Adrenal Gland Flashcards
Describe function of mineralocorticoids
Inc Na+ conc in ECF & consequently inc ECF volume, which is imp in the long-term regulation of BP
On kidney, major site of action, act mainly at the late DCT & the collecting ducts, inc Na+ reabsorption in exchange with secretion of either K+ or H+
Outside kidney, inc Na+ absorption from other body fluids e.g. sweat & saliva as well se from GIT mucosa esp at colon.
Describe regulation of aldosterone secretion
- K+ ion conc in ECF: most potent a small inc in K+ cause severalfold inc in aldosterone. (most potent)
- Ang II: stimulates aldosterone secretion, also promotes growth of zona glomerulosa.(most potent)
- reduced Na+, BP, blood volume :via renin-angiotensin system,
4.ACTH has weak stimulant effect (it regulates aldosterone secretion during stress - ANP: inhibit aldosterone & renin
2ry hyperaldosteronism is caused by……..
Inappropriate high activity of renin-angiotensin system (may be due to dec renal blood flow)
List ionic distrurbances in Conn’s disease & their effect
- Hypernatremia, inc ECF & HTN but no or slight edema due to aldosterone escape
- Hypokalemia: severe muscle weakness, renal damage (hypokalemic nephropathy) as well as cardiac side effects
- Inc H+ secretion-> alkalosis->dec ionized Ca & tetany.
Explain aldosterone escape phenomenon
High doses of aldosterone lead to water retention and inc ECF however in few days this effect disappears & kidney escape from the effect of aldosterone, so the excretion of Na & water inc causing only slight edema this is due to tye inc ECF volume itself which leads to:
1. Pressure diuresis due to inc ABP
2. Naturesis & diuresis by ANP action
Describe transport of cortisol in plasma
75% bound to corticosteroid binding globulin (transcortin)
15% bound to albumin
10% free
The overall effect of cortisol metabolic actions is to……
Increase the blood glucose at tye expense of protein & fat stores.
Effect of cortisol on CHO
- Stimulation of gluconeogenesis & inc glucose release from the liver
- Dec the utilization of glucose by muscle & adipose tissue (anti-insulin effect)
The inc rate of gluconeogenesis & dec glucose utilization lead to rise in glucose & adrenal diabetes.
Describe effect of cortisol on protein metabolism
Cortisol stimulates protein degradation esp in muscle and inc amino acid plasma conc which is used in gluconeogenesis in liver as it dec AAs uptake by extrahepatic tissue. Dec RNA formation & protein synthesis in many tissues esp muscle & lymphoid tissue. Protein stores areduced in all body ex liver cells.
Cortisol inc plasma & liver proteins, its possible effect is to enhance AA transport into liver cells (but not to most other cells) and to enhance the liver enzymes required for protein synthesis.
Describe effect of cortisol on fat metabolism
It has lipolytic action, inc FFA in plasma which inc their utilization for energy.
Cortisol has permissive action to…….on…….
Catecholamines
Vascular smooth muscle (VC), lipolysis & bronchodilation
Mention effect of cortisol on:
1. Nervous system
2. Blood cells
3. Lung maturation
4. Water & electrolyte
- Influences nervous system as changes of electroencephalogram & personality that take place in adrenal insuffieciency are reversed only by cortisol
- Inc RBCs, platelets & neutrophils. Dec eosinophils, basophils, lymphocytes.
- Accelerates the maturation of surfactant in the lungs
- Promotes water excretion in the urine as result of inhibiting ADH, inc GFR, exerts weak mineralocorticoid effect.
List the anti-inflammatory effects
- Stabilizes lysosomal membranes
- Dec permeability of capillaries
- Dec both migration of white blood cells into the inflammed area & phagocytosis of the damaged cells.
- Suppress immune system (marked dec of lymphocyte reproduction)
- Attenuates fever: dec interleukin-1 from WBCs which is principal excitant to hypothalamic temp control system, dec temp reduces VD.
Describe immunosuppressive effect of cortisol
- Reduces circulating basophils & eosinophils
- Dec circulating lymphocytes & size of lymph nodes & thymus by inhibiting lymphocytic mitotic activity
- Reduces secretion of cytokines by inhibiting NF-KB on the nucleus, reduced IL-2 leads to dec proliferation of lymphocytes & these cells undergo apoptosis.
Dec output of T cells leading to dec immunity to all foreign invaders of the body.
Describe control of cortisol secretion
- Hypothalamic control: CRH secreted by hypothalamus in portal circulation
- Pituitary control: ACTH enhances all steps of cortisol synthesis, secreted in irregular bursts
- Negative feedback: long feedback loop
- Stress inc secretion
- Circadian rhythm: high rate of secretion in early morning & lowest in evening. This results from 24hr cyclic alteration in signals from hypothalamus
Causes of hypercortisolism
1ry: adrenocortical tumors that secrete cortisol
2ry: hypersecretion of ACTH from ant pituitary OR ACTH-secreting tumors located in places other than pituitary commonly in lungs
Most ofter iatrogenic by high pharmacological doses
Describe effect of Cushing syndrome on
1. Bone, muscle & skin
2. BP
3. Electrolytes
4. Nervous system
- Fracture with no apparent injury, spindly arms & legs due to muscle loss, purple striae, thin skin, poor wound healing & easy bruises
- Hypervolemia due to Na+ & water retention leading to HTN & edema. VC produced by inc vascular reactivity to CAs
- Hypokalemia & metabolic alkalosis
- Acceleration of basic EEG rhythm & produce mental abnormalities (irritability, anxiety, insomnia, motional disturbance, depression, toxic psychosis
Mention a symptom that differentiates ACTH dependent & independent
Inc skin pigmentation with ACTH
Adrenal androgens are ……
DHEA & androstenedione
Describe role of gonadocorticoids
- Enhancement of growth spurt
- Growth of acillary & pubic hair in m & f
- In adult females, partially, resposible for sex drive
Describe control of DHEA secretion
Stimulated by ACTH but has weak inhibitory effect on it instead has -ve feedback on GnHR
Definition & cause of adrenogenital syndrome
Due to excess adrenal androgen (more common) or estrogen)
In adults occur due to tumor of zona reticularis
In children occurs due to exposure of fetus to excess androgens as a result if congenital adrenal hyperplasia which occurs in deficiency of enzymes for glucocortidcoids synthesis thus thevmetabolic pathways are shunted to androgen production.
Describe features of adrenogenital syndrome in females
- Before birth: pseudohermaphrodite, genetically female with male external genitalia
-Growth of external genitalia (enlarged clitoris with fused labia)
-Penile-like appearance so that it is difficult to determine child sex
-Atrophic uterus, vagina & ovaries
-Presence of some prostatic tissue - Post-puberty: virilism, 2ry male sexual chchs in females as growth in skm, hirsutism, hairline recession up to baldness, deep coarse voice, suppression of female sex hormones with amenorrhea, infertility, atrophy of breast & external genitalia ex clitoris
Describe features of adrenogenital syndrome in males
- In young male: precocious pseudopuberty: development of 2ry sex chchs without sperm production
- Adult male: inapparent
