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Endocrine Pathophysiology

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Katrina Dielman

on 21 May 2016

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Transcript of Endocrine Pathophysiology

Overview of

Endocrine Function

Adrenocortical Disorders:
Cushing Syndrome

vs.

Addison Disease
Thyroid Disorders:
Effects on Metabolism

Endocrine Pathophysiology
NRS 233 - Pathophysiology II
Pre-Diabetes:
Glucose Intolerance
Diabetes
Clinical Manifestations:
Hypo
vs.
Hyperglycemia
Complications:
Acute

vs.

Long-Term
References
Copstead, L. & Banasik, J. (2013).
Pathophysiology
(5th ed.). St. Louis, MO: Elsevier.

Felver, L. (2013). Online Materials:
PROP- Pathophysiology online.
Retrieved from https://evolve.elsevier.com/

Giddens, J. (2013).
Concepts for nursing practice
(1st ed.). St. Louis, MO: Elsevier Mosby.

YouTube videos embedded on some slides.
Cushing Syndrome:
Hypercortisolism
Addison Disease:
Chronic Primary Adrenocortical Insufficiency -
Cortisol
&
Aldosterone
e.g., Gimme' some of that
feedback
!
...and what happens when the feedback loop is bypassed, interrupted, or dysfunctional.
Long-Term Complications:
Microvascular

vs.

Macrovascular
Retinopathy
Nephropathy
Atherosclerosis
Stroke
CAD/MI
Especially appropriate
feedback inhibition
!
Too much...
...or too little.
e.g., T3 & T4 from the thyroid gland
e.g., TRH
e.g., TSH
e.g., CRH
e.g., ACTH
The normal
feedback loop
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:
Diabetic Ketoacidosis

vs.

Hyperosmolar Syndrome
Neuropathy
Monitor & control:
BP
Lipid profile
Glucose
Accelerated!
Comparison:
DMT1

vs.

DMT2
Serum Blood Levels
=
Clues to Source of Altered Secretion
Cortisol
Level
High +
High +
Low +
Low +
ACTH
Level
Low =
High =
High =
Low =
Diagnosis
Tumor
in adrenal gland
Tumor
in anterior pituitary
Damage
to adrenal gland
Hypopituitary adrenal insufficiency
Secondary

Adrenal Insufficiency
Can occur after high-dose glucocorticoid therapy
Primary
Adrenal Insufficiency
Results from damage to the adrenal gland
Causes
The
"fed"
state
Example:
Depression impairs normal feedback inhibition of
cortisol
release
HPA axis
up-regulated
with depression/stress -
CRH receptors
HPA axis feedback from cortisol
down-regulated
-
GRs
Cortisol is designed to promote survival via short-term
catabolism
,
insulin resistance
&
gluconeogenesis
, and
immunosuppression
When inappropriately prolonged, results in the development of
metabolic syndrome

Chronic stress
& the development of
glucose intolerance
from
down-regulation
of GLUT4
glucose transporters
in fat or muscle cell
When
severe
...
SNS activation
Osmotic diuresis
Polyuria
& polydipsia
Kussmaul respirations
Abdominal pain
Nausea/vomiting
Develops < one day
Polyuria

+/- polydipsia
Confusion/lethargy
Develops > one day
More common with
DMT1

- relative absence of insulin = lipolysis and ketoacid production
More common with
DMT2
- some insulin prevents ketoacid production by facilitating complete metabolism of fatty acids by hepatocytes
< Osmotic diuresis >
Microalbuminuria
progresses to proteinuria
Sensory
Motor
Autonomic (e.g., gastroparesis)
Vascular dementia
DMT2 Metabolism
DMT1 Metabolism
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
"
Absolute
lack of insulin"
"
Relative
lack of insulin"
Lack of exercise
Insulin resistant tissues
1. Fat cells
2, Resting skeletal muscle cells
3. Hepatocytes
Dysfunction in chain of events that normally results in GLUT4 glucose transporters being inserted into cell membrane
Cushing
Syndrome
vs.
Disease
Obesity
causes
down-regulation
of
insulin receptors
on cells
Hyperpigmentation
from stimulation of melanocytes by high levels of
ACTH
Loss of
cortisol
=
Hypoglycemia
Hypotension
Loss of
aldosterone
=
ECV deficit
Hyperkalemia
Symptoms by Hormone-Type Deficiency
Adrenal Crisis
- Medical emergency related to acute deficiency of
cortisol
Severe weakness
Postural tachycardia/hypotension
Cardiovascular collapse
Death
Hyperthyroidism:
Graves Disease
Hypothyroidism
Myxedema:

Changes in connective tissue in the dermis and deposition of proteins and lipopolysaccharides cause
doughy edema
throughout the body
Thermoregulation
Increases cellular metabolism
"Thyrotoxicosis"
Type II hypersensitivity
reaction
Autoantibody activation of TSH receptors on thyroid cells
Escapes normal negative feedback loop
Dermopathy:
Pretibial non-pitting edema
Thyroid storm:
Exaggerated symptoms of hyperthyroidism
Increased HR & T
CNS symptoms
Agitation, delirium, psychosis, stupor, coma
GI symptoms
N/V, abdominal pain
Myxedema coma:
Life-threatening hypothyroidism
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
Full transcript