Adrenal Patho And Physio Flashcards
Addison’s disease Definition and symptoms
Adrenal insufficiency / failure to produce hormones
Weight loss-not for diagnosis
Fatigue
Weakness
Dizziness upon standing
Abdominal pain
Suspended menstrual cycles
Dehydration
Increased potassium in blood
Decreased sodium in blood
Low BP
Skin discoloration
Depression
Cushing’s syndrome Definition and symptoms
Hyperadrenocorticism
Weight gain
Lipodystrophy-buffalo hump
Moon face/temporal filling
Dial action of capillaries-telengiectasis- stretch marks
Excessive sweating-hyperhidrosis
Hirsutism
Low libido
Impotence
Amenorrhea/Infertile
Polyuria/dipsia
Hypokalemia
High BP
2 types of glucocorticoids
Cortisol
Corticosterone
1 type Mineralcorticoid and origin
Aldosterone From zona glomerulosa
1 type androgen
Androstenedione
Aldosterone description and what happens in absencence
Required for reabsorbtion of Na in exchange for K
In absence plasma K inc. (arrhythmia)
Plasma Na and Cl dec.
Dec. volume
Dec. CO
RESULTS IN SHOCK/ HYPOTENSION/ DEATH in 2 weeks
MOA Aldosterone
Diffused into tubular cells Bind to proteins Hormone-receptor complex enters nucleus to make mRNA of sodium channels and Na-k ATPase
How to increase aldosterone. 6 ways
High K in ECG
Dec BP
Dec. blood volume
RAAS
Low Na
ACTH-pituitary hormone
Glucocorticoids definition and MOA and origin
Hormones are responsible for RESPONDING TO STRESS
MOA: similar to aldosterone but results in metabolism
* cortisol produces faster effect
Decrease BG/ muscle weakness
Susceptible to stress-death
From zona fasciculata
Glucocorticoids in glucose metabolism
Increase: gluconeogenesis/ glycogen synthesis in liver
Decrease: Glycolysis/ glucose transport into cells Effect:increase blood glucose (adrenal DM)
Glucocorticoids in liver metabolism
Increase: movement of fat FROM adipose tissue / plasma FFA/oxidation of FA
increase hepatic glucose PRODUCTION by inc. substrate availability via proteolysis and lipolysis
****induce hyperinsulemia and insulin resistance, tx as DM2
Decrease: glucose used in adipocytes/TG synthesis
Glucocorticoids in protein metabolism
Increase: catabolism
Decrease: stores in all tissues EXCEPT liver/ synthesis/ AA transport into extra patio tissues/ formation of RNA in extraheoatic tissues In liver: increase AA transport/ synthesis/ plasma proteins/ gluconeogenesis
Effect: transfer of AA FROM MUSCLE TO LIVER
Inflammatory pathway
Increase cell damage
Histamine cause vasodilation Increase capillary permeability
Increase infiltration of leukocytes
Glucocorticoids and inflammation intervention
Increased stabilization of lysosomal membrane = decrease release of enzymes
Cortisol dec. vasodilation
Cortisol decrease capillary permeability
Cortisol dec. migration of leukocytes
Cortisol secretion
- CRH
- ACTH
- Cortisol
- inhibits
- Stimulate
- Promote
- Inhibit
ACTH function/ origin
Adrenocorticotrophic hormone Stimulated by CRH From hypothalamus Released from anterior pituitary
Causes: Cortisol secretion from adrenal cortex (zone fasciculata) Aldosterone secretion from adrenal cortex (zone glomerulosa) Bind to melanocytes to increase melanin
Androgens definition and origin
Weak androgens secreted then converted to testosterone by peripheral tissues. Stimulate pubic and axillary hair growth and sexual drive in females
From zona reticularis
Adrenal Medulla Hormones and function
Epinephrine: Increase blood glucose Increase fat breakdown in fat tissues Dilation of bv in skeletal muscle and cardiac muscle
Epi and NE: Inc. HR and force BV constriction in skin/ kidneys/ GI
Diagnosis of low aldosterone secretion
EKG: T wave is high from K Blood work for aldosterone
Diagnosis of low glucocorticoids
Blood cortisol levels
Increased ACTH
3 Addisons causes
Autoimmune response against cortical tissue
Bacterial infection
Cancer
Addison’s diagnosis and treatment
Dianosis: Measure ACTH will be high
Inject or with 250mcg corticotropin (ACTH) if no rise in cortisol positive diagnosis normal rise is >20mcg/dl
Treatment: Aldosterone injection AND Glucocorticoid injection or oral
Hydrocortisone 300mg IV daily & taper to LIFELONG maintenance dose of 15-20mg AM 5mg PM
2/3 dose in AM 1/3 dose PM (stimulate circadian G production)
Fludricortisone 0.1mg daily
3 causes of Cushing’s disease and effects
Hyperplasia of adrenal corticies (increased ACTH)
Increased cortisol from tumer
Hyperplasia of adrenal corticies in non- pituitary tissues
Brackett’s reasons
systemic inflammatory diseases
solid organ transplant
cancer
steroid administration
Effects: Increased androgens- hair and infertility in women Increased fat movement- buffalo hump Increased BP- b/c mineralcorticoid activity Increased glucose, Increased protein catabolism-muscle-weakness/ low immunity/ osteoporosis
Diagnosis of Cushing’s
Diagnosis:
- Measure plasma cortisol will be high
- normal serum cortisol
- 16-20 mcg/dl in AM
- 6-10 mcg/dl
- Dexamethasone suppression test
- increased ACTH
- normal <80
LDT: 1 mg dexamethasone/ no change in cortisol is abnormal = cushing’s
HDT: 8mg dexamethasone
- less cortisol cushing’s is from pituitaty ACTH producing tumor
- no change in cortisol cushing’s is from adrenal tumor or ectopic ACTH producing tumor
