Download - Diseases of suprarenal gland
Diseases of suprarenal gland
Fedor Šimko
Institute of Pathophysiology LFUK
Disclimer slide –prednáška je určená len na
výučbové potreby medikov LFUK v Bratislave
Fedor Šimko
Hormones of suprarenal gland
Glucocorticoids – fasciculata layer
Mineralocorticoid – glomelurose layer
Androgenes (estrogenes)– reticular layer
Catecholamines- suprarenal medulla
(chromafine cells)
Syntheis of Glk and ALD –in the suprarenal cortex
cholesterol progesteronepregnenolone
11-deoxycorticosterone
Corticosterone
ALDOSTERONE
17-hydroxypregnenolone
11-deoxycortizol
Cortizol
Min
era
loco
rtic
oid
eff
ects
Androgenes synthesis
cholesterol progesteronepregnenolone
androstendione
TESTOSTERONE
11-hydroxy-
androstendion
Dehydroepi-
androsterone
Regulation of corticoid secretion
(ACTH-RH –ACTH-- Gluk – neg. feedback)
Regulation of aldosterone secretion renin – Ang II- AT1R- aldosterone
Androgens regulation
ACTH –trophic effect on suparenal gland
glucocorticoids
ACTH (TSH,STH) ACTH (TSH,STH)
Hypothalamo-adenohypophyseal system
Releasing factors
RF
Trophic hormones-TH
adenohypophysis adenohypophysis
inhibiting factors
IF
Aldosterone-
stimulation
Angiotensin II
HyperkalemiaAdrenocorticothrophic
hormone
Glucocorticoid functions
- gluconeogenesis ( from amino acids)
- Reduction of glycolysis (hexokinase
inhibition)
- Glycogenolysis activation
- inhibition of insuline binding to receptors
- Reduction of glucose reabsrobtion in
distal tubes
•Proteosynthesis / proteolysis
•Lipolysis/lipogenesis- fat redistribution
Hyperglykémia - glykosúria
Glucocorticoid functions
-Atiinflammatory and antialergic effects:
-Proteocatabolism in lymfatic tissue
-Stabilisation of lysosomes
-Reduced capillary permeability
-Reduced bradykine production (by inhibition of
kalikrein in lysosomes)
-Stimulation of hematopoesis
Hyperglykémia - glykosúria
Aldosterone functions
1. Reabsorbtion of Na+ and H2O in
dist. tubuli of kidnies (also in salivary or
swet gland)
2. Na+/K+ exchange – hypokalemia, alkalosis
3. Hypertrophy of vascular musculature and fibrotic proliferation
Androgen functions
-Proteosynthesis
-Musculature growth
-Bone growth – enlargement of bone
longevity – (before closure of growth gaps)
Sex organs growth and maturation
Secondary sex signs
Libido development
Cushing´s sy. a Cushing´s disease
Def: overproduction of corticoids (cortisol)
Etiology and classification:
-Primary (Cush.sy.)- adenoma /
adenocarcinoma of suprarenal cortex – ACTH
reduced
-Secondary (Cushing´s disease)– excessive
production of CRH/ACTH – TU of hypophysis /
hypothalamus / or ectopic production – ACTH
increased
Cushing´s sy. a Cushing´s disease
Clinical manifestations:
Hyperglycemia /steroid diabetes mell.
Hypertension (volume enlargement)
Hypernatremia/ hypokalemia + alkalosis
Strie rubrae – weekness of subcutaneous fibrotic tissue- hemorrhagy
Fat tissue redistribution – buffle type obesity / moon face
Cushing´s sy. / Cushing´s disease
Clinical manifestation
- Osteoporosis (glukoneogenesis from bone amino-acids) + reduced
calcium resorbtion
- Atrophy of musculature and of lymfatic tissue
- Peptic ulcer – (increased HCl + reduced mucin production)
- Polyglobulia + eozinopenia
- Face pletora- (polyglobulia + arteriolar dilatation)
- Oligomenorrhea + loss of libido
- Endocrinne psychosyndrome
Addisson´s syndrome - hypocorticism
Def: insufficiency of suprarenal cortex (defficiency
of Glk, Ald, Andr)
Etiology and classification:
-TBC, hemorrhage, autoimune damage,
meningococcus sepsis
-Sudden withdrawal of corticoid therapy
-pathogenesis: signs of deficit of Glk, Ald, Andr
+ insufficient response to stressors
Addisson´s disease
Classification
- Primary – destruction of suprarenal cortex
ACTH is increased – hyperpigmentations (MSH)
-Secondary – destruction of hypothalamus / hypophysis
-ACTH is decreased, reduced propiomelanocortin – pallor
-Chronic – Addison´s disease
-Acute – Waterhaus-Friderichsen sy. – hemorrhagic
destruction of suprarenal gland / sudden interruption of
hormone - replacement therapy
Addison´s disease – peripheral,
central
Manifestations:
-Weekness, fatigue, loss of weight
-Hypotension/hypovolemia, hypoglycemia
-Anemia / leukopenia /eozinophilia, muscular a-
trophy
-Abdominal pain, vomiting (by reduced NaCl)
-Low Na+, high K+, acidosis
-hyperpigmentations –peripheral / pallor –central
-Bradypsychism, anxiety, end. psychosyndrome
Addison´s crisis
Acute destruction of suprarenal cortex
Etiology: infections-sepsis + hemorrhagy,adrenalectomy/sudden interruption of corticoid therapy
Manifestations:
Depletion of NaCl, hyperkalemia, acidosis hypovolemia
Abdominal pain, weekness
Polyuria, vomitting, diarrhea,
hypotension, shock
Somnolency, sopor
Primary hyperaldosteronism –
Cohn´s sy.
Deffinition: Autonomic increase of
aldosterone production
Etiology: adenoma/adenocarcinoma of
suprarenal cortex
Primary hyperladosteronism –
Cohn´s sy.
Clinical manifestations:
Hypokalemia - muscular weekness,
obstipation, dysrrhytmias
Hypokalemic nephropathy: polyuria,
proteinuria, nykturia, polydipsia, hypo / izostenuria,
alkalosis
Hypernatremia, hypertension (volume), hypertensive heart
Secondary hyperladosteronism
Def: compensatory mechanism in states
with hypovolemia and hypotension
Etiology: heart failure, nephrotic syndrome, liver
cirrhosis
Manifestations:
-hypotension
-hypokalemia
-Increased both - renin and aldosteron
Cause of Ald increase in
HF / liver cirrhosis / nephrotic sy.
Kidney
hypoperfusion-
renin release
decreased
aldosteron degradation
In damaged liver
Secondary hyperaldosteronismheart failure, nephrotic syndr, liver cirrhosis
extravasal loss of fluid –
hypovolemia + hypotension
Renin – angiotensin II – aldosterone
vasoconstriction + fluid retention
increased BP and volume
- hemodynamic improvement fibrotic
remodelling
Feochromocytoma
Def: excessive production of catecholamines (adr, NA)
Etiology: adenoma of suprarenal medulla /adenoma
of sympathetic ganglions
Classification:
paroxysmal (Adr) / continual form (NA)
adenoma / adenocarcinoma(10%)
in suprarenal medulla / in ganglions (10%)
Feochromocytoma
Manifestation:
Paroxysmal hypertension, hypertension crisis
(Adr)
Continual hypertension (NA)
Hypotension, paroxysmal hypotension – Adr
Vasodilatation via β2 receptors
hypovolemia – via postcapillary vasoconstriction followed
by intestitial edema (reduced volume / BP, swetting,
vomitus)
Feochromocytoma
Clinical manifestations:
Hypertension / hypertensive crisis:
- cefalea
- stenocardia, palpitations, tachycardia, dyspnea
- nausea / vomitting / abdominal pain
- pallor / cold swetting
- nervousness, anxiety, anger
- Increased catecholamines in blood and urine
Adr- paroxysmal, NA- continuous