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97 Cards in this Set

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In which 2 conditions do you get aggressive red marks on the abdomen?
-Pregnancy
-Cushings disease
-(some overweight ppl)
Adrenal glands-
2 glands in one
What is made in the adrenal cortex?
-Steroid hormones :- -->GCS(cortisol)
--> mineralocorticoids(aldosterone)
--> some androgens/sex steroids
Adrenal medulla ?
Catecholamine synthesis: epi and norepi.
Disease state assoc. with adrenal medulla?
Pheochromocytomas.
3 parts of cortex?
-Zona Glomerulosa
-Zona Fasciculata
-Zona Reticularis
Zona glomerulosa produces?
Mineralocorticoids-aldos.
Zona fasciculata produces?
GCS(cortisol) + some androgens
Zona reticularis produces?
Sex steroids,androgens and cortisol.
What is common between the structures of aldosterone and cortisol?
both have 4 ring structure common to all steroids.
Cortisone
biologically inactive metabolite of cortisol.
Congenital Adrenal Hyperplasia is due to
Deficiency of 21-OHase -->cortisol and aldos. synthesis decreased--->Increased ACTH-->increase in all other steps=increased synthesis of Testosterone(precocious puberty)
Precocious puberty in CAH is
pseudopuberty as it is not switched on by hypothalamus.
Newly synthetized steroid hormones are
Rapidly secreted from the cell.(little storage)
What % of circulating cortisol is free?
10 %
Cortisol have -ve feedback mechanisms on both
Hypothalamus and pituitary.
DHEA and DHEA sulfate?
Androgen precursors.
Actions of GCS ?
-Stimulation of gluconeogenesis(liver)
-Mobilisation of A.A(muscle)
-Stimulation of lipolysis(adipose tissues)
-Immunosuppression.
Check cycle of GCS on metabolism.
OK!
Effects of GCS on muscle?
-Increased pz degradation
-Decreased protein synthesis
-Decreased glc use
-DECREASED insulin sensitivity
Effects of GCS on liver ?
-Increased glycogen storage
-Increased gluconeogenesis
Effect of GCS on fat?
-Decreased glc use
-DECREASED insulin sensitivity
-Increased lipolysis.
Due to GCS,liver sends
glc to fat and muscles
Due to effects of GCS,fat sends
Increased glycerol to liver
Due to effects of GCS,muscle sends
Increased A.A to liver
Effects of GCS on CNS ?
Decreased CRH and ADH secretion --> sleeplessness,mood changes,psychosis.
Effects of GCS on Cardiovas. system ?
Increased sensitivity to vasoconstrictors causing HT
Effects of GCS on GIT system?
Increased gastric acid secretion causing peptic ulcer.
Effects of GCS on lungs?
Increased surfactant prod. in fetus
Effects of GCS on pituitary ?
Decreased ACTH secretion causing decreased release of other trophic hormones,growth retardation.
Effects of GCS on immune system ?
Decreased inflammatory response causing increased susceptibility to infection.
Cushings disease(hyperadrenocorticism) ?
-HT
-Apparent obesity
-Muscle wasting
-Thin skin
-Metabolic derangements(diabetes)
Most common signs and symptoms of Cushings syndrome?
-Moon facies
-Obesity
-HT
-Menstrual disorders
-hirsutism
-Violaceous striae,bruisability.
-Osteoporosis.
-Ankle edema
-buffalo hump
-Acne
Causes of Cushings ?
-Excessive endogeneous production of cortisol.
-Administration of GCS(SE of tx in asthma,lupus)
Check diagram of Cushings pt in lectures.
OK!
ACTH-secreting pituitary adenomas, which cause adrenals to grow in size and secrete more cortisol, can also
Impinge on optic chiasm.
Addison's disease can be lethal.
True
Addison's disease-
Hypoadrenocorticism where adrenal glands atrophy with deficiency of cortisol and aldosterone.
Clinical findings of Addison's ?
-CVS disease
-Lethargy
-Diarrhea
-Weakness
A pt with Addison's can have increased pigmentation on hands and in buccal mucosa.
True-pigmentation due to increase in ACTH which also act on melanocytes.
In most cases of Addisons,
Adrenals wasted away.
In CAH,what happens to adrenals?
Both increase in size(hyperplastic) due to increased ACTH (but secretion from adrenals blocked)
What is the rule of thumb with trophic hormones?
-if they act long enough,glands get bigger.
-if trophic hormones decrease,glands shrink.
Clinical uses of aldosterone and cortisol ?
-Replacement if inadequate production in pituitary disease and Addison's disease.
-GCS have potent anti-inflammatory properties( asthma,arthritis,dermatitis,autoimmune diseases)
What happens when cortisone is given to pts,even though it is bilogically INACTIVE ?
Metabolized in liver to CORTISOL.(cortisone is a kind of pre-drug)
CGS have quite potent mineralocorticoids properties.
True
Prednisolone is how many times more potent than cortisol ?
5 times more!!
Dexamethasone is
75 times more potent than cortisol.
Which steroid would you give to a pt with deficiency of mineralocorticoids?
Fludrocortisone.
Prednisolone
1 1/2 tablets
GCS have exactly same mineralocorticoid activity as they have glucocorticoid activity.
True(except for synthetic ones)
What regulates aldosterone secretion ?
-Increase K+ conc. in extracellular fluid
-Angiotensin 2
Renin is made from
Juxtaglomerular cells.
Renin acts on
Angiotensinogen which is converted into Angiotensin 1
Angiotensin 2 acts on
pituitary/ACTH levels and adrenal glands.
Aldosterone
Regulates Na+ and K+ conc. in extracR fluids.
Actions of Aldosterone ?
-Increased resorption of Na+
-Increased resorption of water
-Increased EXCRETION of K+ from kidney distal tubule.
Removal of adrenal glands leads to
Death within just a few days due to loss of MINERALOCORTICOID activity.
Secondary hyperaldosteronism is
Very common in old ppl with heart failure,liver disease.
What happens in 2ry hyperaldosteronism(for eg in pt with HF or renal artery stenosis)?
-Decreased intravascular space(body thinks it doesnt have enough salt/water) which leads to increased Aldosterone release---> oedema.
Sequence of events in 2ry hyperaldosteronism in pt with renal stenosis?
Increased renin-->increased Ang 2-->increased aldos.-->increased Na+ retention-->increased K+ loss.
Clinical findings with 2ry hyperaldosteronism ?
-Increased renin
-Increased aldosterone
E.g of primary hyperaldosteronism ?
Adrenal adenoma--> Increased aldos. --> HT ( leads to Conns syndrome)
Mechanism of patho. changes in 1ry hyperaldosteronism ?
Increased aldos. from tumour-->increased Na+ retention-->increased K+ loss-->decreased renin-->decreased Ang. 2
Clinical findings in 1ry hyperaldosteronism ?
-Decreased renin
-Increased aldos. (typical of Conn's syndrome)
Mechanism of GCS and Mineralocorticoid action ?
-Cross cell mb(lipid soluble)
-Enter all cells
-Bind to specific receptors
-Receptors dimerise and bind to coactivator pz
-Receptor complex binds to specific DNA sequences
-Regulate gene expression
-Action is via pz synthesis.
Glucocorticoids and Mineralocorticoids RECEPTORS -
-hormone dependent transcription factors
-steroid action occurs through regulation of responsive genes
-tissue-specific effects occur through diff. genes.
The mineralocorticoid Receptor binds both aldosterone and cortisol with equal affinity.
True
How can aldos. stimulate specific bio. effects when blood conc. of cortisol are 2000-fold higher than aldos. ?
In aldos. responsive cells,cortisol is effectively destroyed to cortisone,allowing aldos. to bind to its receptor w/o competition.
What happens with aldos. resistance to 11beta-hydroxysteroid dehydrogenase ?
Severe HT(excess GCS bind to receptors)-like Conns syndrome
Epinephrine and thyroxine are both derived from which A.A ?
tyrosine
Epinephrine
Cardiovascular and lipolysis.
Adrenaline and Norad. made in same cells.
FALSE-separate cells!
Rate limiting step in synthesis of epi and norepi ?
Tyrosine hydroxylase step
Adrenaline synthetized by
PNMT and SAM
Feedback inhibition is made by ?
Norad. on TH
Sequence of steps in synthesis of Epi ?
-Tyrosine-->DOPA-->Dopamine-->Norepi-->Epi
Adrenal medullary hormones stored in ?
-Chromaffin granules(6 molar)
-with ATP and opiod peptides
Secretion of adrenal medullary hormones via ?
-Splanchnic nerve
Secretion of epi and norepi is stimulated by ?
-ACh released from sympathetic nerve terminals
-In response to exercise,hemorrhage,hypoglycemia,trauma,stress
Elimination of adrenal medullary hormones lasts for
Few min (circulating half life)
Adrenal medullary hormones degraded by
-COMT
-MAO
Adrenal medullary hormones achieve their physiological effects by
Binding to 7 tms metabotropic adrenergic Receptors coupled to G pz.
Adrenal Medullary Hormones mechanism of action ?
-Stimulation or inhibition of intracR signalling pathways(via cAMP)
How does epi achieve fat mobilization in adipose tissue?
-Via cAMP protein kinase stimulation of lipase
How does epi achieve glycogenolysis in muscle tissue?
Via cAMP protein kinase stimulation of Phosphorylase.
Physiological effects of Adrenal medullary hormones :-
-Increased rate and force of contraction of heart muscle(via Beta AR)
-Constriction of BV(NA)
-Dilation of bronchioles
-Increased metabolic rate
-Dilation of pupils
-Inhibition of GIT and motor activity.
Alpha 1 receptor ?
binds epi /norepi --> increased free Ca2+
Alpha 2 receptor ?
binds epi/norepi--> decreased cAMP
Beta 1 receptor ?
binds to epi/norepi-->increased cAMP
Beta 2 receptor ?
binds to EPI only!!--> increased cAMP.
Pheochromocytomas ?
Adrenal medulla tumours producing high levels of Epi.
Cortisol,aldos. and sex hormone precursors secreted in
Adrenal cortex
Cortisol regulated by ?
CRH from hypothalamus and ACTH from pituitary(ant.)
Aldosterone reg. by
K+ and RAAS.
Cortisol and aldos. are ?
Steroids which act via GR and MR.
Epi and Norepi are ?
Stress hormones secreted by adrenal medulla.