nats notes other half Flashcards
Primary adrenal insufficiency-
issue with the gland
secondary adrenal insufficiency
issue stimulating the gland
primary adrenal insufficiency results in
addisons
addisons symptoms
chronic malaise lassitude/lethargy fatigue that is worsened by exertion and improved with bed rest weakness generalised anorexia weight loss
signs
Gastrointestinal complains Hypotension Electrolyte abnormalities Hypoglycaemia Hyperpigmentation
hypoglycaemia in addisons is due to
depleted cortisol
hyperpigmentation in addisons is due to
due to increased ACTH
causes of addisons
auto-immune infection Infiltration Infarction Haemorrhage Adrenoleukodystrophy
diagnosing adrenal insufficiency
Synacthen test
what is Synacthen test
synthetic ACTH
what is increased in addisons
ACTH
where does ACTH come from
anterior pituitary
Autoimmune Poly-glandular Syndromes
group of rare diseases characterized by autoimmune activity against more than one endocrine organ
when is ACTH reduced
secondary adrenal insufficiency
what type of APS is more common in children
APS type 1
APS type 1
chronic mucocutaneous candidiasis
hypoparathyroidism
Addison’s disease
APS type 2
Addison’s disease
autoimmune thyroid disease
diabetes mellitus
what can adrenal crisis in addisons be precipitated by
infection
main factor precipitating adrenal crisis
mineralocorticoid
biggest manifestation of adrenal shock
hypotension
longterm treatment of addisons
Hydrocortisone
Fludrocortisone
Androgen replacement
HPA axis suppression
rules of steroids
never stop taking
carry card
double does in illness
cushings syndrome
prolonged exposure to elevated levels of glucocorticoids
most common cause of cushings
exogenous corticosteroid use
Cushing’s disease
ACTH producing pituitary adenoma causing hypercortisolaemia
ACTH dependant cushings causes
pituitary adenoma or ectopic ACTH production
ACTH independant cushings causes
majority cause by exogenous steroids or adrenal adenomas/carcinomas
diagnosis of cushings
blood abnormalities
raised WBC
hyperglycaemia
hypokalaemic metabolic alkalosis
humeral control of BP
RAAS
naural BP regulation
baroreceptors
where are the baroreceptors
aortic arch carotid bodies
what happens if BP increases (neural regulation)
If BP increases baroreceptors stimulate nucleus of solitary tract which stimulates vagus nerve to reduce HR and reduce BP
shocks
anaphylactic cardiogenic hypovolemic neurogenic septic
cardiac output equation
stroke X heart rate
pressure equation
flow X output
primary problems of hypovolaemia
low volume
fall in cardiac output
compensatory mechs of hypovolaemia
increased resistance (R), tachycardia, but cardiac output falls, hypotension
hypovolaemis signs
cold, clammy, peripheries
tachycardia
prolonged capillary refill time
empty veins
compensation of pump failure
increased resistance (R), tachycardia
clinical pump failure signs
cold, clammy peripheries
tachycardia
prolonged capillary refill time
raised JVP
vasodilation compensation
tachycardia, cardiac output rises
vasodilation signs
warm dry peripheries
tachycardia
short capillary refill time
BOUNDING pulse
signs of shock
oliguria
altered consiousness
intrinsic causes of pump failure
muscle, conduction tissue, valves
extrinsic pump failure
obstruction- pulmonary embolus
compression- tamponade (fluid fills the pericardium)
blood supply
tamponade
fluid fills the pericardium
