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Transcript of Endocrine Pathophysiology
Effects on Metabolism
NRS 233 - Pathophysiology II
Copstead, L. & Banasik, J. (2018).
(6th ed.). St. Louis, MO: Elsevier.
Giddens, J. (2017).
Concepts for nursing practice
(2nd ed.). St. Louis, MO: Elsevier Mosby.
YouTube videos embedded on some slides.
Chronic Primary Adrenocortical Insufficiency -
e.g., Gimme' some of that
...and what happens when the feedback loop is bypassed, interrupted, or dysfunctional.
...or too little.
e.g., T3 & T4 from the thyroid gland
for release of insulin from pancreatic beta cells is the rise and fall of blood glucose stimulating GLUT1 carriers on pancreatic beta cells
Acute Complications of Diabetes:
Monitor & control:
Serum Blood Levels
Clues to Source of Altered Secretion
Can occur after high-dose glucocorticoid therapy
Results from damage to the adrenal gland
Depression impairs normal feedback inhibition of
with depression/stress -
HPA axis feedback from cortisol
Cortisol is designed to promote survival via short-term
When inappropriately prolonged, results in the development of
& the development of
in fat or muscle cell
Develops < one day
Develops > one day
More common with
- relative absence of insulin = lipolysis and ketoacid production
More common with
- some insulin prevents ketoacid production by facilitating complete metabolism of fatty acids by hepatocytes
< Osmotic diuresis >
progresses to proteinuria
Autonomic (e.g., gastroparesis)
Depends upon the speed of beta-cell destruction
Autoimmune attack on the beta-cells - Type IV hypersensitivity
T-cells induce apoptosis
Tissues dependent upon insulin for glucose transport do not have glucose
Body resorts to protein catabolism & lipolysis for energy
lack of insulin"
lack of insulin"
Lack of exercise
Insulin resistant tissues
1. Fat cells
2, Resting skeletal muscle cells
Dysfunction in chain of events that normally results in GLUT4 glucose transporters being inserted into cell membrane
from stimulation of melanocytes by high levels of
Symptoms by Hormone-Type Deficiency
- Medical emergency related to acute deficiency of
Changes in connective tissue in the dermis and deposition of proteins and lipopolysaccharides cause
throughout the body
Increases cellular metabolism
Type II hypersensitivity
Autoantibody activation of TSH receptors on thyroid cells
Escapes normal negative feedback loop
Pretibial non-pitting edema
Exaggerated symptoms of hyperthyroidism
Increased HR & T
Agitation, delirium, psychosis, stupor, coma
N/V, abdominal pain
If due to hypopituitarism, there is often a concommitant adrenal insufficiency
A three-year-old Jack Russell terrier developed a very fat body and began having frequent skin infections.
When his muscles became so weak that he couldn't climb stairs, his owner took him to a veterinarian who referred them to a dog endocrinologist.
The dog's owner reported that the dog was diagnosed with Cushing syndrome and an "electrolyte disorder."
Explain to the dog's owner:
1) Why her dog developed a fat body
2) Why he had frequent infections
3) Why his muscles became weak.
Talk to the Dog's Owner