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endocrine Flashcards

1
Q

what does the anterior pituitary release

A

TSH
adenocorticotropic hormone (ACTH)
FSH and LH
GH
prolactin

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2
Q

what does the posterior pituitary release

A

oxytocin and ADH

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3
Q

thyroid hormone feedback

A

hypothalamus
thyrotropin releasing hormone (TRH)
anterior pituitary
TSH
thyroid gland
triiodothyronine (T3) and thyroxine (T4)
negative feedbacl

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4
Q

adrenal feedback lloop

A

hypothalamus
corticotropin releasing hormone (CRH)
ant pituitary
ACTH
adrenal gland
cortisol
negatibe feedback

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5
Q

what id cortisol and functiond

A

stress hormone
inhibits immune system, inhibits bone formation, increases blood glucose, increases metabolism, increases alertness

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6
Q

how do cortisol levels vary

A

diurnal variation - peaks in early morning, lowest late evening

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7
Q

GH feedback loop

A

hypothalamus
GHRH
ant pituitaty
GH
liver
IGF1

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8
Q

roles of GH

A

stimulates muscle growth
increases bone density and strength
stimulates cell regeration and reproduction
stimulates growth internal organs

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9
Q

when is PTH released

A

low serum Ca/Mg or high phosphate

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10
Q

roles of PTH

A

increase activity and number of osteoclasts
increase Ca reabsorption in kindeys
stimulates kidneys to convert vit D3 into calcitriol (active)

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11
Q

drescribe renin angiotensin system

A

low bp
renin released from juxtaglomerular cells in afferent and efferent arterioles kindey
renin converts angiotensinogen from liver to angiotensin I
angiotensin I converted to angiotensin II in lungs by ACE enzyme
angiotensin II causes vasoconstriction and aldosterone release from adrenal gland

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12
Q

where is renin released from

A

juxtaglomerular cells in afferent and efferent arterioles kidney

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13
Q

roles angiotensin II

A

causes vasoconstriction and aldosterone release from adrenal gland

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14
Q

what is aldosterone

A

mineralocorticoid steroid hormone

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15
Q

role aldosterone

A

acts on nephrons in kidneys to:
increase sodium reabsorption in distal tubule
increase K secretion from distal tubule
increase H secretion from collecting ducts

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16
Q

sx cushings

A

round middle
thin and weak limbs
HTN
cardiac hypertrophy
hyperglycaemia
depression
insmonia
osteoporosis
easy brusing
poor skin healing

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17
Q

cause of cushings

A

prolonged elevated cortisol

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18
Q

causes of cushings syndrome

A

exogenous steroids, cushings disease, adrenal adenoma, paraneoplastic (releases ACTH)

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19
Q

cause of cushings disease

A

pituitary adenoma

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20
Q

diagnosing cushings

A

dexamethasone suppression test: do at 10pm, measure 9am. low dose (1g) if normal (suppressed)=rules out cushings.
then give high dose (8g)

24hr urinary cortisol

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21
Q

results of high dose dexamethasone suppression test

A

if cortisol not suppressed and ACTH low =pituitary,
if cortsol low and ACTH high=adrenal
cortisol not suppressed and ACTH high=ectopic

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22
Q

cause of adrenal insufficiency

A

not enough steroid hormones

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23
Q

types adrenal insufficiency

A

primary=addisons, often AI
secondary=damaged pituitary
tertiary=inadequate CRH from hypothalamus-usually due to oral steroid

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24
Q

sx adrenal insufficiency

A

fatigue
nausea
abdo pain
bronze skin
decreased blood pressure
decreased na
increased k

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25
ix adrenal insufficiency
if AI: adrenal cortex Ab and 21-hydroxylase Ab short synacthen test: in morning give synacthen (ACTH) and measure cortisol at base, 30m, 60m. if cortisol rises less than 2xbaseline = primary insufficiency
26
mx adrenal insufficeincy
hydrocortisone (for cortisol), fludrocortisone (for aldosterone) double dose in acute illness
27
sx addisonian/adrenal crisis
decreased consciousness, increased bp, decreased glucose, decreased na, increased k
28
mx addisonina/adrenal crisis
IV hydrocortisone 100mg stat, then 100mg 6hrly IV fluids
29
hormone levels hyperthyroif
low TSH, increased T3 and 4
30
hormone levels primary hypothyroid
increased TSH, low T3 and 4
31
hormone levels secondary hypothyroid
low TSH, T3 and T4
32
thyroid problems with anti-TPO Ab
graves, hashimotos
33
thyroid problems with antithyroglobulin Ab
graves, hashimotos, cancer,
34
thyroid problems with TSH receptor Ab
graves
35
graves thyroid radioisotope scan
diffuse high uptake
36
what thyroid prpblems have focal high uptake on radiisotope scan
toxic multinodular goitre adenoma
37
thyroid cancer radioisotope scan
'cold ' area = low uptake
38
thyrotoxicosis
abnormal and excessive thyroid hormone in body
39
sx graves
diffuse goitre, eye disease, exopthalmos, pretibial myxoedema
40
cause de quervains thyroiditis
viral infection
41
sx de quervains thyroiditis
fever, neck pain, dysphagia, features hyperthyroid
42
mx de quervains thyroiditis
self limiting BB, NSAIDs
43
sx thyroid storm/thyrotoxic crisis
hyperthyroid and pyrexia increase HR delirium
44
mx thyroid storm/thyrotoxic crisis
tx hyperthyroid fluids BB anti-arrhythmic
45
mx hyperthyroidism
1. carbimazole: if block all will need levothyroxine 2. propylthiouracil: risk severe hepatic rxn 3. radioactive iodine 4. propanolol (tx sx not cause) 5. surgery
46
causes hypothyroidd
hashimotos too little iodine se hyperthyroid tx lithium amiodarone tumour infection sheehans syndrome
47
mx hypothyroidism
levothyroxine (synthetic T4, metabolises to T3)
48
ideal blood glucose
4.4-6.1
49
insulin
produced by B cells in islets of langerhans in pancreas decreases blood glucose
50
glucagon
produced by alpha cells in islets of langerhans in pancrease increases blood glucose by glycogenolysis and gluconeogenesis
51
ketogenesis
no glucose so FA->ketons - can cross BBB
52
what is T1DM
no insulin produced
53
causes T1DM
genetic coxsackie B virus enterovirus
54
mx T1DM
background long acting and short acting insulin need to monitor HbA1c and capillary glucose
55
Hba1c
glucose levels avg over 3m
56
what is DKA
ketoacidosis from ketogenesis and dehydration (due to hyperglycaemia causing polyuria) and potassium imbalance (insulin normal drives K into cells)
57
sx DKA
polyuria polydipsia N+V acetone breath LOC
58
diagnosis DKA
blood glucose >11 and ketosis (ketones >3) and acidosis (ph<7.3)
59
mx DKA
fluids: IV saline - 1L stat then 4L +K over 12h insulin infusion at 0.1unit/kg/hr monitor glucose, add desxtrose when <14 monitor K tx trigger .g. infrction chart fluid balance monitor ketones restart normal insulin regime before stop infusion
60
short term complications DM
hypoglycaemia hyperglycaemia
61
long term complications DM
hyperglycaemia ->leaky endothelial cells macrovascular: coronary arter disease, ischaemic feet, HTN, stroke microvascualr: peripheral neuropathy, retinopathy, glomerulosclerosis infection: UTI, pneumonia, fungal (oral/vagina, feet)
62
T2DM
body resistant to insulin
63
pre diabetes
HbA1c 42-47 impaired fasting glucose: 6.1-6.9 impaired glucose tolerance (@2h): 7.8-11.1 OGTT
64
diagnosing DM
HbA1c>48 random glucose >11 fasting glucose >7 OGTT>11
65
aim for T2DM tx
HbA1c <48 if on more than just metformin <53
66
mx T2DM
1. diet and exercise 2. metformin 3. + sulfonylurea, pioglitazone, DPP4i, SGLT2i 4. metformin +2 or metformin and insulin patients with CVD: use SGLT2i or GLP1 mimetics
67
drug class metformin and actions
biguanide increases insulin sensitivity, decreases liver glucose production
68
SE metformin
diarrhoea abdo pain lactic acidosis
69
give an e.g. sulfoylurea and actions
gliclazide increases insulin release
70
SE sulfonylureas
increased wt hypoglycamiea CVD MI
71
class drug pioglitazone and actions
thiazolidinedione increased insuline sensitivity, decreased liver glucose
72
SE pioglitazone
increased wt increased fluid anaemia HF
73
give e.g. DPP4i and action
sitogliptin increased GLP1 activity
74
SE DPP4 i
GI upset sx urti pancreatitis
75
e.g. SGLT2i and action
empagliflozin block glucose reapsorption from urine
76
SE SGLT2i
glucosuria, uti decreased wt DKA
77
e.g. GLP1 mimetics
Liraglutide
78
SE GLP1 mimetics
GI upset decreased wt dizzy
79
cause acromegaly
increased GH pituitary adenoma
80
sx acromegaly
bitemporal hemianopia large HTN T2DM
81
mx acromegaly
surgery pegvisomant(GH antagonist) somatostatin analogue (block GH release) octreotide bromocriptine (dopamine agonists-block GH release)
82
what produces PTH
chief cells
83
primary hyperparathyroid
caused by tumour increased PTH and Ca
84
mx hyperparathyroid
primary=surgery for tumour secondary=correct vit d or renal transplant tertiary=surgery
85
secondary hyperparathyroid
caused by low vit D or CKD increased PTH, normal or decreased Ca
86
tertiary hyperparathyroid
caused by hyperplasia high PTH and Ca
87
primary hyperaldosteronism
conns syndrome adrenal glands produce too much aldosterone so low serum renin cause=adrenal adenoma, hyperplasia, familial, adrenal carcinoma
88
secondary hyperaldosteronism
excessive renin cause: renal artery stenosis/obstruction, HF
89
ix hyperaldosteronism
renin:aldosterone ratio HTN decreased K alkalosis CT/MRI
90
mx hyperaldosteronism
aldosterone antagonists: eplerenone, spironolactone tx cause-surgery
91
SIADH causes
caused by too much ADH - post op, infection (atypical pneumonia), HI, medication (thiazide diuretics, carbazepine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs), malignancy (SCLC), meningitis
92
sx SIADH
headache fatigue cramps low sodium->seizure, LOC
93
mx SIADH
slow correction na to avoid central pontine myelinolysis fluid restriction: <500ml-1l tolvaptan: ADH receptor blocker
94
what is diabetes insipidus
low/lack of response to ADH
95
sx DI
polyuria polydipsia dehydration decreased BP increased Na
96
types/causes DI
nephrogenic: kidneys dont respond-lithium, genes, kidney disease, low K, increased Ca cranial: hypothalamus doesnt produce ADH-brain tumour, HI, brain infection, brain surgery
97
ix DI
low urine osmolality, increased serum osmolality water deprivation/desmopressin stimulation: no fluid for 8h, give desmopressin, measure urine osmolality 8h later
98
results water deprivation/desmopressin stimulation in DI
cranial DI: urine osmolality low after deprivation but high after ADH nephrogenic DI: urine osmolality low after deprivation and after ADH primary polydipsia: urine osmolality high after deprivation and ADH
99
mx DI
tx cause desmopressin
100
what is phaeochromocytoma
tumour of chromaffin cells (produce adrenaline in adrenal gland) so secrete unregulated and excessive adrenaline associated with multiple endocrine neoplasia type 2
101
sx phaeochromocytoma
fluctuate: sweating, headache, HTN, tremor, palpitations, Increased HR, paroxysmal AF
102
ix phaeochromocytoma
24hr urine catecholamines, plasma free metanephrines
103
mx phaeochromocytoma
alpha blocker: phenoxybenzamine BB adrenalectomy
104
What to do with diabetic meds on VRIII
Only continue long acting and basal insulin Stop all others: oral, short acting, pre mixed
105
When to stop VRIII
NORMAL VBG eating and drinking
106
How to stop VRIII
give meal related long acting insulin Remove VRIII one hr later Review and restart other diabetics meds
107
VRIII set up
Constant rate glucose and K in one cannula Variable insulin in other based on hourly CBG
108
When to give insulin in T2DM
HBa1c over 58 after 3m dual oral therapy
109
Starting total daily dose for T1DM
Total number units over 24h on VRIII - however often overestimating 0.5 units per kg wt
110
Insulin regimes T2DM
LONG ACTING only= if still produce some insulin Mixed BD = if struggle with hyperglycaemia after meals
111
How is basal bolus regime split T1DM
Usually half units long acting - morn and evening Half units short acting which correlate with meals (so usually split into 3)
112
When are pre mixed insulin given
Always with meals as risk of hypos Never before bed
113
hyperosmolar hyperglycaemic state
hypovolaemia gluc>30 osmolality >320 no ketonaemia/acidosis
114
mx hyperosmolar hyperglycaemic state
1. IV access, U+E, LFTs, clotting, CRP, CXR, urine C&S, BC, lab glu and osm, VBG 2. IV NaCl IV insuline (0.05 units/kg) when BG stopped falling with IV saline - aim to fall less than 5 /hr 4. aim for fluid balance 3-6 L by 12 h 5. eat and drink asap
115
what can adrenal haemorrhage cause
primary adrenal insufficiency
116
emergency mx preimary adrenal insufficeincy
hydrocortisone 100mg IV STAT then 50mg 6hrly IV fluids 0.9% NaCL tx hypoglycaemia refer endo
117
mx sev hyponatraemia
170ml 2.7% hypertonic saline over 20m repeat if seizures/low GCS/cardiaresp arrest otherwise only repeat if VBG rise Na<5 stop infusion when sx improve or Na increases >10 or total >130 (whichever first) monitor Na until stabe (6h, 12h, daily)
118
what should Na rise be limited to in low Na tx
less than 10 in first 24h then less than 8 in next 24h risk myelinolysis
119
what can cause pituitary apoplexy
prolactinoma
120
what is pituitary apoplexy
bleeding into pituitary imapired blood supply pituitary
121
sx pituitary apoplexy
sudden headache and visual field defects/double vision
122
mx pituitary apoplexy
steroids: 100mg IM hydrocortisone then 50-100 mg QDS IM surgery if severe reduced visual acuity, persistent visual field defects, deteriorating GCS HDU/ITU
123
hypercalcaemia mx
IV fluid: 4-6L NaCl 24h bisphosponate: zolendronic acid 4mg over 15m calcium nadir from 2-4d tx cause
124
what diabetes meds can cause euglycaemia ketoacidosis
SGLT2i
125
HDU referral DKA
potassium <3.5 pH <7.1, HCO3 <5, ketones>6 18-25y or elderly pregnant GCS<12 HR>100/<60, SBP<90, oxygen <92%
126
what to be aware of in DKA mx
hypoglycaemia - is why you need dextrose cover when give insulin

finals (31 decks)

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