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phase 2a clinical > endocrinology > Flashcards

endocrinology Flashcards

1
Q

acromegaly: epidemiology

A

male:female 1:1

5% associated with MEN-1

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2
Q

acromegaly: causes

A

excess growth hormone from pituitary tumour (99%) or hyperplasia

if occurs before epiphyses fuse- gigantism

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3
Q

acromegaly: symptoms

A 
resp: snoring
GI: wonky bite- malocclusion
MSK: arthralgia, backache 
neuro: headache, acroparaethesia
increase in sweating and weight
decrease in libido
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4
Q

acromegaly: signs

A 
skin darkening
big supraorbital ridge
interdental separation
macroglossia
progathism
laryngeal dyspnoea
OSA
spade like hands and feet
carpal tunnel syndrome
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5
Q

acromegaly: complications

A

impaired glucose tolerance- 40%
diabetes mellitus- 15%
arrhythmias, cardiomyopathy, stroke
colon cancer

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6
Q

acromegaly: investigations

A

IGF-1 and OGTT test
don’t rely on GH as pulsatile secretion
MRI pituitary fossa
look at old photos

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7
Q

acromegaly: treatment

A

trans-sphenoidal surgery to remove tumour
somatostatin analogue
radiotherapy
pegvisomant

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8
Q

acromegaly: acroparaethesia

A

a condition of burning, tingling or prickling sensations in the extremities

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9
Q

endocrine tumours: epidemiology

A

incidence 10/100,000/year
women effected more than men
prevalence 90/100,000

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10
Q

endocrine tumours: symptoms caused by

A 
pressure on local structures
pressure on normal pituitary 
functioning tumours
local effect of tumour
effect of hyperprolactinaemia
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11
Q

endocrine tumours: pressure on normal pituitary

A

hypopituitarism

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12
Q

endocrine tumours: functioning tumours examples

A

prolactinoma
acromegaly
cushing’s disease

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13
Q

endocrine tumours: local effect of tumours

A

headache
visual field defect
CSF leak

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14
Q

endocrine tumours: effect of hyperprolactinaemia

A 
menstrual irregularity
infertility 
galactorrhoea
low libido
low testosterone in men
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15
Q

endocrine tumours: causes of hyperprolactinaemia

A

non-functioning pituitary tumour: compresses pituitary stalk

antidopaminergic drugs: don’t measure prolactin on these but a careful drug history needed

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16
Q

endocrine tumours: management

A

dopamine agonists

shrinkage usual with macroadenoma- sight saving

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17
Q

carcinoid tumours

A

diverse group of tumours of enterochromaffin origin
produce serotonin
also secrete bradykinin, tachykinin, insulin etc.
appendix 45%, ileum 30%, rectum 20%

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18
Q

prolactinoma

A

benign tumour of the pituitary gland that produces prolactin

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19
Q

hypokalaemia levels

A

K+ <3.5mmol/L

severe= <2.5 mmol/L

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20
Q

hypokalaemia: causes

A 
diuretics
cushing's
conn's
pyloric stenosis
alkalosis
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21
Q

hypokalaemia: symptoms

A 
muscle weakness
muscle cramps 
decrease in muscle tone and reflexes
palpitations
arrhythmias
constipations
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22
Q

hypokalaemia: investigations

A

Bloods

ECG: U have no Pot and no Tea BUT and long PR and a long QT

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23
Q

mild hypokalaemia: treatment

A

oral K+ supplements
review K after 3 days
if taking thiazide diuretic and K>3mmol/L consider repeating and/or K+ sparing diuretic

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24
Q

severe hypokalaemia: treatment

A

IV K+ cautiously

no more than 20mmol/Hour and not more concentrated than 40mmol/L

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25
Q

hyperkalaemia levels

A

K+ >5.5mmol/L

severe= >6.5mmol/L

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26
Q

hyperkalaemia: causes

A 
oliguric renal failure
K-sparing diuretics
rhabsomyolysis 
addisons
burns
metabolic acidosis
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27
Q

hyperkalaemia: symptoms

A

myocardial excitability- VF and cardiac arrest

concerning:
fast irregular pulse, chest pain, weakness, palpitations, light-headedness

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28
Q

hyperkalaemia: investigations

A

Bloods
ECG:
Tall tented T waves, small P waves, wide QRS

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29
Q

hyperkalaemia: non-urgent treatment

A

treat underlying cause
review meds
polystyrene sulfonate resin- binds K+ in gut

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30
Q

hyperkalaemia: emergency treatment

A

stabilise cardiac membrane with 10ml 10% calcium gluconate

drive K+ into cells with 10U actrapid (insulin) and 50ml 20% glucose

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31
Q

puberty

A

describes the physiological, morphological and behavioural changes as the gonads switch from infantile to adult

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32
Q

definitive signs of puberty in females

A

menarche- first menstrual bleeding
breast bud noted/palpable
secondary characteristics:
- oestrogen regulates growth of breast and female genitalia
- ovarian and adrenal androgens control pubic hair

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33
Q

definitive signs of puberty in males

A

first ejaculation, often nocturnal
testicular volume >3ml

secondary characteristics:

  • testicular androgens
  • external genitalia and pubic hair growth
  • laryngeal muscles enlarge
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34
Q

early puberty

A

onset of secondary characteristics before 8 (girls), 9 (boys)

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35
Q

true precocious puberty

A

GnRH increase
idiopathic
CNS tumours or disorders
secondary central precocious puberty

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36
Q

precocious pseudo- puberty

A 
autonomous production of oestrogen- GnRH independent 
increased androgen secretion
secreting tumours
ovarian cyst
hypothyroidsism
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37
Q

early puberty investigations

A

GnRH stimulation test to see if dependent(stimulation) or independent (no stimulation)

bone age- advanced in precocious

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38
Q

early puberty treatment

A

precocious- GnRH super-agonist to suppress pulsatility of GnRH

psuedo- treat underlying cause

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39
Q

delayed puberty

A

absence of secondary sexual characteristics by 14 years for girls or 16 years for boys

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40
Q

types of delayed puberty

A

constitutional delay of growth and puberty
hypergonadotropic hypogonadism
hypogonadotropic hypogonadism

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41
Q

constitutional delay of growth and puberty

A

delayed activation of hypothalamic pulse generator

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42
Q

hypergonadotropic hypogonadism

A

primary hypogonadism:

  • gonadal disorder
  • hypergonadotropic as increase in GnRH, FSH and LH to increase gonadal sex hormone
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43
Q

hypogonadotropic hypogonadism

A

secondary/tertiary hypogonadism

sexual infantilism related to gonadotrophin deficiency

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44
Q

constitutional delay of growth and puberty causes

A

inherited from multiple genes

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45
Q

hypergonadotropic hypogonadism causes

A

males= klinefelters, testicular failure, chemotherapy

females= turners

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46
Q

hypogonadotropic hypogonadism causes

A

CNS disorders such as tumours
isolated gonadotropin deficiency
Idiopathic and Genetic Forms of Multiple Pituitary Hormone Deficiencies

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47
Q

delayed puberty investigations

A 
red blood count
LH, FSH
testosterone/ oestradial
thyroid function
karyotyping
bone age
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48
Q

delayed puberty treatment for females

A

ethinyl estradiol or oestrogen

oral tablets

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49
Q

delayed puberty treatment for males

A

testosterone enanthate

IM injection

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50
Q

delayed puberty treatment for fertility

A

GnRH-TX

parental combination of gonadotropin TX

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51
Q

Cushing’s syndrome

A

chronic glucocorticoid excess

loss of normal feedback mechanisms and circadian rhythm

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52
Q

ACTH dependent causes of Cushing’s syndrome

A

cushing’s disease- bilateral adrenal hyperplasia from ACTH secreting adenoma

ectopic ACTH production

ectopic CRH production

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53
Q

ACTH independent causes of Cushing’s syndrome

A

adrenal adenoma/carcinoma

adrenal nodular hyperplasia

iatrogenic- steroids

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54
Q

cushing’s syndrome symptoms

A 
acne
increased weight
gonadal dysfunction
proximal weakness
recurrent achilles tendon rupture
mood change- depression, lethargy, irritability
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55
Q

cushing’s syndrome signs : fat distribution

A

central obesity
moon face
buffalo neck hump
supraclavicular fat distribution

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56
Q

cushing’s syndrome signs: skin changes

A

skin and muscle atrophy
bruises
purple abdominal striae

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57
Q

other cushing’s syndrome signs

A 
osteoporosis
hypertension
hyperglycaemia
infection prone
poor healing
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58
Q

Cushings syndrome investigations

A

bloods- increased plasma cortisol

overnight or 48 hour dexamethasone suppression test

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59
Q

treating iatrogenic causes for cushings

A

stop steroids

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60
Q

cushing’s disease treatment

A

trans-sphenoidal surgery or bilateral adrenalectomy

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61
Q

adrenal adenoma treatment

A

adrenalectomy

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62
Q

adrenal carcinoma treatment

A

adrenalectomy, adrenolytics

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63
Q

ectopic ACTH treatment

A

surgery

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64
Q

adrenal insufficiency

A

adrenal glands do not produce adequate amounts of steroid hormones- primarily cortisol

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65
Q

types of adrenal insufficiency

A

primary
secondary
tertiary

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66
Q

primary adrenal insufficiency

A

adrenal gland disorder

aka addison’s disease:

  • primary adrenocortical insufficiency
  • destruction of adrenal cortex
  • decrease in glucocorticoids and mineralocorticoids
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67
Q

primary adrenal insufficiency: causes

A

autoimmune- 80%, most common in UK
TB= most common worldwide

adrenal metastases
lymphoma
opportunistic infections in HIV
adrenal haemorrhage

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68
Q

adrenal insufficiency: symptoms

A
  • abdominal pain, constipation/diarrhoea
  • tanned skin
  • lean build
  • MSK weakness, myalgia
  • dizzy, fainting
  • tired, tearful, anorexic, depressed
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69
Q

adrenal insufficiency: signs

A

pigmented palmar creases and buccal mucosa
vitiligo
postural hypotension

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70
Q

primary adrenal insufficiency: investigations

A

Bloods:

  • FBC (anaemia, eosinophilia)
  • U&E ( low Na, high K, Ca and urea)
  • BM glucose (low)

short ACTH stimulation test (excluded if 30 min cortisol is >550nmol/L)

9am ACTH levels- will be high in addison’s

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71
Q

primary adrenal insufficiency: treatment

A

replace steroids with 15-25mg hydrocortisone daily

replace mineralocorticoids (aldosterone) with fludocortisone

drug card and bracelet

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72
Q

secondary adrenal insufficiency

A

inadequate secretion of ACTH by the pituitary gland

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73
Q

secondary adrenal insufficiency: causes

A

most common cause is iatrogenic- long term steroid therapy suppresses HPA axis

pituitary disorders

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74
Q

secondary adrenal insufficiency: investigations

A

Bloods:

  • FBC (anaemia and eosinophilia)
  • U&E (high Ca)
  • BM glucose (low)

short ACTH stimulation (>550nmol/L)

9am ACTH levels (low)

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75
Q

secondary adrenal insufficiency: treatment

A

replace steroids with 15-25mg of hydrocortisone daily

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76
Q

tertiary adrenal insufficiency

A

impaired hypothalamic release of corticotropin-releasing hormone- CRH

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77
Q

tertiary adrenal insufficiency: causes

A

hypothalamo-pituitary disease

suppression of HPA

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78
Q

tertiary adrenal insufficiency: investigations

A

Bloods:

  • FBC (anaemia and eosinophilia)
  • U&E (high Ca)
  • BM glucose (low)

short ACTH stimulation (>550nmol/L)

9am ACTH levels (low)

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79
Q

tertiary adrenal insufficiency: treatment

A

replace steroids with 15-25mg of hydrocortisone daily

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80
Q

Adrenal crisis

A

constellation of symptoms caused by insufficient levels of cortisol

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81
Q

Adrenal crisis: causes

A

adrenal insufficiency

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82
Q

Adrenal crisis: symptoms

A 
hypotension
fatigue
fever
hypoglycaemia
hyponatraemia
hyperkalaemia
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83
Q

Adrenal crisis: treatment

A

immediate IV hydrocortisone 100mg
fluid resuscitation- 1L N/Saline 1 hour
hydrocortisone 50-10mg 6 hourly

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84
Q

Conn’s syndrome

A

excess aldosterone independent of RAAS

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85
Q

Conn’s syndrome: causes

A

solitary aldosterone-producing adenoma

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86
Q

Conn’s syndrome: symptoms

A

increased retention of sodium and water
may have signs of low potassium
often asymptomatic

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87
Q

Conn’s syndrome: investigations

A

U&E
Renin
Aldosterone

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88
Q

Conn’s syndrome: treatment

A

laparoscopic adrenalectomy

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89
Q

actions of ADH

A

vasoconstriction

increased water reabsorption

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90
Q

Diabetes insipidus

A

when secretion of, or response to, vasopressin is impaired

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91
Q

Diabetes insipidus: types

A

Cranial
nephrogenic
other

92
Q

Cranial diabetes insipidus:

A

lack of vasopression

93
Q

nephrogenic diabetes insipidus

A

resistance to vasopressin

94
Q

other forms of diabetes insipidus

A

gestational- excessive vasopressinase activity

dipsogenic- disordered thirst

95
Q

Cranial diabetes insipidus: causes

A 
tumour
lack of blood supply
impact/fracture
surgical
autoimmune
96
Q

nephrogenic diabetes insipidus: causes

A

lithium toxicity
release of obstruction
hypercalcaemia
hypokalaemia

97
Q

Diabetes insipidus: symptoms

A

polydipsia- excessive or abnormal thirst
polyuria- abnormally large volumes of dilute urine

dehydration
hypernatraemia

98
Q

Diabetes insipidus: investigations

A

water deprivation test to diagnose DI

water deprivation with desmopressin (ADH agonist):

  • cranial= urine output falls and osmolality increases
  • nephrogenic= no change
99
Q

Cranial diabetes insipidus: treatment

A

desmopressin

treat underlying condition

100
Q

Nephrogenic diabetes insipidus: treatment

A

thiazide diuretics and amiloride- encourages salt and water uptake

high dose of desmopressin

free access to water

101
Q

syndrome of inappropriate ADH secretion: SIADH

A

excessive ADH production

102
Q

SIADH: causes

A

CNS disorders- infection, bleed, MS

pulmonary- infection, abscess, asthma, CF

103
Q

SIADH: symptoms

A 
small volumes of concentrated urine
hyponatraemia 
anorexia
nausea
aches and weakness
104
Q

SIADH: investigations

A

euvolaemic with hyponatraemia
urine osmolarity >100mOsm/Kg
urine sodium >40mEq/L

105
Q

SIADH: treatment

A

fluid restriction- increases Na concentration

tolvaptin- v2 vasopressin blocker

106
Q

hyponatraemia

A

serum sodium <135mmol/L

107
Q

hyponatraemia: causes

A

fluid overload
SIADH
dehydration
malignancy

108
Q

hyponatraemia symptoms: Na 130-135mmol/L

A

asymptomatic

109
Q

hyponatraemia symptoms: Na 125-130mmol/L

A

headache
lethargy
abdominal pain
weakness

110
Q

hyponatraemia symptoms: Na<1255mmol/L

A

confusion
hallucinations
agitation
decreased consciousness

111
Q

hyponatraemia symptoms: Na<115mmol/L

A

fitting

coma

112
Q

hyponatraemia: acute vs chronic

A

acute= 48 hours, rapid correction is safer

chronic= CNS has adapted so correction must be slow

113
Q

hyponatraemia: investigations

A 
plasma osmolality
urine osmolality
plasma glucose
urine sodium
urine dip test for protein
114
Q

hyponatraemia: treatment

A

restrict fluids if fluid overload

saline replacement if dehydrated

115
Q

thyroid disease epidemiology

A 
most common endocrine disorders
female preponderance is 5-10 fold
hyperthyroidism, 2.5% prevalence
hypo= 5%
goitre=5-10%
116
Q

autoimmune thyroid disease

A

2% of women will get grave’s disease or autoimmune hypothyroidism

5% will have postpartum thyroiditis

20% will have positive thyroid antibodies

117
Q

hypothyroidism

A

abnormally low activity of the thyroid gland

118
Q

primary hypothyroidism: causes

A

(over 99% of cases, low T4 due to absence or dysfunction of thyroid gland)

hashimoto’s thyroiditis
primary atrophic hypothyroidism
iodine deficiency
TH resistance

119
Q

secondary hypothyroidism: causes

A

(low TSH due to pituitary/ hypothalamic dysfunction)

hypopituitarism

120
Q

hypothyroidism: symptoms

A 
hoarse voice
constipation
cold intolerance
weight gain
myalgia
tired
low mood
abnormally heavy bleeding at menstruation (menorrhagia)
121
Q

hypothyroidism: signs

A

think BRADYCARDIC

Bradycardic
Reflexes relax slowly
Ataxia
Dry thin hair and skin
Yawning, drowsy
Cold hands
Ascites
Round puffy face
Defeated demeanour
Immobile
CCF
122
Q

hypothyroidism: investigations

A

thyroid function tests
lipids/cholesterol
↓T3, ↓T4 = ↑TSH (secondary/tertiary TSH low)

123
Q

hypothyroidism: inherited associations

A

turner’s syndrome
down’s syndrome
cystic fibrosis

124
Q

hypothyroidism: autoimmune associations

A

type 1 diabetes
addison’s
pernicious anaemia

125
Q

hypothyroidism: treatment

A

levothyroxine (T4)

126
Q

hyperthyroidism

A

excess of thyroid hormones in blood due to overactivity of the thyroid gland

127
Q

hyperthyroidism: causes

A

graves’ disease (75-80%)
toxic multinodular goitre
toxic adenoma
ectopic thyroid tissue

128
Q

hyperthyroidism: symptoms

A 
palpitations
diarrhoea
heat intolerance
weight loss
tremor
irritability
129
Q

hyperthyroidism: signs

A 
warm, moist skin
palmar erythema
tachycardia
thin hair
lid lag/retraction
goitre
130
Q

hyperthyroidism: Graves’ specific signs

A

diffuse goitre
thyroid eye disease
pretibial myxoedema
acropachy

131
Q

hyperthyroidism: MNG specific signs

A

multinodular goitre

132
Q

hyperthyroidism: adenoma specific signs

A

solitary nodule

133
Q

hyperthyroidism: investigations

A

linked with liver failure
thyroid function tests
thyroid autoantibodies
isotope uptake scan

134
Q

hyperthyroidism: treatment

A

beta-blockers
antithyroid medication
radioiodine
thyroidectomy

135
Q

thyroid eye disease

A

autoimmune inflammatory disorder of the orbit and periorbital tissues

swelling of extraocular muscles

136
Q

thyroid eye disease: causes

A

25-50% have graves’ disease
main risk factor is smoking
eye and thyroid disease may not correlate

137
Q

thyroid eye disease: symptoms

A

eye discomfort
grittiness
diplopia

138
Q

thyroid eye disease: signs

A

exophthalmos
proptosis
ophthalmoplegia

139
Q

thyroid eye disease: tests

A

clinical diagnosis

140
Q

thyroid eye disease: management

A 
stop smoking
sunglasses
IV methylprednisolone
surgical decompression
eyelid surgery
141
Q

goitre

A

swelling of neck resulting from enlargement of the thyroid gland

142
Q

goitre presentation:

A

palpable and visible thyroid enlargement

endemic in iodine deficient areas

143
Q

diffuse goitre causes:

A

physiological
graves’ disease
hashimoto’s thyroiditis

144
Q

nodular goitre causes:

A

multinodular
adenoma
cyst
carcinoma

145
Q

thyroid cancers

A 
papillary- 60%
follicular- <25%
medullary- 5%
lymphoma- 5%
anaplastic
146
Q

hyperparathyroidism

A

abnormally high concentration of parathyroid hormone in the blood

147
Q

primary hyperparathyroidism

A

one or more of the parathyroid glands are overactive

148
Q

primary hyperparathyroidism: causes

A

80% due to adenoma

15-20% due to four gland hyperplasia

149
Q

primary hyperparathyroidism: symptoms

A

STONES- kidney
BONES- osteitis fibrosa cystica, osteoporosis
MOANS- abdominal, constipation, pancreatitis
GROANS- confusion

150
Q

primary hyperparathyroidism: investigations

A

PTH high-> calcium is high
phosphate usually low
phosphatase usually high

151
Q

primary hyperparathyroidism: treatment

A

treat underlying cause- usually surgical

152
Q

secondary hyperparathyroidism

A

excessive secretion of PTH by the parathyroid glands in response to hypocalcaemia and associated hyperplasia of the glands

153
Q

secondary hyperparathyroidism: causes

A

CKD and vitamin D deficiency is most common

GI bypass and crohn’s disease also possible causes

154
Q

secondary hyperparathyroidism: symptoms

A

usually asymptomatic

symptoms are predominantly bony- joint pain, osteomalacia

155
Q

secondary hyperparathyroidism: investigations

A

PTH high -> calcium low
phosphate high
phosphatase high

156
Q

treating secondary hyperparathyroidism

A

treat underlying cause

bisphosphonates to protect bones

157
Q

tertiary hyperparathyroidism

A

a state of excessive secretion of PTH after a long period of secondary hyperparathyroidism

results in high blood calcium level

158
Q

hypoparathyroidism

A

diminished concentration of parathyroid hormone in the blood

159
Q

hypoparathyroidism: causes

A 
surgical
autoimmune
DiGeorge
infiltration
familial forms
magnesium deficiency
160
Q

hypoparathyroidism: symptoms

A 
paraesthesia- abnormal sensation or prickles
convulsions
arrhythmia
tetany
numb
161
Q

hypoparathyroidism: differential diagnosis

A

many other potential reasons calcium might be low

kidney disease, vit d malabsorption, drugs, CCB overdose

162
Q

pseudohypoparathyroidism

A

resistance to PTH

PTH levels okay, peripheral resistance

163
Q

pseudopseudohypoparathyroidism

A

RARE
osteodystrophy without resistance of PTH
skeletal defects

164
Q

hypoparathyroidism: treatment

A

calcium and vitamin D long term

165
Q

hypocalcaemia

A

deficiency of calcium in the bloodstream

166
Q

hypocalcaemia: causes

A 
actual vitamin d deficiency
functional vitamin d deficiency
magnesium deficiency 
hypoparathyroidism
pseudohypoparathyroidism
drug therapy
alkalosis
167
Q

hypocalcaemia: due to actual vitamin D deficiency

A

dietary
lack of sunlight
malabsorption

168
Q

hypocalcaemia: due to functional vitamin D deficiency

A

renal disease

liver disease

169
Q

hypocalcaemia: due to hypoparathyroidism

A

autoimmune

post-surgery

170
Q

hypocalcaemia: from drug therapy

A

bisphosphonates calcitonin

anticonvulsant therapy

171
Q

hypocalcaemia: by alkalosis

A

because albumin dissociates from hydrogen and picks up calcium

172
Q

hypocalcaemia: symptoms

A 
paraesthesia 
convulsions
arrhythmia
tetany
numb
173
Q

hypocalcaemia: signs

A

chvostek’s sign:
-tap over facial nerve and look for spasm of facial muscles

trousseau’s sign:

  • inflate BP cuff to 20mmHg above systolic for 5 minutes
  • hand will go into spasm
174
Q

hypocalcaemia: treatment

A

admit if severe

calcium replacement with calcium glucoronate

175
Q

hypercalcaemia: main causes

A

90% are either malignancy- bone mets, myeloma, lymphoma

or primary hyperparathyroidism

176
Q

hypercalcaemia: other causes

A 
thiazides
thyrotoxocosis
sarcoidosis
adrenal insufficiency
immobilisation
177
Q

hypercalcaemia: symptoms

A 
thirst
nausea
constipation
confusion
renal stones
ECG abnormalities- short QT
178
Q

normal range of blood glucose

A

3.5-8mmol/L

179
Q

diabetes mellitus

A

syndrome of chronic hyperglycaemia due to relative insulin deficiency or resistance

180
Q

primary diabetes mellitus

A

type 1 or type 2 diabetes

181
Q

secondary diabetes mellitus

A

pancreatic disease
endocrine disease
drug induced
maturity onset diabetes of youth

182
Q

type 1 diabetes

A

beta cell destruction in islet of langerhans

insulin deficiency

183
Q

type 1 diabetes: epidemiology

A

manifests in childhood
patient is usually lean
increased in those of northern european ancestry

184
Q

type 1 diabetes: causes

A

autoimmune

185
Q

type 1 diabetes: risk factors

A

family history

associated with other autoimmune diseases

186
Q

type 1 diabetes: pathophysiology

A

autoimmune destruction by autoantibodies of pancreatic insulin-secreting beta cells in the islets of langerhans

187
Q

type 2 diabetes

A

combination of insulin resistance and less severe insulin deficiency

188
Q

type 2 diabetes: epidemiology

A
  • common in all populations of an affluent lifestyle
  • usually diagnosed at an older age
  • overweight around the abdomen
  • prevalent in south asian, african and caribbean ancestry
189
Q

type 2 diabetes: causes

A

decreased insulin secretion
increased insulin resistance
associated with obesity, lack of exercise, calorie and alcohol excess
polygenic disorder

190
Q

type 2 diabetes: risk factors

A

family history
obesity
poor exercise
ethnicity

191
Q

type 1 diabetes: presentations

A

leaner

present with more marked polydipsia, polyuria, weight loss and ketosis

192
Q

type 2 diabetes: presentations

A

overweight in abdominal area

193
Q

type 2 diabetes: presentations

A

overweight in abdominal area
polydipsia, polyuria
weight loss and ketosis in advanced

194
Q

type 2 diabetic retinopathy

A

microaneurysms are seen as tiny red dots:

  • intramural pericyte death and thickening of basement membrane of small blood vessels
  • reduction in junctional contact with endothelial cells
  • fluid leakage

haemorrhages seen as blots:

  • when there is a breach of the microaneurysms
  • fluid is cleared into the retinal veins, leaving protein and lipid deposits
  • these become hard exudates which are yellow/white
195
Q

type 2 diabetic nephropathy

A

thickening of basement membrane causes glomerular damage

causes microalbuminuria

196
Q

type 2 diabetic neuropathy

A

isolated mononeuropathies are thought to result from occlusion of vasa nervorum (arteries that supply peripheral nerves)

197
Q

type 2 diabetes: infections

A

poorly controlled diabetes impairs the function of polymorphonuclear leucocytes and confers and increased susceptibility to infections

198
Q

type 2 diabetes: investigations

A

HbA1c
random plasma glucose
fasting plasma glucose
oral glucose tolerance tests

199
Q

type 2 diabetes: HbA1c

A

measured amount of glycated haemoglobin
pre-diabetes= 42-47 (6.1-6.4%)
diabetes= >48 (6.5%)

200
Q

type 2 diabetes: random plasma glucose

A

> 11.1mmol/L is diabetes
in symptomatic individuals- one abnormal result is needed
2 if they are asymptomatic

201
Q

type 2 diabetes: fasting plasma glucose

A

> 7mmol/L is diabetes
in symptomatic individuals- one abnormal result is needed
2 if they are asymptomatic

202
Q

type 2 diabetes: oral glucose tolerance tests

A

diabetes diagnosis:
fasting >7mmol/L
2 hours after glucose >11.1mmol/L

203
Q

type 2 diabetes: treatment

A 
lifestyle and dietary changes
metformin
sulfonylurea
DPP-4 inhibitors
pioglitazone
triple therapy (sulfonylurea, DPP-4 inhibitors and pioglitazone)
insulin
secondary prevention
204
Q

type 2 diabetes treatment: lifestyle and dietary changes

A

decreased carbs and sugar intake
nutrient load
BP control
hyperlipidaemia control

205
Q

type 2 diabetes treatment: metformin

A

increases insulin sensitivity
helps lose weight
reduces rate of gluconeogenesis in the liver
reduces CVS risk

206
Q

type 2 diabetes treatment: secondary prevention

A 
eye screening
foot screening
kidney tests
BP checks
appropriate aggressive management
statins
207
Q

ketoacidosis

A

biochemical triad of hyperglycaemia, ketonaemia and acidaemia
with rapid onset

208
Q

ketoacidosis: causes

A

uncontrolled hyperglycaemia and catabolic state

undiagnosed diabetes
interruption of insulin therapy
stress of intercurrent illness

more likely in type 1

209
Q

ketoacidosis: risk factors

A 
stopping insulin
infection
surgery
MI
pancreatitis
undiagnosed diabetes
210
Q

ketoacidosis: pathophysiology

A
  • state of uncontrolled catabolism associated with insulin deficiency
  • there is an increase in hepatic gluconeogenesis and reduced peripheral uptake by tissues
  • ketones produced as body requires glucose in cells
  • accumulation of ketone bodies produces metabolic acidosis
211
Q

ketoacidosis: investigations

A

hyperglycaemia: blood glucose >11mmol/L
raised plasma ketones: >3mmol/L
acidaemia: pH <7.3
metabolic acidosis with bicarbonate: <15mmol/L

212
Q

ketoacidosis: treatment

A

first priority= replace fluid loss and electrolytes:

  • 0.9% saline, 500ml
  • aim for fall in ketones of 0.5mmol/hr and rise in bicarb of 3mmol/hour
  • when glucose hits 10-14, add glucose and insulin to prevent hypos

second priority= replace deficient insulin:
-actrapid 0.1u/kg/hr IV

213
Q

hyperosmolar, hyperglycaemic state

A

life threatening emergency marked by hyperglycaemia, hyperosmolality and mild ketosis

uncontrolled type 2 diabetes

214
Q

hyperosmolar, hyperglycaemic state: epidemiology

A

patients present in middle or later life

undiagnosed diabetes

215
Q

hyperosmolar, hyperglycaemic state: risk factors

A

infection- particularly pneumonia
consumption of glucose rich fluids
concurrent medication such as thiazide diuretics or steroids

216
Q

hyperosmolar, hyperglycaemic state: pathophysiology

A

endogenous insulin levels are reduced but still sufficient to inhibit hepatic ketogenesis
but insufficient to inhibit hepatic glucose production

217
Q

hyperosmolar, hyperglycaemic state: symptoms

A 
dehydration
decreased level of consciousness
hyperglycaemia
hyperosmolality
no ketones
coma
bicarb is not lowered
218
Q

hyperosmolar, hyperglycaemic state: diagnosis

A

blood glucose >11mmol/L
urine stick testing shows heavy glycosuria
high plasma osmolality

219
Q

hyperosmolar, hyperglycaemic state: treatment

A

fluid replacement
low molecular weight heparin
restore electrolytes

220
Q

hypoglycaemia

A

plasma glucose <3mmol/L

221
Q

hypoglycaemia: diabetic causes

A

due to insulin or sulphonylurea treatment

increased activity, missing meals, accidental/nonaccidental overdose

222
Q

hypoglycaemia: non-diabetic causes

A

EXPLAIN

EXogenous drugs (insulin, alcohol)
Pituitary insufficiency 
Liver failure
Addison's disease
Islets cell tumour
Non-pancreatic neoplasm
223
Q

hypoglycaemia: symptoms

A

autonomic= sweating, anxiety, hunger, tremor, dizziness

neuroglycopenic= confusion, drowsiness, visual trouble, seizures, coma

224
Q

hypoglycaemia: diagnosis

A

fingerprick blood
drug history
general bloods

225
Q

hypoglycaemia: treatment

A

oral sugar
long acting starch
if they cannot swallow- 50% glucose IV
IM glucagon if no IV access

226
Q

ketoacidosis: symptoms

A 
ketonuria
dehydration
drowsiness 
vomiting
polyuria
confusion
abdo pain
coma 
kussmaul breathing- deep and rapid to compensate (hyperventilating)

phase 2a clinical (8 decks)

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