1
Q
Endocrine disorders
A
Diabetes Thyroid diseases Parathyroid diseases Pituitary disorders Adrenal dysfunction
2
Q
Insulin is released by _____ of the ______
A
B cells of the pancreas
3
Q
Pancreas
A
Accessory organ in GI
Releases blood sugar homeostasis hormones and GI enzymes
Groups of cells called islets of langerhans release hormones
4
Q
What does insulin consist of
A
A, B, C chain
5
Q
During production of insulin, what is removed
A
C chain
- secreted with insulin
- can be used to tell about type I and type II DM
6
Q
When is insulin secreted
A
When blood glucose is high
7
Q
What transports glucose into B cells
A
GLUT2
8
Q
What happens when glucose is transported in to the B cells
A
- glucose oxidized to produce ATP
- High ATP levels cause closure of K channels
- store
9
Q
What does insulin bind
A
Receptor tyrosine kinase
-receptors phosphorylate themselves and become active
-phosphorylate other proteins insicde the cell
—IRS-1 and other activcated proteins affect cellular function
—
10
Q
What does insulin cause
A
Storage of excess energy
11
Q
Decreased blood glucose
A
Causes GLUT4 to be instrted in cell membranes
Glucose is taken up by cells and stored as glycogen
Reduced gluconeogensis
12
Q
What does insulin ultimately do
A
Decreases blood glucose levels
Decreases blood fat levels
Decreases blood amino acid levels
13
Q
Group of diseases with common presentation of hyperglycemia
A
DM
14
Q
Normal FBGL
A
> 70-100
15
Q
Blood glucose >100-150
A
Prediabetic
16
Q
Fasting blood glucose <125
A
Diabetic
17
Q
Expense of diabetics
A
245 bill a year
18
Q
Diabetics are predisposed to numerous other diseases and complication
A
Retinopathy, cataracts, glaucoma
MI, HTN, stroke, atherosclerosis
Impaired wound healing, gangrene, neuropathy
19
Q
How do we divide the types of DM
A
Based on why someone is hyperglycemia
20
Q
Insulin dependent diabetes
A
- 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
21
Q
Treatment of insulin dependent type I diabetes
A
Lifelong insulin therapy
22
Q
Most common DM
A
Non-insulin dependent diabetes-90% of all diabetes cases
23
Q
Non-insulin dependent DM- type II
A
- 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
24
Q
Treatment of DMII
A
Blood glucose control
- wt loss, exercise, inproved dietary control
- metformin
- sulfonylureas
- thiazolidinedione
- SGLT2 inhibitors
25
What is the most important drug for DMII
Metformin
26
What does metformin do
Tells liver to stop making glucose. Increases insulin sensitivity too
27
What do sulfonyureas do
Increase insulin production, but at expense of B cells
28
What do thiazolidinediones do
Increases insulin sensitivity
29
SGLT2 inhibitor does what
Reduce kidney reuptake of glucose
30
Which of the following is true for type I but not type II DM?
Administration of exogenous insulin resolved the hypoglycemia
31
Where do we want to keep plasma glucose
Above 60ish
| -dont go too high though bc DM
32
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
33
what releases TRH
Hypothalamus
34
What releases T-SHIRT
Anterior pituitary
35
What releases T3 and T4
Thyroid
36
Which is more potent? T3 or T4
T3
37
HPT axis
Production of thyroid hormone (T3/T4)
38
What are the master metabolic hormones
T3/T4
39
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
40
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
41
Disease of thyroid
Hyperthyroidism
| Hypothyroidism
42
Too much T3/T4
Hyperthyroidism
43
Graves’ disease
Hyperthyroidism
| -Ab bind to activate TSH receptor on thyroid
44
Problems with hyperthyroidism
```
Weight loss, increased appetite
Heat intolerance, sweating
Increased CO
Exopthalmos (overactive SNS to lids)
Goiter
```
45
How is hyperthyroidism Dx
Measuring serum TSH and T3/T4 levels
46
TX of hyperthyroidism
Remove the thyroid/tumor
| -appears as a goiter
47
Not enough T3/T4
Hypothyroidism
48
Hashimotos
Hypothyroidism
| -most common
49
What are the tow most common types of hypothyroidism
Hashimotos
| Iodine deficiency
50
Most common hypothyroidism in underdeveloped countries
Iodine deficiency
51
Symptoms of hypothyroidism
- weight gain, cold intolerance
- low CO
- mental slowness, lack of energy
- myxedema: swollen puffy skin
52
Dx of hypothyroidism
Requires TSH serum levels
53
Treatment of hypothyroidism
Give them exogenous T3/T4 or iodine
54
Cretinism
Congenital hypothyroidism due to poor diet of mother
55
Symptoms of cretinism
Learning disabilities
Growth inhibited
Protruding tongue
Umbilical hernia
56
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
57
First signs of hypothyroidism (hashimotos)
Goiter
58
Enlarged thyroid gland, most often caused by low iodine, also by too much cabbage
Goiter
59
When do you get a goiter
Hyper or hypothyroidism
60
What can a goiter lead to
Tumors due to increased cellular proliferation, hypertrophy, and stress
61
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
62
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
63
4 glands under the thyroid
Parathyroid glands
64
What do parathyroid glands release
PTH from chief cells
65
What does PTH respond to
Serum ionized calcium levels
- release in response to low levels
- works to raise blood calcium levels
66
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
67
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
68
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
69
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
70
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
71
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
72
Anterior posterior pituitary release
A lot of stimulating hormones as well as growth hormone
73
Non-functioning tumor, congenital, due to ischemic, or radiation damage
Hypopituitarism
74
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
75
What hormone axis can hypopituitarism affect
Can affect only a single hormone axis or many
| -secondary hypo-whatever-ism
76
Usually due to a tumor in the pituitary gland, most are one cell type and will produce too much of only one hormone
Hyperpituitarism
77
What hormone does not have a downstream gland from the pituitary
GH
78
Mechanism of GH
JAK STAT
| -alter transcription and translation
79
Regulates blood levels of all energy sources, causes protein synthesis and organ growth, causes linear bone growth
GH
80
What does GH produce
Somatomedins which function like GH in some target tissues
81
GH deficiency
Usually due to pituitary damage
82
Congenital GH deficiency
Failure to grow and develop normally in first months
| Must give GH allow to catchup growth
83
Children-acquired GH deficiency
- short stature, possible dwarfism if not corrected
- underdeveloped features
- poor bone density
- low muscle mass
- late to puberty
84
Adults-acquired GH defiance
- loss of lean muscle, obesity
- poor bone density
- increased risk of cardiovascular disease
85
GH excess
Due to tumor
| -syomtpsm Demond on time of excess
86
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
87
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
88
Paired organs on top of kidneys
Adrenal glands
89
What do adrenal glands produce
Glucocorticoids (cortisol)
NE and Epi
Mineralocorticoids (aldosterone)
-under control of RAAS and K
90
Stress hormone that increases protein catabolism, FA utilization and maintaineence of blood glucose levels
Cortisol
91
Starvation hormone
Cortisol
92
Stimulates gluconeogensis by liver
Cortisol
- liver produces glucose from other sources like fat, and proteins
- causes muscle breakdown to provide AA to liver
93
Anti-inflammatory and immunosuppression in cortisol
- inhibits production of inflammatory molecules
- inhibits proliferation of lymphocytes
- inhibits platelets activation
94
Hypercortioslim
Monst common cause is taking glucocorticoids (cortisol)
95
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
96
What is hypocortisolism due to
Autoimmune destruction of adrenal cortex
| -also common after TB
97
Addison’s diseases
Hypocortisolim
- adrenals dont produce enough cortical hormones
- hypoglycemia and weight loss, muscle weakness
- Hypotension, hyperkalemia, metabolic acidosis
- hyperpigmentation
98
Hyperpigmentation from Addison’s
Course due to overproduction of ACTH
- ACTH and MSH come from same protein
- bronze skin and dark gums
99
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
100
Tumors of chromaffin cells
Pheochromocytoma
101
What do chromoffin cells make
NE and epi
102
Where are chromaffin cells reside
Adrenal medulla
| -can come from any neural crest derived cell
103
Predominant symptom of pheochromocytoma
HTN
- usually episodic with tachycardia, sweating, HA, and apprehension
- increases risk of sudden MI and cardiac arrest
104
Dx of pheochromocytoma
Imaging and serum levels of Ne and EPi metabolites
105
How do you five pheochromocytoma
Remove the tumor
Pathology Block 11
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