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endocrinology key points Flashcards

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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
how does insulin work?
facilitates glucose entry into muscle cells and adipocytes promotes formation of glycogen and triglycerides facilitates protein synthesis
26
when is glucagon released?
in response to raised blood glucose conc | acts to raise
27
how does glucagon work?
glycogenolysis and gluconeogenesis in liver | lipolysis and ketone synthesis
28
somatostatin
functions as a local hormone, inhibiting insulin and glucagon secretion effects seem to be separate from action of inhibiting GH release from AP
29
Addison's disease
destruction of adrenal cortex tissue | - inadequate secretion
30
Cushing's syndrome
excess cortisol
31
therapeutic corticosteroids
suppression of adrenal action | steroid adverse effects
32
what stimulates release from hypothalamus?
neurogenic and systemic forms of stress
33
how does cortisol feedback work?
it feeds back and inhibits its own release | negative feedback
34
aldosterone
enhances Na+ resorption and K+ loss H2O retention = indirectly increases bp renin-angiotensin system
35
drugs which inhibit aldosterone action
ACE inhibitors | AT2 blockers
36
side effects of ACE inhibitors
cough angio-oedema oral lichenoid drug reactions
37
cortisol release pattern
circadian release - nocturnal peak
38
actions of cortisol
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
39
Conns syndrome
excess aldosterone salt and water retention and hypertension adrenal tumour/hyperplasia
40
Cushing's syndrome
excess cortisol
41
primary gland failure - adrenal hypofunction
AI gland destruction, infection, infarction | often Addisons
42
adrenal hypofunction - secondary pituitary failure
can't make ACTH compression from non-fct adenoma sheehan's syndrome
43
Sheehan's syndrome
pituitary gland damaged during childbirth | haemorrhage - reduce bp - pituitary infarction
44
link between ACTH and MSH
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
45
tx of hypopituitarism
``` 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 ```
46
cushing's syndrome gender distribution
F 4:1 M
47
causes of cushings syndrome
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)
48
cushings disease
form of CS caused by a fct pituitary adenoma (ACTH). 70% spontaneous cushings pts
49
signs of cushings syndrome
``` centripetal obesity moon face hypertension thin skin purpura muscle weakness osteoporotic changes and fractures ```
50
symptoms of cushings syndrome
DM features poor infection resistance - opportunistic infections back pain and bone fractures psychiatric disorders - depression, emotional lability, psychosis hirsuitism amenorrhoea, impotence, infertility
51
when can you get skin and mucosal pigmentation in Cushings?
only if high ACTH level - not a SE of steroid medicines
52
causes of Addisons
TB - worldwide UK - 90% AI adrenalitis (organ-specific AI disease) slow onset - months, gradual destruction
53
signs of Addisons
``` 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 ```
54
symptoms of Addisons
weakness anorexia loss of body hair (F)
55
investigating Cushings syndrome
high 24hr urinary cortisol excretion abnormal dexamethasone suppression tests - tumour CRH tests - Cushings disease show rise in ACTH with CRH
56
investigating Addisons disease
high ACTH | negative synACTHen tests - no plasma cortisol rise in response to ACTH injection
57
diagnosing hyperfunction
pituitary adenoma, ectopic ACTH production - high ACTH, high cortisol gland adenoma - low ACTH, high cortisol
58
diagnosing hypofunction
pituitary failure - low ACTH, low cortisol, synACTHen positive gland destruction - high ACTH, low cortisol, synACTHen negative
59
Addison crisis
when levels of cortisol in body fall significantly hypotension, hypovolaemic shock, hyponatraemia, vomiting, coma, hyperkalaemia absence of mineralocorticoid and mineralocorticoid effects of glucocorticoid
60
treating an addison crisis
tx the problem/ppt event e.g. infection fluid resuscitation corticosteroids IV correct hypoglycaemia
61
Addison's disease treatment
hormone replacement - hydrocortisone - cortisol - fludrocortisone - aldosterone
62
doubling addison's disease steroid dose
dose increased by physical/psychological stress and infection if significant double oral cortisol dose during illness
63
steroid prophylaxis/cover in Addisons
when increased physiological requirement anticipated - surgery, infection, physiological stress 1 day + tx day + 1 day = double dose
64
Addisons in pregnancy
double oral dose in labour for 24hrs, increase dose for few days
65
when in dentistry would you consider steroid dose increase for Addisons?
MOS spreading dental/facial infection NOT for simple dental extractions
66
Addisons vs steroid as a tx
``` Addisons - physiological replacement - tendency to hypotension steroids - supraphysiological - tendency to hypertension ```
67
what should you always ask re steroids?
steroid use in prev 6m
68
therapeutic steroids
``` 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
therapeutic steroids adverse effects
``` 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
causes of oral pigmentation
``` 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
MEN
malignancy in 1 endocrine gland - v likely malignancy in another - develop from same tissue as an embryo MEN2b - oral mucosal neuromas
72
pituitary tumours
functional adenomas - make hormone excess | non-fct adenomas - space occupying
73
fct adenomas <40yrs
prolactin or ACTH | amenorrhoea - Galctorrhoea or Cushings disease
74
fct adenomas >40yrs
GH | acromegaly
75
non-fct adenomas
``` mass effects visual field defects - pituitary gland under optic chiasma - tumour could compress optic nerve - lose peripheral vision other hormone deficiencies ```
76
tx of pituitary tumours
trans-sphenoidal surgery
77
insufficient GH
growth failure children metabolic changes adults - increased fat, reduced vitality
78
excess GH
gigantism or acromegaly
79
assessing GH levels
IGF-1 - shows resemblance to overnight peak GH level
80
acromegaly onset
insidious peak 30-50years benign pituitary tumour
81
acromegaly features
``` get bigger coarse features enlarged hands - carpal tunnel syndrome T2 diabetes - GH antagonistic to insulin CV disease visual field defects hyperprolactinaemia hypopituitarism ```
82
IO acromegaly features
``` enlarged tongue interdental spacing 'shrunk' dentures changes in occlusion reverse overbite - mandible keeps growing ```
83
thyrotoxicosis without hyperthyroidism
thyroid tablets to increase metabolism as quick fix diet pills
84
causes of hyperthyroidism
``` Graves disease - 70-80%, AI disease, diffuse goitre - autoABs match TSH receptor toxic multi-nodular goitre toxic adenoma pituitary tumour - rare (secondary) ```
85
what other organ is affected in Graves disease?
ophthalmopathy - scleral injection - proptosis - periorbital oedema - conjunctival oedema
86
effects of hyperthyroidism
increased metabolism | often bouts
87
symptoms of hyperthyroidism
``` hot and sweating weight loss palpitations muscle weakness irritable, manic, anxious diarrhoea ```
88
signs of hyperthyroidism
``` warm moist skin tachycardia and AF increased bp and HF tremor and hyperreflexia eyelid retraction and lid lag ```
89
causes of primary hypothyroidism
``` 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
AI hashimoto's thyroiditis
``` antibody targets gland - destruction goitre, hypothyroidism older women associations - FH of AI disease - Down Syndrome ```
91
causes of secondary hypothyroidism
hypothalamic/pituitary disease | rare
92
effects of hypothyroidism
reduced metabolism | v gradual onset
93
symptoms of hypothyroidism
``` tired cold intolerance weight gain constipation hoarse goitre (in Hashimotos - inflammation) angina 'slow', poor memory hair loss ```
94
signs of hypothyroidism
``` dry coarse skin bradycardia hyperlipidaemia psychiatric/confusion delayed reflexes myxoedema ```
95
investigating thyroid disease
blood: TSH, T3, T4 imaging: US (cysts), radioisotope scans (gland uptake) tissue: FNA/biopsy, see what damage is
96
T3
triiodothyronine
97
T4
thyroxine
98
hormones in hyperthyroidism
``` Graves/adenoma: reduced TSH, increased T3 pituitary cause (rare): increased TSH, increased T3 ```
99
hormones in hypothyroidism
``` gland failure: increased TSH, reduced T4 pituitary cause (rare): reduced TSH, reduced T4 ```
100
tx of hyperthyroidism
carbimazole B-blockers radioiodine surgery
101
tx of hypothyroidism
T4 tablets thyroxine slow response - weeks increase dose slowly (IHD risk - heard attack) test 6m-1yr to check levels stable
102
thyroid enlargement
goitre - diffuse enlargement | solitary nodule enlargement - adenoma, carcinoma, cyst formation
103
thyroid cancer
usually thyroid swelling be suspicious in children or elderly papillary or follicular in young undifferentiated in elderly
104
dental aspects of hyperthyroidism
pain anxiety and psychiatric problems | caution for tx until controlled
105
dental aspects of hypothyroidism
avoid sedatives if severe
106
DM
abnormality of glucose regulation
107
DI
abnormality of renal fct - lack of ADH
108
T1 DM
insulin deficiency
109
T2 DM
insulin resistance
110
symptoms of DM
polyuria polydipsia tiredness - can't move glucose efficiently into cells
111
general features T1
``` younger thin ? FH ? FH of AI disease diabetic symptoms easily get ketosis ```
112
general features T2
``` older obese strong FH ?diabetic symptoms present with complications rarely get ketosis ```
113
diabetes diagnosis
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
IGT
on way to becoming diabetic | need lifestyle changes
115
definition of T1 DM
immune mediated pancreatic B-cell destruction - autoantibodies - hyperglycaemia - ketoacidosis
116
T1 circulating ABs
GAD - glutamic acid decarboxylase ICA - islet cell antibodies IAA - insulin autoantibodies
117
aetiology of T1
genetic - HLA associated | env - low twin concordance
118
T1 child/adolescence onset
higher ICA, IAA, more severe decompensation
119
T1 adult onset
gradual onset, GAD, less weight loss and ketoacidosis, LADA
120
acute presentation T1
hyperglycaemia with diabetic symptoms | ketoacidosis - metabolic acidosis you get from dissolving fat in body
121
T2 onset
``` usually >40yrs, gradual onset often found by accident often retinal damage at diagnosis unusual infections, diabetic complications MODY possible ```
122
T2 FH
strong
123
T2 pathogenesis
poorly fct insulin receptors - hypersecrete - B-cell exhaustion bit of insulin in background - don't get ketoacidosis
124
T2 as a metabolic disorder
defect in insulin resistance defect in insulin secretion basal hepatic glucose output increased insulin stimulated muscle glucose uptake reduced
125
effects of T2
``` IGT hyperinsulinaemia hypertension obesity (abdo distribution) dyslipidaemia procoagulant epithelial markers early and accelerated atherosclerosis ```
126
management of diabetes
``` education targets drugs, insulin nutrition exercise monitoring ```
127
importance of diabetic control
good control = less future complications | but pts often keep slightly higher blood sugar as they don't like hypo
128
T2 management
``` weight loss diet restriction 'diet pills' - orlistat, sibutramine surgery - gastric bypass oral hypoglycaemic agents - insulin secretagogues - insulin sensitisers insulin ```
129
insulin secretagogues
increase pancreatic insulin secretion small hypoglycaemia risk sulphonylureas e.g. gliclazide, tolbutamide
130
insulin sensitisers
thiazolidinediones - rosiglitazone biguanides - metformin - enhances cell insulin sensitivity - reduces hepatic gluconeogenesis
131
insulin regimes
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
HbA1c aim
48mmol/mol | 6.5%
133
hypoglycaemia
``` adrenaline sweating, tremor confusion coma warnings often get less as get older - nerve dysfct worse ```
134
what are chronic diabetic complications due to?
prolonged hyperglycaemia
135
chronic diabetic complications
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
what causes the microvascular disease?
don't know | something to do with toxicity to endothelial cells
137
diabetes care in surgery
fasting problem in T1 higher risks of complications - heart attack and infection metabolic changes increased insulin requirement T1 (T2)
138
dental aspects of diabetes
food intake disruption acute emergencies complications infection risk and poor wound healing

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