Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

finals > endocrine > Flashcards

endocrine Flashcards

1
Q

what does the anterior pituitary release

A

TSH
adenocorticotropic hormone (ACTH)
FSH and LH
GH
prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does the posterior pituitary release

A

oxytocin and ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

thyroid hormone feedback

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

adrenal feedback lloop

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what id cortisol and functiond

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how do cortisol levels vary

A

diurnal variation - peaks in early morning, lowest late evening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GH feedback loop

A

hypothalamus
GHRH
ant pituitaty
GH
liver
IGF1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

roles of GH

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

when is PTH released

A

low serum Ca/Mg or high phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where is renin released from

A

juxtaglomerular cells in afferent and efferent arterioles kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

roles angiotensin II

A

causes vasoconstriction and aldosterone release from adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is aldosterone

A

mineralocorticoid steroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

sx cushings

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cause of cushings

A

prolonged elevated cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

causes of cushings syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

cause of cushings disease

A

pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cause of adrenal insufficiency

A

not enough steroid hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

types adrenal insufficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

sx adrenal insufficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ix adrenal insufficiency

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mx adrenal insufficeincy

A

hydrocortisone (for cortisol), fludrocortisone (for aldosterone)
double dose in acute illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

sx addisonian/adrenal crisis

A

decreased consciousness, increased bp, decreased glucose, decreased na, increased k

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

mx addisonina/adrenal crisis

A

IV hydrocortisone 100mg stat, then 100mg 6hrly
IV fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

hormone levels hyperthyroif

A

low TSH, increased T3 and 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

hormone levels primary hypothyroid

A

increased TSH, low T3 and 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

hormone levels secondary hypothyroid

A

low TSH, T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

thyroid problems with anti-TPO Ab

A

graves, hashimotos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

thyroid problems with antithyroglobulin Ab

A

graves, hashimotos, cancer,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

thyroid problems with TSH receptor Ab

A

graves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

graves thyroid radioisotope scan

A

diffuse high uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what thyroid prpblems have focal high uptake on radiisotope scan

A

toxic multinodular goitre
adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

thyroid cancer radioisotope scan

A

‘cold ‘ area = low uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

thyrotoxicosis

A

abnormal and excessive thyroid hormone in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

sx graves

A

diffuse goitre, eye disease, exopthalmos, pretibial myxoedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

cause de quervains thyroiditis

A

viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

sx de quervains thyroiditis

A

fever, neck pain, dysphagia, features hyperthyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

mx de quervains thyroiditis

A

self limiting
BB, NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

sx thyroid storm/thyrotoxic crisis

A

hyperthyroid and pyrexia
increase HR
delirium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

mx thyroid storm/thyrotoxic crisis

A

tx hyperthyroid
fluids
BB
anti-arrhythmic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

mx hyperthyroidism

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

causes hypothyroidd

A

hashimotos
too little iodine
se hyperthyroid tx
lithium
amiodarone
tumour
infection
sheehans syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

mx hypothyroidism

A

levothyroxine (synthetic T4, metabolises to T3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

ideal blood glucose

A

4.4-6.1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

insulin

A

produced by B cells in islets of langerhans in pancreas
decreases blood glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

glucagon

A

produced by alpha cells in islets of langerhans in pancrease
increases blood glucose by glycogenolysis and gluconeogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

ketogenesis

A

no glucose so FA->ketons - can cross BBB

52
Q

what is T1DM

A

no insulin produced

53
Q

causes T1DM

A

genetic
coxsackie B virus
enterovirus

54
Q

mx T1DM

A

background long acting and short acting insulin
need to monitor HbA1c and capillary glucose

55
Q

Hba1c

A

glucose levels avg over 3m

56
Q

what is DKA

A

ketoacidosis from ketogenesis and dehydration (due to hyperglycaemia causing polyuria) and potassium imbalance (insulin normal drives K into cells)

57
Q

sx DKA

A

polyuria
polydipsia
N+V
acetone breath
LOC

58
Q

diagnosis DKA

A

blood glucose >11 and ketosis (ketones >3) and acidosis (ph<7.3)

59
Q

mx DKA

A

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
Q

short term complications DM

A

hypoglycaemia
hyperglycaemia

61
Q

long term complications DM

A

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
Q

T2DM

A

body resistant to insulin

63
Q

pre diabetes

A

HbA1c 42-47
impaired fasting glucose: 6.1-6.9
impaired glucose tolerance (@2h): 7.8-11.1 OGTT

64
Q

diagnosing DM

A

HbA1c>48
random glucose >11
fasting glucose >7
OGTT>11

65
Q

aim for T2DM tx

A

HbA1c <48
if on more than just metformin <53

66
Q

mx T2DM

A
  1. diet and exercise
  2. metformin
    • sulfonylurea, pioglitazone, DPP4i, SGLT2i
  4. metformin +2 or metformin and insulin

patients with CVD: use SGLT2i or GLP1 mimetics

67
Q

drug class metformin and actions

A

biguanide
increases insulin sensitivity, decreases liver glucose production

68
Q

SE metformin

A

diarrhoea
abdo pain
lactic acidosis

69
Q

give an e.g. sulfoylurea and actions

A

gliclazide
increases insulin release

70
Q

SE sulfonylureas

A

increased wt
hypoglycamiea
CVD
MI

71
Q

class drug pioglitazone and actions

A

thiazolidinedione
increased insuline sensitivity, decreased liver glucose

72
Q

SE pioglitazone

A

increased wt
increased fluid
anaemia
HF

73
Q

give e.g. DPP4i and action

A

sitogliptin
increased GLP1 activity

74
Q

SE DPP4 i

A

GI upset
sx urti
pancreatitis

75
Q

e.g. SGLT2i and action

A

empagliflozin
block glucose reapsorption from urine

76
Q

SE SGLT2i

A

glucosuria,
uti
decreased wt
DKA

77
Q

e.g. GLP1 mimetics

A

Liraglutide

78
Q

SE GLP1 mimetics

A

GI upset
decreased wt
dizzy

79
Q

cause acromegaly

A

increased GH
pituitary adenoma

80
Q

sx acromegaly

A

bitemporal hemianopia
large
HTN
T2DM

81
Q

mx acromegaly

A

surgery
pegvisomant(GH antagonist)
somatostatin analogue (block GH release)
octreotide
bromocriptine (dopamine agonists-block GH release)

82
Q

what produces PTH

A

chief cells

83
Q

primary hyperparathyroid

A

caused by tumour
increased PTH and Ca

84
Q

mx hyperparathyroid

A

primary=surgery for tumour
secondary=correct vit d or renal transplant
tertiary=surgery

85
Q

secondary hyperparathyroid

A

caused by low vit D or CKD
increased PTH, normal or decreased Ca

86
Q

tertiary hyperparathyroid

A

caused by hyperplasia
high PTH and Ca

87
Q

primary hyperaldosteronism

A

conns syndrome
adrenal glands produce too much aldosterone so low serum renin
cause=adrenal adenoma, hyperplasia, familial, adrenal carcinoma

88
Q

secondary hyperaldosteronism

A

excessive renin
cause: renal artery stenosis/obstruction, HF

89
Q

ix hyperaldosteronism

A

renin:aldosterone ratio
HTN
decreased K
alkalosis
CT/MRI

90
Q

mx hyperaldosteronism

A

aldosterone antagonists: eplerenone, spironolactone
tx cause-surgery

91
Q

SIADH causes

A

caused by too much ADH - post op, infection (atypical pneumonia), HI, medication (thiazide diuretics, carbazepine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs), malignancy (SCLC), meningitis

92
Q

sx SIADH

A

headache
fatigue
cramps
low sodium->seizure, LOC

93
Q

mx SIADH

A

slow correction na to avoid central pontine myelinolysis
fluid restriction: <500ml-1l
tolvaptan: ADH receptor blocker

94
Q

what is diabetes insipidus

A

low/lack of response to ADH

95
Q

sx DI

A

polyuria
polydipsia
dehydration
decreased BP
increased Na

96
Q

types/causes DI

A

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
Q

ix DI

A

low urine osmolality, increased serum osmolality
water deprivation/desmopressin stimulation: no fluid for 8h, give desmopressin, measure urine osmolality 8h later

98
Q

results water deprivation/desmopressin stimulation in DI

A

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
Q

mx DI

A

tx cause
desmopressin

100
Q

what is phaeochromocytoma

A

tumour of chromaffin cells (produce adrenaline in adrenal gland) so secrete unregulated and excessive adrenaline
associated with multiple endocrine neoplasia type 2

101
Q

sx phaeochromocytoma

A

fluctuate:
sweating, headache, HTN, tremor, palpitations, Increased HR, paroxysmal AF

102
Q

ix phaeochromocytoma

A

24hr urine catecholamines, plasma free metanephrines

103
Q

mx phaeochromocytoma

A

alpha blocker: phenoxybenzamine
BB
adrenalectomy

104
Q

What to do with diabetic meds on VRIII

A

Only continue long acting and basal insulin
Stop all others: oral, short acting, pre mixed

105
Q

When to stop VRIII

A

NORMAL VBG
eating and drinking

106
Q

How to stop VRIII

A

give meal related long acting insulin
Remove VRIII one hr later
Review and restart other diabetics meds

107
Q

VRIII set up

A

Constant rate glucose and K in one cannula
Variable insulin in other based on hourly CBG

108
Q

When to give insulin in T2DM

A

HBa1c over 58 after 3m dual oral therapy

109
Q

Starting total daily dose for T1DM

A

Total number units over 24h on VRIII - however often overestimating
0.5 units per kg wt

110
Q

Insulin regimes T2DM

A

LONG ACTING only= if still produce some insulin
Mixed BD = if struggle with hyperglycaemia after meals

111
Q

How is basal bolus regime split T1DM

A

Usually half units long acting - morn and evening
Half units short acting which correlate with meals (so usually split into 3)

112
Q

When are pre mixed insulin given

A

Always with meals as risk of hypos
Never before bed

113
Q

hyperosmolar hyperglycaemic state

A

hypovolaemia
gluc>30
osmolality >320
no ketonaemia/acidosis

114
Q

mx hyperosmolar hyperglycaemic state

A
  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
  3. aim for fluid balance 3-6 L by 12 h
  4. eat and drink asap
115
Q

what can adrenal haemorrhage cause

A

primary adrenal insufficiency

116
Q

emergency mx preimary adrenal insufficeincy

A

hydrocortisone 100mg IV STAT then 50mg 6hrly
IV fluids 0.9% NaCL
tx hypoglycaemia
refer endo

117
Q

mx sev hyponatraemia

A

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
Q

what should Na rise be limited to in low Na tx

A

less than 10 in first 24h
then less than 8 in next 24h
risk myelinolysis

119
Q

what can cause pituitary apoplexy

A

prolactinoma

120
Q

what is pituitary apoplexy

A

bleeding into pituitary
imapired blood supply pituitary

121
Q

sx pituitary apoplexy

A

sudden headache and visual field defects/double vision

122
Q

mx pituitary apoplexy

A

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
Q

hypercalcaemia mx

A

IV fluid: 4-6L NaCl 24h
bisphosponate: zolendronic acid 4mg over 15m
calcium nadir from 2-4d
tx cause

124
Q

what diabetes meds can cause euglycaemia ketoacidosis

A

SGLT2i

125
Q

HDU referral DKA

A

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
Q

what to be aware of in DKA mx

A

hypoglycaemia - is why you need dextrose cover when give insulin

finals (31 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions