungal infections
  • Syphilis
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32
Q

What are some other causes of Addison’s disease?

(Not autoimmune or infective)

A
  • Haemorrhage
  • Meningitis
  • Maliganancy invasion
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33
Q

What is an Addisonian crisis?

A
  • Life-threatening presentation of Addison’s disease
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34
Q

What occurs during an Addisonian crisis?

A
  • Significant deficiency in mineral/glucocorticoids
  • Can occur after withdrawl of exogenous steroids
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35
Q

What are symptoms of an Addisonian crisis?

A
  • Confusion
  • Pyrexia
  • Abdominal pain
  • Hypotension
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36
Q

What are the symptoms of chronic Addison’s disease?

A
  • Anorexia
  • Fatigue
  • Postural dizziness
  • Abdominal pain
  • Nausea and vomiting
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37
Q

What are the clinical signs seen in acute onset Addison’s disease?

A
  • Hypotension
  • Shock
  • Pyrexia
  • Dehydration
  • Hyperpigmentation
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38
Q

What are some clinical signs seen in chronic Addison’s disease?

A
  • Hyperpigmentation
  • Postural HTN
  • Weight loss
  • Muscular dystrophy
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39
Q

What symptoms are seen in females with Addison’s disease?

A
  • Hair loss in pubic area and axillary regions
  • Amenorrhea = androgen deficiency
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40
Q

What are some causes of an Addisonian crisis?

A
  • Stress
  • Trauma
  • Illness
  • Abrupt cessation of steroid after chronic use
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41
Q

What happens to U&E levels in Addison’s disease?

A
  • Elevated due to dehydration
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42
Q

What results are seen in relation to sodium and potassium levels in Addison’s disease?

A
  • HYPOnatraemia
  • HYPERkalaemia
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43
Q

What level of cortisol serum is indicative of adrenal insufficiency?

A
  • <50nmol/L @ 9am = Adrenal insuffciency
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44
Q

How is primary and secondary Addison’s disease differentiated between using ACTH levels?

A
  • Primary = HIGH
  • Secondary = LOW
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45
Q

What do the results of a SST/LST test show?

A
  • Insufficient rise = adrenal insuffciency
  • No rise = primary adrenal failure
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46
Q

What is synthacten?

A
  • Synthetic ACTH analogue
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47
Q

What is main management principle for the treatment of Addison’s disease?

A
  • Replacement of deficient hormones in the body
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48
Q

What are deficient glucocorticoids replaced by?

A
  • Hydrocortisone
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49
Q

What are deficient mineralcorticoids replaced by?

A
  • Fludrocortisone
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50
Q

What are deficient androgens replaced by?

A
  • DHEA
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51
Q

What important patient education is given in Addison’s disease?

A
  • Lifelong treatment
  • How to identify a crisis
  • Carry a steroid card
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52
Q

What should be done to the steroid dose of someone with Addison’s disease if their temperature exceeds 37.5°?

A
  • Steroid dose should be doubled
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53
Q

What is the treatment for an Addisonian crisis?

A
  • IV hydrocortisone (100mg)
  • IV Fluid rehydration
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54
Q

What monitoring should be arranged in Addison’s disease?

A
  • Cardiac
  • Electrolyte
  • Blood sugar monitoring
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55
Q

What are the complications associated Addison’s disease?

A
  • Severe abdominal pain
  • Extreme weakness
  • Low BP
  • Kidney failure
  • Shock (Crisis)
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56
Q

What is Cushing’s disease?

A
  • Hypercortisolism caused by exposure to an excess of glucocorticoids
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57
Q

What is endogenous Cushing’s disease?

A
  • Derived internally from excess production of glucocortocoids
  • Rare
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58
Q

What is exogenous Cushing’s disease?

A
  • Derived externally due to excess intake of synthetic glucocorticoids either as medication or misuse
  • Most common cause
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59
Q

What are the two types of Cushing’s disease?

A
  • ACTH dependant
  • ACTH independant
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60
Q

What are the causes of ACTH dependant Cushing’s disease?

A
  • Pituitary adenoma
  • Ectopic ACTH/CRH producing tumour (Eg. Bronchial carcinoma)
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61
Q

What are the causes of ACTH independant Cushing’s disease?

A
  • Therapeutic corticosteroid administration
  • Adrenal tumours (Adenoma, Carcinoma, Hyperplasia)
  • Excess cortisol release
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62
Q

What are the symptoms associated with Cushing’s disease?

A
  • Tiredness
  • Depression
  • Weight gain
  • Easy bruising
  • Amenorrhoea
  • Reduced libido
  • Striae
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63
Q

What are the clinical features associated with Cushing’s disease?

A
  • Moon face
  • Buffalo hump
  • Acne
  • Plethora (Excess blood in skin)
  • HTN
  • Proximal muscle weakness
  • Hyperpigmentation (ACTH dependant)
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64
Q

What are the inclusion criteria for testing for Cushing’s disease?

A
  • Unusual features for age
  • Children with increased weigh percentile and decreased weight percentile
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65
Q

What test can be used to prove hypercortisolism?

A
  • Overnight dexamethasone test
  • Give 1mg at of Dex. at 11pm
  • Measure at 9am
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66
Q

What is the normal value for cortisol?

A
  • <50nmol/L
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67
Q

What are some symptoms of pseudocushings?

A
  • Happens with a false positive
  • Obesity
  • Acute illness
  • Depression
  • Alcoholism
  • Renal failure
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68
Q

How is a plasma ACTH used distinguish between dependant and indendant Cushing’s disease?

A
  • ACTH dependant = High
  • ACTH independant = Low
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69
Q

What other tests can be performed in cases of suspected Cushing’s disease?

A
  • 24 hour urinary free cortisol
  • Late night salivary test
  • Longer low dose DST (2mg/d for 48 hours)
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70
Q

Which test can be used to distinguish between Cushing’s disease and HPA axis dysregulation?

A
  • Dexamethasone-CRH test
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71
Q

What is the definitive management strategy for exogenous Cushing’s disease?

A
  • Withdrawl of glucocoticoids
  • Tapered withdrawl
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72
Q

What is the gold standard treatement for Cushing’s disease?

A
  • Transsphenoidal surgery
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73
Q

What are the two types of transsphenoidal surgery?

A
  1. Microadenectomy
  2. Subtotal resection of the anterior pituitary
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74
Q

What is the pharmcological management involved in Cushing’s disease?

A
  • Metyrapone
  • 11B-hydrolase inhibitor
  • Leads to less cortisol production
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75
Q

Why must steroid use be tapered?

A
  • If stopped abruptly it can causes an Addisonian crisis?
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76
Q

What is Conn’s syndrome?

A
  • Primary hyperaldosteronism - Excess aldosterone in the body
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77
Q

What is the function of aldosterone in the body?

A
  • Promotes Na+ reabsorption in the kidneys
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78
Q

How does aldosterone causes excess Na+ reabsorption?

A
  • Binds to principle cells
  • Causes an increase in sodium channels
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79
Q

What are the outcomes of increased Na+ reabsorption?

A
  • Hypertension
  • Hypernatremia
  • Hypokalaemia
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80
Q

What are the symptoms associated with Conn’s syndrome?

A
  • Muscle weakness
  • Pins and needles
  • Increased urination
  • Mood disturbances (Due to hypokalaemia)
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81
Q

What are the different causes of Conn’s syndrome?

A
  • Bilateral idiopathic adrenal hyperplasia (Most common)
  • Adrenal adenomas
  • Adrenal hyperplasia
  • These cancers produce aldosterone independant of the body’s normal functions
  • Unilateral hyperplasia
  • Familial hyperaldosteronism (T1/T2/T3(KCN55))
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82
Q

How is screening used in the investigation of Conn’s syndrome?

A
  • Aldosterone:Renin ratio
  • Raised >20mg/dL = Diagnosis confirmed
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83
Q

What tests are used in confirmatory testing for Conn’s syndrome?

A
  • Oral sodium loading test
  • Saline infusion test
  • Catopril challenge test
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84
Q

How is a CT scan used in the diagnosis of Conn’s syndrome?

A
  • Used to distinguish if unilateral or bilateral
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85
Q

What is the definitive management for Conn’s syndrome?

A
  • Either a unilateral or bilateral adrenalectomy
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86
Q

What must be used if a bilateral adrenalectomy is performed?

A
  • Mineralcorticoid receptor anatagonists
  • Eg. Spironolactone, Eplerenone (Don’t cause gynaecomastia)
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87
Q

What are the pharmacological treatment options for Conn’s syndrome?

A
  • Mineralcorticoid receptor antagonists
  • ENaC inhibitors - Amiloride (Potassium sparing diuretic)
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88
Q

What complications can arise from HTN caused by Conn’s syndrome?

A
  • CKD
  • CVD
  • Heart failure
  • Retinopathy
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89
Q

What can hypokalaemia lead to in Conn’s syndrome?

A
  • Metabolic alkalosis
90
Q

What is a phaeochromocytoma?

A
  • A neuroendocrine tumour that arises from chromaffin cells of the adrenal medulla
  • These secrete catecholamines
91
Q

Where else are phaeochromocytomas found in the body?

A
  • Sympathetic paravertebral ganglia of the thorax, abdomen and pelvis
92
Q

What is the ratio between genetic and sporadic phaeochromocytoma?

A
  • Genetic - 40%
  • Sporadic - 60%
93
Q

What are the effects of increased catecholamines on alpha adrenergic receptors?

A
  • Increased BP
  • Increased cardiac contractility
  • Increased glucose utilisation
94
Q

What are the effects of increased catecholamines on beta adrenergic receptors?

A
  • Increased HR
  • Increased cardiac contractility
95
Q

What can increased catecholamines secretions ultimately lead to?

A
  • HTN
  • Phaeochromocytoma crisis
  • Circulatory collapse
96
Q

What triad of symptoms are associated with phaeochromocytoma?

A
  • Episodic headaches
  • Sweating
  • Tachycardia
97
Q

What symptoms are seen in phaeochromocytoma?

A
  • Headaches
  • Sweating
  • Tachycardia
  • Palpitations
  • Dyspnoea
  • Weakness
  • Tremor
  • Nausea
98
Q

What can a phaeochromocytoma resemble?

A
  • Can resemble a panic attack
99
Q

What are the clinical signs seen in phaeochromocytoma?

A
  • HTN
  • Postural HTN
  • Weight loss
  • Pallor
  • Arrhythmias
  • Fever
  • Tremor
100
Q

What are the clinical signs seen in a phaeochromocytoma crisis?

A
  • HTN
  • Hyperthermia
  • Confusion
  • End-organ dysfunction
101
Q

What syndromes are associated with phaeochromocytoma?

A
  • Multiple endocrine neoplasia (MEN) type II
  • Von Hippel-Lindau (VHL) syndrome
  • Neurofibromatosis (NF) type I
102
Q

Whar are some causes of phaeochromocytoma?

A
  • Drugs
  • Opiates
  • Dopamine antagonists
  • Beta blockers
  • Cocaine
  • Tricyclic antidepressants
103
Q

What physical/direct causes are there for phaeochromocytoma?

A
  • Direct pressure during surgery
  • Endotracheal intubation
104
Q

What biochemical tests can be used for phaeochromocytoma?

A
  1. Urinary fractionated metanephrines
  2. Plasma free metanephrines
105
Q

What imaging is used in the diagnosis of phaeochromocytoma?

A
  • CT scan
  • MRI scan
  • MIBG scintigraphy
  • FDG-PET
106
Q

What are the symptoms associated with hyperadrenergic spells?

A
  • Palpitations
  • Sweating
  • Headaches
  • Tremor
  • Pallor
107
Q

What is the definitive management for phaeochromocytoma?

A
  • Surgical resection
108
Q

What must be achieved before a resection is performed?

A
  • Blood pressure optimisation
109
Q

What medications are used in BP optimisation?

A
  1. Alpha blockers
  2. Beta blockers
  3. Calcium channel blockers
  4. Metgrosine
110
Q

What are patients encourgaed to do to compensate for volume loss with excessive catecholamines?

A
  • High sodium diet
111
Q

What complications are associated with phaeochromocytoma?

A
  • Cardiac
  • Metabolic
  • Neurological
  • Post-surgical
112
Q

What is the method of action associated with metgrosine?

A
  • Inhibits catecholamine synthesis
  • Associated with many strong side effects
113
Q

What are the two parts of the pituitary gland?

A
  • Anterior (adenohypophysis)
  • Posterior (neurohypophysis)
114
Q

What is the function of the pituitary gland?

A
  • Regulation of several endocrine organs
115
Q

What hormones are secreted from the anterior pituitary gland?

A
  • Growth hormone
  • TSH
  • FSH
  • LH
  • ACTH
  • Prolactin
  • Melanocyte stimulating hormone
116
Q

What hormones are secreted from the posterior pituitary gland?

A
  • Antidiuretic hormone (ADH)
  • Oxytocin
117
Q

What is the function of growth hormone?

A
  • Stimulates growth, cell production and cell regeneration
118
Q

What is the function of TSH?

A

Stimulates the thyroid gland to produce and release thyroid hormones (T3 and T4)

119
Q

What is the function of ACTH?

A
  • Stimulates the adrenal cortex to produce and release cortisol
120
Q

What is the function of FSH?

A
  • Females - Growth of ovarian follicles
  • Males - Spermatogenesis
121
Q

What is the function of LH?

A
  • Females - Triggers ovulation and production of oestrogen and progesterone
  • Males - Production of testerone
122
Q

What is the function of prolactin?

A
  • Promotes lactation in the mammary gland
123
Q

What is the function of MSH?

A
  • Influences the pigmentation of the skin
124
Q

What is the function of ADH?

A
  • Regulates water balance in the body by increasing water reabsorption in the kidneys
  • Reduces urine output
  • Also known as vasopressin
125
Q

What is the function of oxytocin?

A
  • Stimulates uterine contractions in childbirth
  • Triggers let-down reflex
  • Involved in social bonding
126
Q

How can TB induce Addison’s disease?

A
  • When lesions travel from lungs to the adrenal glands
  • Causes inflammation, necrosis, destruction of adrenal cortical tissue
  • Usually infects bilaterally
127
Q

What is waterhouse-fridericksen syndrome?

A
  • An adrenal haemorrhage caused by severe bacterial infection which then causes arenal gland failure
128
Q

What is the most common cause of waterhouse-fridericksen syndrome?

A
  • Neissera meningitidis
129
Q

What can waterhouse-fridericksen syndrom lead to?

A
  • Adrenal crisis
130
Q

Which two hormones are involved in the regulation of blood glucose?

A
  • Insulin
  • Glucagon
131
Q

What happens when there is a low blood glucose?

A
  • Glucagon released from alpha cells in the pancreas
  • Liver releases glucose into blood
  • Normal level restored
132
Q

What happens when there is a high blood glucose?

A
  • Insulin released by beta cells in the pancreas
  • Fat cells take in glucose from the blood
  • Normal levels restored
133
Q

What are the two main functions of the pancreas?

A
  • Exocrine (digestive)
  • Endocrine (hormonal)
134
Q

Which part of the pancreas is intraperitonal?

A
  • Tail
135
Q

What are the different parts of the pancreas?

A
  • Head
  • Neck
  • Body
  • Tail
  • Ucinate process
136
Q

Which vessels supply blood to the pancreas?

A
  • Pancreatic branches of the splenic artery
  • Sup/Inf branches of the pancreatoduodenal arteries
137
Q

What cells are the most abundant in the pancreas?

A
  • Acini cells
138
Q

What five cell types are found in the islets or langerhans?

A
  • Alpha
  • Beta
  • Delta
  • Gamma
  • Epsilon
139
Q

What is released by alpha cells and what is its role?

A
  • Glucagon
  • Increase blood glucose
140
Q

What is released by beta cells and what is its role?

A
  • Insulin
  • Reduce blood glucose
141
Q

What is released by delta cells and what is its role?

A
  • Somatostatin
  • Regulates islet secretion
142
Q

What is released by gamma cells and what is its role?

A
  • Pancreatic polypeptide
  • GI functionality
143
Q

What is released by epsilon cells and what is its role?

A
  • Ghrelin
  • Increase appetite (Hunger hormone)
144
Q

What is the function of leptin?

A
  • Suppresses appetite
  • Opposite of ghrelin
145
Q

What proportion of the pancreas is made up of islets?

A
  • Around 5%
146
Q

What is T1DM?

A
  • Inability to produce or secrete insulin
147
Q

When is T1DM usually diagnosed?

A
  • In children and adolescents
148
Q

What is the main cause of T1DM?

A
  • Autoimmune destruction of beta cells which are responsible for the production of insulin
149
Q

Which HLA antigens are associated with T1DM?

A
  • HLA-DR3
  • HLA-DR4
150
Q

When does hypoglycaemia occur in T1DM?

A
  • When up to 90% of beta cell mass has been destroyed
151
Q

What does an decrease in insulin cause?

A
  • Increased rate of glucose production in liver
  • Reduced peripheral glucose uptake causes weight loss and hypergylcaemia
152
Q

What are the symptoms of osmotic diuresis seen in T1DM?

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Electrolyte derangement
153
Q

What happens to fatty acids in T1DM?

A
  • Converted by hepatocytes into ketone bodies
154
Q

What are the genetic causes of T1DM?

A
  • HLA-DR3
  • HLA-DR4
155
Q

What is the identical twin concordance of T1DM?

A
  • Between 30%-50%
156
Q

What are the autoimmune causes of T1DM?

A
  • Associated with other factors
  • AITD, Coeliac, Addisons, Pernicious anaemia
157
Q

What are the environmental causes of T1DM?

A
  • Increased rates in Europe
  • Enteroviruses
  • Vitamin D deficiencies
  • Diet problems
158
Q

What is the normal range of glucose seen in health?

A
  • 3.5 mmol/L - 8.0 mmol/L
159
Q

What are the symptoms seen in T1DM?

A
  • Polyuria
  • Very thirsty
  • Very tired
  • Unexplained weight loss
  • Itchiness in genital area
  • Slow healing wounds
  • Blurred vision (Lens becomes dry)
160
Q

What are the clinical features seen in T1DM?

A
  • Mild-moderate dehydration
  • BMI <25
  • Polyuria
  • Polydipsia
  • Weight loss
  • Vomiting from circulating ketones
  • Lethargy
161
Q

What autoantobodies are tested for in T1DM?

A
  • Islet cell antibodies (ICA)
  • GAD
  • Insulin antibodies (IAA)
  • IA-2 antibodies
162
Q

When should a patient be screened for pancreatic cancer in relation to T1DM?

A
  • If over 60 with new onset T1DM
163
Q

What does the management of T1DM require?

A
  • Life long exogenous insulin
164
Q

What are the five different types of insulin?

A
  • Rapid acting
  • Short acting
  • Intermediate acting
  • Long acting
  • Mixed (Long and short)
165
Q

What are the two types of glucose monitoring available?

A
  • Real-time continous
  • Intermitent
166
Q

What is the expected glucose value at waking up?

A
  • 5-7 mmol/L
167
Q

What is the expected glucose value before a meal?

A
  • 4-7 mmol/L
168
Q

What is the expected glucose value 90 mins after a meal?

A
  • 5-9 mmol/L
169
Q

What are the 3 different types of insulin regime available?

A
  1. Basal-bolus
  2. 1/2/3 per day
  3. Continuous infusion
170
Q

What is a basal-bolus regime in T1DM?

A
  • Rapid acting given before meals
  • Long acting given for basal requirements
171
Q

What is a 1/2/3 regime used in T1DM?

A
  • Either 1/2/3 injections given every day
  • Using both short acting and intermediate acting insulin
172
Q

What is a continuous insulin infusion in T1DM?

A
  • Continual delivery via a pump
  • Rapid or short acting
  • Used when patients have hypos with other regimes
173
Q

How is long term management of T1DM measured?

A
  • Using a HbA1c test which indicates blood glucose average over three months
174
Q

What are the exacerbations that are associated with T1DM?

A
  • Retinopathy
  • Nephropathy
  • Diabetic foot problems
  • CVS risks
  • Thyroid disease
  • Dental disease
175
Q

What are the two major complications associated with T1DM?

A
  • Hypoglycaemia
  • Diabetic ketoacidosis
176
Q

What is hypoglycaemia?

A
  • Abnormally low blood/plasma glucose concentration
  • <4 mmol/L = hypo
177
Q

At what glucose levels can serious and long term consequences be caused?

A
  • <3.0 mmol/L
178
Q

What is Whipple’s triad and how is it used in the formal diagnosis of hypoglycaemia?

A
  • Used to make a formal diagnosis
    1. Low blood glucose concentration
    2. Symptoms of hypoglycaemia
    3. Reversal of symptoms on restoration
179
Q

What are the main counter-regulatory mechanisms utilised in hypoglycaemia?

A
  • Decreasing insulin scretion
  • Increase glucagon secretion
  • Increase in adrenaline secretion
  • Secretion of cortisol and GH
180
Q

What are some common causes of hypoglycaemia in T1DM?

A
  • Medication changes
  • Concurrent illnesses
  • Dietary/Activity changes
181
Q

What is an insulinoma?

A
  • Tumour of beta cells within the islets of langerhans in the pancreas
182
Q

What are the autonomic symptoms of hypoglycaemia and when are they seen?

A
  • < 3 mmol/L
  • Tremor
  • Palpitations
  • Anxiety
  • Sweating
  • Hunger
  • Paresthesia
183
Q

What are the neuroglycopaenic symptoms of hypoglycaemia and when are they seen?

A
  • < 2.8 mmol/L
  • Dizziness
  • Weakness
  • Drowsiness
  • Confusion
  • Altered mental state
  • Seizures
  • Coma
184
Q

What are some side effects of insulin therapy?

A
  • Weight gain
  • Hypernatremia
  • Hypokalaemia
185
Q

What test forms the basis of a hypoglycaemia diagnosis?

A
  • Capillary/serum blood glucose measurement
186
Q

What other tests are used in hypoglycaemia diagnosis?

A
  • 72 hr fast
  • Insulin test
  • C-Peptide test
  • Pro-insulin
  • Sulfonylurea
  • Beta-hydroxybutyrate
187
Q

What is the management of hypoglycaemia dependant on?

A
  • Depends on their level of alertness which is determined using the GCS scale
188
Q

What is the management on an alert patient with hypoglycaemia?

A
  • Oral glucose load
  • Complex carbohydrate meal
  • Monitor capillary blood glucose
  • Consider IV dextrose
  • Determine the cause
189
Q

What is the management of a comatose patient with hypoglycaemia?

A
  • ABCDE assessment
  • IV glucose load
  • Consider 1mg glucagon
  • Reassess
  • Consider IV glucose infusion
  • Continue monitoring
  • Determine the underlying cause
190
Q

What is diabetic ketoacidosis?

A
  • Life threatening diabetic emergency
191
Q

What triad of clinical features are seen in diabetic ketoacidosis?

A
  • Hyperglycaemia = > 11.0 mmol/L
  • Ketonaemia = ≥ 3 mmol or ketonuria
  • Acidosis = Bicard < 15.0 mmol/L or venous pH < 7.3
192
Q

What percentage of patients with T1DM develop diabetic ketoacidosis each year?

A
  • Around 4%
193
Q

What are some precipitating factors that can cause diabetic ketoacidosis?

A
  • Infection
  • Non-compliance
  • Inappropriate dose alteration
  • New diabetes diagnosis
  • MI
194
Q

What are the symptoms associated with diabetic ketoacidosis?

A
  • Nausea
  • Vomiting
  • Polyuria
  • Polydipsia
  • Abdominal pain
  • Leg cramps
  • Headache
195
Q

What are some clinical features seen in diabetic ketoacidosis?

A
  • Abdominal tenderness
  • Dehydration
  • Hypotension
  • Kussmaul breathing
  • Ketotic breath (Pear drops)
  • Reduced consciousness or coma
196
Q

What is a diagnosis of diabetic ketoacidosis based on?

A
  • Biochemical triad:
    1. Hyperglycaemia
    2. Acidaemia
    3. Ketonaemia/ketonuria
197
Q

What are the main investigations performed in the diagnosis of diabetic ketoacidosis?

A
  • Laboratory glucose testing
  • VBG/ABG
  • Ketone measurement either in blood or urine
198
Q

What are the goals in management of diabetic ketoacidosis?

A
  1. Restore circulating volume
  2. Clear ketones / Halt ketogenesis
  3. Decrease serum glucose towards normal level
  4. Correct electrolyte derangements
  5. Identify and treat underlying cause
199
Q

What is T2DM?

A
  • Combination of inadequate insulin secretion and peripheral insulin resistance
200
Q

What other conditions is T2DM associated with?

A
  • Obesity
  • Metabolic syndromes
201
Q

How many people are estimated to be effected by T2DM in the UK?

A
  • Around 3.9 million people
202
Q

What risk does obesity present in relation to the development of T2DM?

A
  • Accounts for around 80% of risk
203
Q

What environmental factor play a role in the development of T2DM?

A
  • Poor diet
  • Low birth weight
  • Medications
  • PCOS
  • History of GDM
204
Q

What is the pathophysiology behind insulin resistance seen in T2DM?

A
  • Hyperglycaemia due to reduced glucose uptake
205
Q

What is the pathophysiology behind insulin deficiency in T2DM?

A
  • Initially there is an increase in secretion
  • Then there is gradual beta cell destruction
206
Q

What are beta cells replace with in T2DM?

A
  • Replaced with amyloid
207
Q

What is a major diagnostic tool used in T2DM and what do the results mean?

A
  • HbA1c test for glycated haemoglobin
  • > 48 mmol/mol = diagnostic
  • 43-47 mmol/mol = pre-diabetic
208
Q

What are some possible interrupting comorbidities in T2DM?

A
  • Erythropoiesis
  • Haemoglobin structure
  • Glycation
  • Red cell survival
209
Q

Other than HbA1c, what are other test used in the diagnosis of T2DM?

A
  1. Fasting plasma glucose
  2. Random plasma glucose
  3. Oral glucose tolerance test
210
Q

What is needed to confirm a T2DM diagnosis?

A
  • 2 x abnormal HbA1c test
  • 1 x abnormal HbA1c test + 1 other diagnostic test
211
Q

What are the main focuses in T2DM treatment?

A
  1. Lifestyle advice
  2. Antidiabetic drugs
  3. Insulin use in T2DM
  4. Treatment targets
  5. Complication monitoring
212
Q

How can lifestyle advice alone improve T2DM?

A
  • Ability to reverse symptoms in 5 years with lifestyle advice alone
213
Q

What is the first line pharmacological treatment for T2DM?

A
  • Metformin
214
Q

What is the mechanism of action for metformin?

A
  • Inhibits hepatic gluconeogenesis
  • Increased peripheral insulin sensitivity
  • Increased peripheral uptake of glucose
215
Q

What is the second line pharmacological treatment for T2DM?

A
  • Metformin + second antidiabetic
  • Aim for < 53 mmol/mol
216
Q

What are some examples of antidiabetic drugs?

A
  • Metformin
  • Sulfonylurea
  • DPP-4i
  • Pioglitazone
  • SGLT-2i
217
Q

What is the third line pharmacological treatment of T2DM?

A
  • Second intensification
  • Consider triple antidiabetic therapy if > 58 mmol/L
218
Q

When is insulin therapy not used as a first step of management?

A
  • Those at risk of hypoglycaemia
  • May exacerbate weight issues
219
Q

What is a side effect of metformin?

A
  • CKD -> Lactic acidosis
220
Q

What are some possible side effects seen in the management of T2DM?

A
  • CVS disease
  • Limb neuropathy
  • Kidney disease
  • Eye damage
  • Skin conditions
  • Slow wound healing
  • Hearing impairment
221
Q
A

Year 2 Medicine @ Lancaster Uni (15 decks)

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