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Endocrine > endocrine diseases-adrenal > Flashcards

endocrine diseases-adrenal Flashcards

1
Q

difference cushing syndrome and cushing disease

A

cushing syndrome= adrenal gland excess cortisol

cushing disease= pituitary excess ACTH

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2
Q

symptoms of cushing syndrome

A 
anabolic= elevated glucose- DM
catabolic=
muscle weakness
poor wound healing
easy brusing
infertility
stretch marks 
high cholesterol 
depression
memory loss 
skin ulcers
uncontrolled muscle protein breakdown
increased fat 
osteoporosis
unctonrolled appetitie
central fat deposition
moonface
excess mineralocorticoid action= hypertension
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3
Q

2 main types of hypertension

A

primary=idiopathic

secondary=endocrine, vascular damage and neoplastic disease, aldosteronism

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4
Q

3 causes of primary hyperaldosternoism

A

conn’s syndrome
bilateral adrenal hyperplasia
Glucocorticoid remediable aldosteronism

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5
Q

what is conn’s syndrome

A

unilateral adrenal tumour

aldosterone producing adenoma

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6
Q

phenotype of conn’s

A 
high aldosterone
high sodium
low renin
low potassium
ECF expansion
hypertension
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7
Q

management of conn’s syndrome

A

surgical
venous sampling
ct scan
unilateral adrenalectomy

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8
Q

what is bilateral adrenal hyperplasia

A

idiopathic

most common PA 60-70%

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9
Q

phenotype for bilateral adrenal hyperplasia

A 
high aldosterone
low renin
high sodium
low potassium
ECF expansion
hypertension
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10
Q

treatment for bilateral adrenal hyperplasia

A

anti-hypertensives
MR blockers
spironalactone
eplernone

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11
Q

what is glucocorticoid remediable aldosteronism

A

ACTH driven
autosomal dominant genetic disorder
-hybrid gene of unequal meiotic exchange so get 11obhase promoter and AS coding region
- aka driven by ACTH not angiotensin II

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12
Q

phenotype of glucocorticoid remediable aldosteronism

A 
high aldosterone
high sodium
low potassium
low renin
ecf expansion
hypertension
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13
Q

treatment for glucocoritcoid remediable aldosteronism

A

suppress pituitary ACTH secretion

-synthetic glucocorticoid dexamethasone

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14
Q

causes of secondary hyperaldosteronism

A

high renin

  • renin secreting JG tumour
  • renal arterial stenosis
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15
Q

what is a renin secreting JG tumour

A

renin hypersecretion

increase RAAS

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16
Q

phenotype for secondary aldosteronism

A 
high renin
high aldosterone
MR activation
high na
low k
ecf expansion
hypertension
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17
Q

treatment for secondary aldosteronism

A

surgical removal of tumour

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18
Q

what is renal arterial stenosis

A

low perfusion pressure so get increased renin
secretion
cycle: vasoconstriction increased stenosis

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19
Q

treatment for renal arterial stenosis

A 
anti-hbp
MR blockers
statins
anti-platelets
balloon angioplasty
stent
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20
Q

excess cortisol 2 types

A

cushing syndrome= adrenal problem

cushing disease=pituitary tumour

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21
Q

phenotype for cushing’s

A 
high cortisol
low k
high na
low aldosterone and renin 
high bp
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22
Q

cushing syndrome versus cushing disease phenotype

A

cushing syndrome=low plasma ACTH high cortisol

cushing disease= high acth and cortisol

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23
Q

treatment for cushing disease plus 3 main drugs

A
  • trans-sphenoidal hypophysectomy
  • adrenalectomy
  • pituitary radiotherapy
  • adrenal synthesis inhibitors: metyrapone and ketoconazole
  • somatostatin analogue: pasireotide
24
Q

treatment for cushing syndrome

A

stop steroids
remove tumour
radiotherapy tumour

25
Q

metabolic syndrome and link to 11bHSD

A

11bhsd type 1 found in fat, liver and brain
increased in obesity
activates cortisol

26
Q

11bhsd inhibitors function

A

improve hba1c and reduce cortisol improving memory

27
Q

how does cortisol elevate hypertension

A
  1. inhibits vascular nitric oxide production from arginine by eNOS (nitric oxide synthase)
  2. potentiate catecholamine action increasing Cardiac output, resistance and adrenaline
  3. activate the kidney MR normally prevented by converting to cortisone- increase NA pull
28
Q

causes of glucocorticoid hyperactivity 6

A
  1. cushing syndrome
  2. cushing disease
  3. apparent mineralocorticoid excess
  4. liquorice ingestion and drugs
  5. CAH 11obhase deficiency
  6. Pheocromrocytoma
29
Q

what is apparent mineralocorticoid excess

A

autosomal recessive loss of function in 11bhsd2

-loss of conversion of cortisol to cortisone

30
Q

phenotype apparent mineralocorticoid excess

A 
high Na
Ecf expansion
low k
low renin
low aldosterone
severe childhood hypertension
31
Q

treatment for apparent mineralocorticoid excess

A

MR antagonists
spironalactone
eplerone
low sodium and k+ diet

32
Q

what causes hypertension from liquorice ingestion

A

glycyrrhizinc acid
and carbenoxolone
inhibitors of 11bhsd2

33
Q

phenotype liquorice ingested hypertension

A

high sodium
low potassium, renin, aldosterone
episodic HBP

34
Q

what is congenital adrenal hyperplasia 11obhase deficiency

A

blocks in ZF formation of cortisol

35
Q

how does 11b ohase cause hypertension

A

decrease cortisol

increase ACTH as decrease feedback so increase substrates DOC and deocortisol that act weakly at MR increase receptors

36
Q

what type of gene disorder are the CAH

A

autosomal recessive

37
Q

what does CAH 21 ohase cause

A

increased ACTH causes hyperplasia

  • enlarged adrenals
  • steroidogenesis towards androgens= virilisation
  • low sodium
  • low blood p
  • high renin and potassium
38
Q

what is pheochromocytoma

A

catecholaime secreting tumour of adrenal medulla

chromaffin cell tumour secretes adrenaline

39
Q

phenotype of pheochromocytoma- increase catecholamies adrenaline

A 
increase glucagon
decrease insulin
increase HR
vasoconstriction
increase glycogen and lipid breakdown
peripheral resistance
40
Q

treatment for pheochromoctyoma

A

alpha and beta blockers

41
Q

what MEN syndrome is pheochromocytoma

A

MEN 2b

multiple endocrine neoplasia

42
Q

what genetic inheritance is MEN

A

autosomal dominant causes overactivity and enlargement of some endocrine glands leading to hormonal changes

43
Q

symptoms of pheochromocytoma

A 
PHE
palpitation
headache
episodic swelling
hypertension
DM
44
Q

how much does endocrine hypertension count for hypertension

A

10-15%

45
Q

testing for cushing’s disease

A

overnight dexamethasone suppression test
-give glucocorticoid dexamethasone as should negative feedback ACTH
-low dose suppress pituitary ACTH in normal
-high dose suppress in pituitary adenoma but not ectopic adenoma ACTH
<50

46
Q

what is the test for Addison’s disease

A

synACTHen stimulation test
-give ACTH
if addison’s disease then won’t respond to ACTH <430

47
Q

tests for acromegaly

A

OGTT and GH will NOT be suppressed

-glucagon stimulation test

48
Q

conn’s syndrome test

A

saline suppression test

49
Q

difference between primary and secondary adrenal insufficiency and their phenotype

A

primary=lack of steroids and MR due to adrenal-Addison’s disease
secondary= hypopituitarism lack glucocorticoids but normal mineralocorticoid

50
Q

causes Addison’s disease

A
  • autoimmune 80%
  • infection HIV or TB
  • metastases
  • amyloid
  • haemorrhage waterhouse-friederichsen
  • congenital
  • surgery
51
Q

5t’s of addison’s disease

A 
tired
tears
tummy 
thin 
tanned
52
Q

symptoms of primary adrenal insufficiency

A 
weakness
tired
anorexia
nausea and vomiting
weight loss
hyperpigmentation 
postural hypotension
vitiligo and other autoimmune conditions
53
Q

symptoms of secondary adrenal insufficiency

A 
weak, tired
anorexia
nausea and vomiting
hypopigmentation
weight loss
postural hypotension
other hypopituritarism signs
54
Q

treatment for adrenal insufficiency emergencey

A

IV access 2-3 litre saline

hydrocorisone 100mg IV 6hrly

55
Q

treatment maintenance for adrenal insufficiency

A

hydrocortisone 10-15mg on waking
5-10mg in evening
fludrocortisone 0.95-0.1mg

56
Q

sick day rules for adrenal insufficiency

A

double your dose for 2 days

57
Q

what is an incidentaloma

A

tumour that is found incidentally on CT when investigating for other

Endocrine (14 decks)

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