Diseases of suprarenal gland
Transcript of 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