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BDS2 bams > endocrinology key points > Flashcards

endocrinology key points Flashcards

1
Q

body systems

A 
interact with external env - behaviour
 - nervous, reproductive
regulate internal env - homeostasis
 - CV, respiratory, immune
control other systems 
 - nervous, endocrine
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2
Q

chemical communication

A

synapse
paracrine
endocrine

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3
Q

process at a chemical synapse

A

impulse arrives at terminal of pre-synaptic cell
transmitter released from storage vesicles
diffuses in synaptic cleft
binds to receptor on post-synaptic cell
alters post-synaptic cell
- excitatory/inhibitory
transmitter action terminated

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4
Q

drug actions on synapse

A

may enhance/suppress synapse

  • synthesis/storage/release of tx
  • action of tx on receptor
  • 2nd messenger system
  • inactivation of tx
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5
Q

autocrine

A

chemical acts on cell releasing it

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6
Q

nerve control

A

specific, localised, rapid, short duration
reflexes
sensory systems
salivary secretion

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7
Q

hormonal control

A 
co-ordinated, body wide actions
slow to act, but effect persists
metabolism
growth
menstrual cycle
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8
Q

nerve and hormone combined control

A

bp
blood loss
thermoregulation

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9
Q

examples of 2nd messengers

A

G-proteins and cAMP

Ca2+

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10
Q

steroid hormones

A

can pass through membrane

change transcription in nucleus

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11
Q

peptide transmitters

A

1st messengers

act on receptor protein on membrane

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12
Q

hyperfunction

A

excess production and secretion

upregulation of receptors

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13
Q

hypofunction

A

reduced production and secretion
down regulation of receptors
receptors not functioning

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14
Q

posterior pituitary - how are hormones released?

A

hypothalamus
nerve axons
PP
released into circulation

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15
Q

which hormones are released from the posterior pituitary?

A

ADH

oxytocin

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16
Q

how are hormones released from anterior pituitary?

A

hypothalamus
releasing hormones travel along hypothalamic - pituitary portal vessels
AP target cells
hormones released

hormonal local feedback system

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17
Q

function of hypothalamic hormones

A

control release of AP hormones

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18
Q

hypothalamic hormones

A 
corticotropin RH
gonadotropin RH
thyrotropin RH
growth hormone RH
prolactin RH
somatostatin
dopamine
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19
Q

which hormone inhibits GH?

A

somatostatin

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20
Q

which hormone inhibits prolactin?

A

dopamine

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21
Q

anterior pituitary hormones

A 
adrenocorticotropic hormone
follicle stimulating hormone
luteinizing hormone
thyroid stimulating hormone
growth hormone
prolactin
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22
Q

structure of adrenal gland

A

endocrine, neuronal and epithelial tissue
capsule
cortex
- zona glomerulosa - aldosterone
- zona fasiculata - cortisol
- zona retiuclaris - sex hormones- androgens, DHEA
medulla - modified sympathetic ganglion - epinephrine (acetylcholine chemical signal for secretion)

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23
Q

islets of langerhans

A

a cells glucagon
B cells insulin
d cells somatostatin

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24
Q

when is insulin released?

A

in response to increased blood glucose conc

acts to lower it

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25
Q

how does insulin work?

A

facilitates glucose entry into muscle cells and adipocytes
promotes formation of glycogen and triglycerides
facilitates protein synthesis

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26
Q

when is glucagon released?

A

in response to raised blood glucose conc

acts to raise

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27
Q

how does glucagon work?

A

glycogenolysis and gluconeogenesis in liver

lipolysis and ketone synthesis

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28
Q

somatostatin

A

functions as a local hormone, inhibiting insulin and glucagon secretion
effects seem to be separate from action of inhibiting GH release from AP

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29
Q

Addison’s disease

A

destruction of adrenal cortex tissue

- inadequate secretion

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30
Q

Cushing’s syndrome

A

excess cortisol

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31
Q

therapeutic corticosteroids

A

suppression of adrenal action

steroid adverse effects

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32
Q

what stimulates release from hypothalamus?

A

neurogenic and systemic forms of stress

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33
Q

how does cortisol feedback work?

A

it feeds back and inhibits its own release

negative feedback

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34
Q

aldosterone

A

enhances Na+ resorption and K+ loss
H2O retention
= indirectly increases bp

renin-angiotensin system

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35
Q

drugs which inhibit aldosterone action

A

ACE inhibitors

AT2 blockers

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36
Q

side effects of ACE inhibitors

A

cough
angio-oedema
oral lichenoid drug reactions

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37
Q

cortisol release pattern

A

circadian release - nocturnal peak

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38
Q

actions of cortisol

A

antagonist to insulin - maintains blood glucose levels
inhibits protein synthesis, increases proteolysis
inhibits immune response, anti-inflammatory
raises bp
inhibits bone synthesis
stimulates erythropoietin synthesis
ADH antagonist
inhibits reproductive function

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39
Q

Conns syndrome

A

excess aldosterone
salt and water retention and hypertension
adrenal tumour/hyperplasia

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40
Q

Cushing’s syndrome

A

excess cortisol

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41
Q

primary gland failure - adrenal hypofunction

A

AI gland destruction, infection, infarction

often Addisons

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42
Q

adrenal hypofunction - secondary pituitary failure

A

can’t make ACTH
compression from non-fct adenoma
sheehan’s syndrome

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43
Q

Sheehan’s syndrome

A

pituitary gland damaged during childbirth

haemorrhage - reduce bp - pituitary infarction

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44
Q

link between ACTH and MSH

A

both made from the same protein precursor
aMSH identical to part of ACTH
if make lots of ACTH causes melanocytes to make a lot more melanin - pigmentation

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45
Q

tx of hypopituitarism

A 
ACTH - cortisol
TSH - thyroxine
GH - only give to children
FSH and LH - depends on age - may give O/P
ADH - ddAVP, desmopressin
oxytocin - replace during birth
prolactin - don't replace
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46
Q

cushing’s syndrome gender distribution

A

F 4:1 M

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47
Q

causes of cushings syndrome

A

cushings disease - form of CS caused by a fct pituitary adenoma (ACTH). 70% spontaneous cushings pts
adrenal adenoma
adrenal hyperplasia
ectopic ACTH production (lung tumours)

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48
Q

cushings disease

A

form of CS caused by a fct pituitary adenoma (ACTH). 70% spontaneous cushings pts

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49
Q

signs of cushings syndrome

A 
centripetal obesity
moon face
hypertension
thin skin
purpura
muscle weakness
osteoporotic changes and fractures
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50
Q

symptoms of cushings syndrome

A

DM features
poor infection resistance - opportunistic infections
back pain and bone fractures
psychiatric disorders - depression, emotional lability, psychosis
hirsuitism
amenorrhoea, impotence, infertility

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51
Q

when can you get skin and mucosal pigmentation in Cushings?

A

only if high ACTH level - not a SE of steroid medicines

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52
Q

causes of Addisons

A

TB - worldwide
UK - 90% AI adrenalitis (organ-specific AI disease)
slow onset - months, gradual destruction

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53
Q

signs of Addisons

A 
postural hypotension
hyponatraemic (risk of seizures)
hypoglycaemia and hyperkalaemic acidosis
weight loss and lethargy
hyperpigmentation (only in primary - keep making more ACTH to try and stimulate gland)
vitiligo - AI destruction of melanocytes
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54
Q

symptoms of Addisons

A

weakness
anorexia
loss of body hair (F)

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55
Q

investigating Cushings syndrome

A

high 24hr urinary cortisol excretion
abnormal dexamethasone suppression tests - tumour
CRH tests - Cushings disease show rise in ACTH with CRH

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56
Q

investigating Addisons disease

A

high ACTH

negative synACTHen tests - no plasma cortisol rise in response to ACTH injection

57
Q

diagnosing hyperfunction

A

pituitary adenoma, ectopic ACTH production - high ACTH, high cortisol
gland adenoma - low ACTH, high cortisol

58
Q

diagnosing hypofunction

A

pituitary failure - low ACTH, low cortisol, synACTHen positive
gland destruction - high ACTH, low cortisol, synACTHen negative

59
Q

Addison crisis

A

when levels of cortisol in body fall significantly
hypotension, hypovolaemic shock, hyponatraemia, vomiting, coma, hyperkalaemia
absence of mineralocorticoid and mineralocorticoid effects of glucocorticoid

60
Q

treating an addison crisis

A

tx the problem/ppt event e.g. infection
fluid resuscitation
corticosteroids IV
correct hypoglycaemia

61
Q

Addison’s disease treatment

A

hormone replacement

  • hydrocortisone - cortisol
  • fludrocortisone - aldosterone
62
Q

doubling addison’s disease steroid dose

A

dose increased by physical/psychological stress and infection
if significant double oral cortisol dose during illness

63
Q

steroid prophylaxis/cover in Addisons

A

when increased physiological requirement anticipated
- surgery, infection, physiological stress
1 day + tx day + 1 day = double dose

64
Q

Addisons in pregnancy

A

double oral dose in labour for 24hrs, increase dose for few days

65
Q

when in dentistry would you consider steroid dose increase for Addisons?

A

MOS
spreading dental/facial infection
NOT for simple dental extractions

66
Q

Addisons vs steroid as a tx

A 
Addisons
 - physiological replacement
 - tendency to hypotension
steroids
 - supraphysiological
 - tendency to hypertension
67
Q

what should you always ask re steroids?

A

steroid use in prev 6m

68
Q

therapeutic steroids

A 
hydrocortisone (cortisol equivalent 1)
prednisolone (4)
triamcinolone (5)
dexamethasone (25)
betamethasone (30)

adrenal suppression
stops adrenal gland being able to respond to ACTH
enhanced glucocorticoid and mineralocorticoid effects

69
Q

therapeutic steroids adverse effects

A 
hypertension
T2 diabetes - if already have then harder to control
osteoporosis
increased infection risk
peptic ulceration
thinning of skin
easy bruising
cataracts and glaucoma
hyperlipidaemia (atherosclerosis)
increased cancer risk
psychiatric disturbance - sleeping problems
70
Q

causes of oral pigmentation

A 
racial 
SMOKING
melanotic macule
drugs
 - OCP
 - minocycline
 - antimalarials
 - AZT (antiretroviral)
pigmented naevus
pregnancy
chronic trauma
melanoma
 - Addisons not most common reason for oral pigmentation
71
Q

MEN

A

malignancy in 1 endocrine gland - v likely malignancy in another - develop from same tissue as an embryo
MEN2b - oral mucosal neuromas

72
Q

pituitary tumours

A

functional adenomas - make hormone excess

non-fct adenomas - space occupying

73
Q

fct adenomas <40yrs

A

prolactin or ACTH

amenorrhoea - Galctorrhoea or Cushings disease

74
Q

fct adenomas >40yrs

A

GH

acromegaly

75
Q

non-fct adenomas

A 
mass effects 
visual field defects
 - pituitary gland under optic chiasma
 - tumour could compress optic nerve - lose peripheral 
   vision
other hormone deficiencies
76
Q

tx of pituitary tumours

A

trans-sphenoidal surgery

77
Q

insufficient GH

A

growth failure children
metabolic changes adults
- increased fat, reduced vitality

78
Q

excess GH

A

gigantism or acromegaly

79
Q

assessing GH levels

A

IGF-1 - shows resemblance to overnight peak GH level

80
Q

acromegaly onset

A

insidious
peak 30-50years
benign pituitary tumour

81
Q

acromegaly features

A 
get bigger
coarse features
enlarged hands - carpal tunnel syndrome
T2 diabetes - GH antagonistic to insulin
CV disease
visual field defects
hyperprolactinaemia
hypopituitarism
82
Q

IO acromegaly features

A 
enlarged tongue
interdental spacing
'shrunk' dentures
changes in occlusion
reverse overbite - mandible keeps growing
83
Q

thyrotoxicosis without hyperthyroidism

A

thyroid tablets to increase metabolism as quick fix diet pills

84
Q

causes of hyperthyroidism

A 
Graves disease - 70-80%, AI disease, diffuse goitre
 - autoABs match TSH receptor
toxic multi-nodular goitre
toxic adenoma
pituitary tumour - rare (secondary)
85
Q

what other organ is affected in Graves disease?

A

ophthalmopathy

  • scleral injection
  • proptosis
  • periorbital oedema
  • conjunctival oedema
86
Q

effects of hyperthyroidism

A

increased metabolism

often bouts

87
Q

symptoms of hyperthyroidism

A 
hot and sweating
weight loss
palpitations
muscle weakness
irritable, manic, anxious
diarrhoea
88
Q

signs of hyperthyroidism

A 
warm moist skin
tachycardia and AF
increased bp and HF
tremor and hyperreflexia
eyelid retraction and lid lag
89
Q

causes of primary hypothyroidism

A 
AI Hashimoto's thyroiditis (90%)
idiopathic atrophy
radioiodine tx (to treat hyper)
thyroidectomy surgery
iodine deficiency
drugs - carbimazole, amiodarone, lithium
congenital (can cause cretinism)
90
Q

AI hashimoto’s thyroiditis

A 
antibody targets gland - destruction
goitre, hypothyroidism
older women
associations
 - FH of AI disease
 - Down Syndrome
91
Q

causes of secondary hypothyroidism

A

hypothalamic/pituitary disease

rare

92
Q

effects of hypothyroidism

A

reduced metabolism

v gradual onset

93
Q

symptoms of hypothyroidism

A 
tired
cold intolerance
weight gain
constipation
hoarse
goitre (in Hashimotos - inflammation)
angina
'slow', poor memory
hair loss
94
Q

signs of hypothyroidism

A 
dry coarse skin
bradycardia
hyperlipidaemia
psychiatric/confusion
delayed reflexes
myxoedema
95
Q

investigating thyroid disease

A

blood: TSH, T3, T4
imaging: US (cysts), radioisotope scans (gland uptake)
tissue: FNA/biopsy, see what damage is

96
Q

T3

A

triiodothyronine

97
Q

T4

A

thyroxine

98
Q

hormones in hyperthyroidism

A 
Graves/adenoma: reduced TSH, increased T3
pituitary cause (rare): increased TSH, increased T3
99
Q

hormones in hypothyroidism

A 
gland failure: increased TSH, reduced T4
pituitary cause (rare): reduced TSH, reduced T4
100
Q

tx of hyperthyroidism

A

carbimazole
B-blockers
radioiodine
surgery

101
Q

tx of hypothyroidism

A

T4 tablets thyroxine
slow response - weeks
increase dose slowly (IHD risk - heard attack)
test 6m-1yr to check levels stable

102
Q

thyroid enlargement

A

goitre - diffuse enlargement

solitary nodule enlargement - adenoma, carcinoma, cyst formation

103
Q

thyroid cancer

A

usually thyroid swelling
be suspicious in children or elderly
papillary or follicular in young
undifferentiated in elderly

104
Q

dental aspects of hyperthyroidism

A

pain anxiety and psychiatric problems

caution for tx until controlled

105
Q

dental aspects of hypothyroidism

A

avoid sedatives if severe

106
Q

DM

A

abnormality of glucose regulation

107
Q

DI

A

abnormality of renal fct - lack of ADH

108
Q

T1 DM

A

insulin deficiency

109
Q

T2 DM

A

insulin resistance

110
Q

symptoms of DM

A

polyuria
polydipsia
tiredness - can’t move glucose efficiently into cells

111
Q

general features T1

A 
younger
thin
? FH
? FH of AI disease
diabetic symptoms
easily get ketosis
112
Q

general features T2

A 
older
obese
strong FH
?diabetic symptoms
present with complications
rarely get ketosis
113
Q

diabetes diagnosis

A

RPG - >11.1mmol/L on 2 occasions diagnostic
GTT
- 75g load after fasting
- amount of time body spends in high blood sugar levels
- levels before test and 2hr plasma glucose

114
Q

IGT

A

on way to becoming diabetic

need lifestyle changes

115
Q

definition of T1 DM

A

immune mediated pancreatic B-cell destruction - autoantibodies

  • hyperglycaemia
  • ketoacidosis
116
Q

T1 circulating ABs

A

GAD - glutamic acid decarboxylase
ICA - islet cell antibodies
IAA - insulin autoantibodies

117
Q

aetiology of T1

A

genetic - HLA associated

env - low twin concordance

118
Q

T1 child/adolescence onset

A

higher ICA, IAA, more severe decompensation

119
Q

T1 adult onset

A

gradual onset, GAD, less weight loss and ketoacidosis, LADA

120
Q

acute presentation T1

A

hyperglycaemia with diabetic symptoms

ketoacidosis - metabolic acidosis you get from dissolving fat in body

121
Q

T2 onset

A 
usually >40yrs, gradual onset
often found by accident
often retinal damage at diagnosis
unusual infections, diabetic complications
MODY possible
122
Q

T2 FH

A

strong

123
Q

T2 pathogenesis

A

poorly fct insulin receptors
- hypersecrete
- B-cell exhaustion
bit of insulin in background - don’t get ketoacidosis

124
Q

T2 as a metabolic disorder

A

defect in insulin resistance
defect in insulin secretion
basal hepatic glucose output increased
insulin stimulated muscle glucose uptake reduced

125
Q

effects of T2

A 
IGT
hyperinsulinaemia
hypertension
obesity (abdo distribution)
dyslipidaemia
procoagulant epithelial markers
early and accelerated atherosclerosis
126
Q

management of diabetes

A 
education
targets
drugs, insulin
nutrition
exercise
monitoring
127
Q

importance of diabetic control

A

good control = less future complications

but pts often keep slightly higher blood sugar as they don’t like hypo

128
Q

T2 management

A 
weight loss
diet restriction
'diet pills' - orlistat, sibutramine
surgery - gastric bypass
oral hypoglycaemic agents
 - insulin secretagogues
 - insulin sensitisers
insulin
129
Q

insulin secretagogues

A

increase pancreatic insulin secretion
small hypoglycaemia risk
sulphonylureas e.g. gliclazide, tolbutamide

130
Q

insulin sensitisers

A

thiazolidinediones - rosiglitazone
biguanides - metformin
- enhances cell insulin sensitivity
- reduces hepatic gluconeogenesis

131
Q

insulin regimes

A

basal-bolus
- long acting, give spikes when have food
- more injections, better control
split-mixed control
- fewer injections, poorer control
- insulin that lasts 12hrs and gives spikes
SC injection - gradually taken up into circulation

132
Q

HbA1c aim

A

48mmol/mol

6.5%

133
Q

hypoglycaemia

A 
adrenaline
sweating, tremor
confusion
coma
warnings often get less as get older - nerve dysfct worse
134
Q

what are chronic diabetic complications due to?

A

prolonged hyperglycaemia

135
Q

chronic diabetic complications

A

CV risk - macrovascular disease
- atheroma, angina, MI, claudication, aneurysm
infection risk - microvascular disease
- poor wound healing
- impaired neutrophil phagocytosis
renal disease - microvascular
- atherosclerosis renal artery, glomeruli
eye disease
- cataracts
- maculopathy
- diabetic proliferative retinopathy
neuropathy - microvascular
- general sensation - hands and feet, ischaemia to
nerves, pain and numbness
- motor - weakness and wasting of muscles
- autonomic regulation - awareness of hypoglycaemia
lost, postural reflexes, bladder and bowel dysfct

136
Q

what causes the microvascular disease?

A

don’t know

something to do with toxicity to endothelial cells

137
Q

diabetes care in surgery

A

fasting problem in T1
higher risks of complications - heart attack and infection
metabolic changes
increased insulin requirement T1 (T2)

138
Q

dental aspects of diabetes

A

food intake disruption
acute emergencies
complications
infection risk and poor wound healing

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