Endocrine Path Flashcards
Endocrine disorders
Diabetes Thyroid diseases Parathyroid diseases Pituitary disorders Adrenal dysfunction
Insulin is released by _____ of the ______
B cells of the pancreas
Pancreas
Accessory organ in GI
Releases blood sugar homeostasis hormones and GI enzymes
Groups of cells called islets of langerhans release hormones
What does insulin consist of
A, B, C chain
During production of insulin, what is removed
C chain
- secreted with insulin
- can be used to tell about type I and type II DM
When is insulin secreted
When blood glucose is high
What transports glucose into B cells
GLUT2
What happens when glucose is transported in to the B cells
- glucose oxidized to produce ATP
- High ATP levels cause closure of K channels
- store
What does insulin bind
Receptor tyrosine kinase
-receptors phosphorylate themselves and become active
-phosphorylate other proteins insicde the cell
—IRS-1 and other activcated proteins affect cellular function
—
What does insulin cause
Storage of excess energy
Decreased blood glucose
Causes GLUT4 to be instrted in cell membranes
Glucose is taken up by cells and stored as glycogen
Reduced gluconeogensis
What does insulin ultimately do
Decreases blood glucose levels
Decreases blood fat levels
Decreases blood amino acid levels
Group of diseases with common presentation of hyperglycemia
DM
Normal FBGL
> 70-100
Blood glucose >100-150
Prediabetic
Fasting blood glucose <125
Diabetic
Expense of diabetics
245 bill a year
Diabetics are predisposed to numerous other diseases and complication
Retinopathy, cataracts, glaucoma
MI, HTN, stroke, atherosclerosis
Impaired wound healing, gangrene, neuropathy
How do we divide the types of DM
Based on why someone is hyperglycemia
Insulin dependent diabetes
- 10% of all DM cases
- autoimmune disorder
- type I (juvenile)
- no insulin produced
- increases blood levels of glucose, lipids, and proteins
- muscle wasting
- diabetic ketoacidosis due to utilization of fats as energy source
- diuretics, acidosis, and hyperkalemia
Treatment of insulin dependent type I diabetes
Lifelong insulin therapy
Most common DM
Non-insulin dependent diabetes-90% of all diabetes cases
Non-insulin dependent DM- type II
- adult
- loss of insulin sensitivity due to chronic high levels of blood glucose (insulin resistance)
- make insulin, body does not respond to
- usually in older, abuses, HTN individuals
- retinal problems due to loss of auto regulation of blood flow
Treatment of DMII
Blood glucose control
- wt loss, exercise, inproved dietary control
- metformin
- sulfonylureas
- thiazolidinedione
- SGLT2 inhibitors
What is the most important drug for DMII
Metformin
What does metformin do
Tells liver to stop making glucose. Increases insulin sensitivity too
What do sulfonyureas do
Increase insulin production, but at expense of B cells
What do thiazolidinediones do
Increases insulin sensitivity
SGLT2 inhibitor does what
Reduce kidney reuptake of glucose
Which of the following is true for type I but not type II DM?
Administration of exogenous insulin resolved the hypoglycemia
Where do we want to keep plasma glucose
Above 60ish
-dont go too high though bc DM
A patient presents to the office with a fasted blood glucose of 300 and a high serum insulin level. Which of the following is also likely?
The patient is overweight
what releases TRH
Hypothalamus
What releases T-SHIRT
Anterior pituitary
What releases T3 and T4
Thyroid
Which is more potent? T3 or T4
T3
HPT axis
Production of thyroid hormone (T3/T4)
What are the master metabolic hormones
T3/T4
How does TS3/T4 work
- signals through a steroid pathway
- bone growth and maturation
- CNS maturation
- increases BMR and heat production
- increases all body metabolism
- increases CO
Why is different about T3/T4?
It is a peptide hormone, but acts like a steroid
- carried by binding proteins
- activates intracellular receptor
- directly initiates transcriptional changes
Disease of thyroid
Hyperthyroidism
Hypothyroidism
Too much T3/T4
Hyperthyroidism
Graves’ disease
Hyperthyroidism
-Ab bind to activate TSH receptor on thyroid
Problems with hyperthyroidism
Weight loss, increased appetite Heat intolerance, sweating Increased CO Exopthalmos (overactive SNS to lids) Goiter
How is hyperthyroidism Dx
Measuring serum TSH and T3/T4 levels
TX of hyperthyroidism
Remove the thyroid/tumor
-appears as a goiter
Not enough T3/T4
Hypothyroidism
Hashimotos
Hypothyroidism
-most common
What are the tow most common types of hypothyroidism
Hashimotos
Iodine deficiency
Most common hypothyroidism in underdeveloped countries
Iodine deficiency
Symptoms of hypothyroidism
- weight gain, cold intolerance
- low CO
- mental slowness, lack of energy
- myxedema: swollen puffy skin
Dx of hypothyroidism
Requires TSH serum levels
Treatment of hypothyroidism
Give them exogenous T3/T4 or iodine
Cretinism
Congenital hypothyroidism due to poor diet of mother
Symptoms of cretinism
Learning disabilities
Growth inhibited
Protruding tongue
Umbilical hernia
Hashimotos
- autoimmune destruction of thyroid gland
- more common in 50ish year old women
- generation of anti-thyroid Abs, excessive inflammation and cell death in thyroid gland
- usually first signs are a goiter
First signs of hypothyroidism (hashimotos)
Goiter
Enlarged thyroid gland, most often caused by low iodine, also by too much cabbage
Goiter
When do you get a goiter
Hyper or hypothyroidism
What can a goiter lead to
Tumors due to increased cellular proliferation, hypertrophy, and stress
A patient presents to the clinic complaint of excessive sweating, reading heart, and weight loss. They also have bulging eyes. This patient could also have
Low serum TSH levels
You join a medical mission which travels the world aiding the poor in underdeveloped countries. One of your patients presents with a large mass on their neck, what is most likely cause
Low dietary iodine
4 glands under the thyroid
Parathyroid glands
What do parathyroid glands release
PTH from chief cells
What does PTH respond to
Serum ionized calcium levels
- release in response to low levels
- works to raise blood calcium levels
Actions of PTH
- increase phosphate excretion an caslcium reacbsoprtion from kidney and bone
- increases osteoclasts activity
- activates vitamin D to allow for better absorption of dietary calcium
Primary hyperparathyroidism
Usually due to a parathyroid tumor
-part of MEN1 and MEN2 pathologies
Hyperkalemia, weakened bones
Hypophosphotemia
Renal stones that may block the ureter
Constipation, depression
TX; remove tumor
Secondary hyperparathyroidism
- due to renal failure
- vit D must be activated in kidney
- initially a hypokalemia due to failed dietary absorption which increases PTH levels
- bones are dissolved and serum calcium is restored
- weakened bones
- possible calcification of some vessels
Hypoparathyroidism
-rare
-usually due to thyroid problem and removing it
-congenital or autoimmune destruction possible
Symptoms
-hypokalemia, huperphosphatemia
-muscle spasms and tetany
-cardiac arrhythmias
-increased ICP
-seizures
-clotting disroders q
A patient presents to the clinic with abnormally high PTH levels due to a tumor. His symptoms would most likely tremble which ionic balance
Hypercalcemia
A patient suffers a massive heart attack and goes into heart failure. After several years, his kidneys also begins to fail. Which fo the following would occur due to this
Loss of bone strength
Anterior posterior pituitary release
A lot of stimulating hormones as well as growth hormone
Non-functioning tumor, congenital, due to ischemic, or radiation damage
Hypopituitarism
What can hypopituitarism result in
Slow loss of most downstream glandular function
- FSH and LH are usually lost first
- GH is second
- thyroid and ACTH are usually lost
What hormone axis can hypopituitarism affect
Can affect only a single hormone axis or many
-secondary hypo-whatever-ism
Usually due to a tumor in the pituitary gland, most are one cell type and will produce too much of only one hormone
Hyperpituitarism
What hormone does not have a downstream gland from the pituitary
GH
Mechanism of GH
JAK STAT
-alter transcription and translation
Regulates blood levels of all energy sources, causes protein synthesis and organ growth, causes linear bone growth
GH
What does GH produce
Somatomedins which function like GH in some target tissues
GH deficiency
Usually due to pituitary damage
Congenital GH deficiency
Failure to grow and develop normally in first months
Must give GH allow to catchup growth
Children-acquired GH deficiency
- short stature, possible dwarfism if not corrected
- underdeveloped features
- poor bone density
- low muscle mass
- late to puberty
Adults-acquired GH defiance
- loss of lean muscle, obesity
- poor bone density
- increased risk of cardiovascular disease
GH excess
Due to tumor
-syomtpsm Demond on time of excess
Newborns and children GH excess
- pituitary gigantism
- rare
- increases linear growth, very tall
- usually early death due to overgrowth if organs
- predisposition to DM, HTN, osteoporosis
GH excess in adults
- acromegaly
- pituitary tumor
- growth of all soft tissues and organs
- cardio issues
- characteristics physical features
- growth of fingers, nose, wars
- no gain in height
- insulin resistance
- if pituitary tumor is large, can cause peripheral vision loss
Paired organs on top of kidneys
Adrenal glands
What do adrenal glands produce
Glucocorticoids (cortisol)
NE and Epi
Mineralocorticoids (aldosterone)
-under control of RAAS and K
Stress hormone that increases protein catabolism, FA utilization and maintaineence of blood glucose levels
Cortisol
Starvation hormone
Cortisol
Stimulates gluconeogensis by liver
Cortisol
- liver produces glucose from other sources like fat, and proteins
- causes muscle breakdown to provide AA to liver
Anti-inflammatory and immunosuppression in cortisol
- inhibits production of inflammatory molecules
- inhibits proliferation of lymphocytes
- inhibits platelets activation
Hypercortioslim
Monst common cause is taking glucocorticoids (cortisol)
Cushings
- hypercortosolisms
- adrenals produce too much cortisol
- hyperglycemia and weight gain
- central obesity, moon face, buffalo hump
- muscle wasting, HTN, striae
Virilization in women due to androgen production
What is hypocortisolism due to
Autoimmune destruction of adrenal cortex
-also common after TB
Addison’s diseases
Hypocortisolim
- adrenals dont produce enough cortical hormones
- hypoglycemia and weight loss, muscle weakness
- Hypotension, hyperkalemia, metabolic acidosis
- hyperpigmentation
Hyperpigmentation from Addison’s
Course due to overproduction of ACTH
- ACTH and MSH come from same protein
- bronze skin and dark gums
A patient presents with bronzed skin, weight loss and hypotension. As you review their medical chart which of the following would you likely see that may have controbiuted to their symptoms
Tuberculosis
Tumors of chromaffin cells
Pheochromocytoma
What do chromoffin cells make
NE and epi
Where are chromaffin cells reside
Adrenal medulla
-can come from any neural crest derived cell
Predominant symptom of pheochromocytoma
HTN
- usually episodic with tachycardia, sweating, HA, and apprehension
- increases risk of sudden MI and cardiac arrest
Dx of pheochromocytoma
Imaging and serum levels of Ne and EPi metabolites
How do you five pheochromocytoma
Remove the tumor
