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Pathology Block 11 > Endocrine Path > Flashcards

Endocrine Path Flashcards

1
Q

Endocrine disorders

A 
Diabetes 
Thyroid diseases 
Parathyroid diseases 
Pituitary disorders 
Adrenal dysfunction
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2
Q

Insulin is released by _____ of the ______

A

B cells of the pancreas

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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

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4
Q

What does insulin consist of

A

A, B, C chain

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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
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6
Q

When is insulin secreted

A

When blood glucose is high

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7
Q

What transports glucose into B cells

A

GLUT2

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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
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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
—

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10
Q

What does insulin cause

A

Storage of excess energy

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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

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12
Q

What does insulin ultimately do

A

Decreases blood glucose levels
Decreases blood fat levels
Decreases blood amino acid levels

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13
Q

Group of diseases with common presentation of hyperglycemia

A

DM

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14
Q

Normal FBGL

A

> 70-100

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15
Q

Blood glucose >100-150

A

Prediabetic

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16
Q

Fasting blood glucose <125

A

Diabetic

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17
Q

Expense of diabetics

A

245 bill a year

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18
Q

Diabetics are predisposed to numerous other diseases and complication

A

Retinopathy, cataracts, glaucoma
MI, HTN, stroke, atherosclerosis
Impaired wound healing, gangrene, neuropathy

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19
Q

How do we divide the types of DM

A

Based on why someone is hyperglycemia

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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
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21
Q

Treatment of insulin dependent type I diabetes

A

Lifelong insulin therapy

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22
Q

Most common DM

A

Non-insulin dependent diabetes-90% of all diabetes cases

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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
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24
Q

Treatment of DMII

A

Blood glucose control

  • wt loss, exercise, inproved dietary control
  • metformin
  • sulfonylureas
  • thiazolidinedione
  • SGLT2 inhibitors
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25
Q

What is the most important drug for DMII

A

Metformin

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26
Q

What does metformin do

A

Tells liver to stop making glucose. Increases insulin sensitivity too

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27
Q

What do sulfonyureas do

A

Increase insulin production, but at expense of B cells

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28
Q

What do thiazolidinediones do

A

Increases insulin sensitivity

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29
Q

SGLT2 inhibitor does what

A

Reduce kidney reuptake of glucose

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30
Q

Which of the following is true for type I but not type II DM?

A

Administration of exogenous insulin resolved the hypoglycemia

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31
Q

Where do we want to keep plasma glucose

A

Above 60ish

-dont go too high though bc DM

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32
Q

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?

A

The patient is overweight

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33
Q

what releases TRH

A

Hypothalamus

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34
Q

What releases T-SHIRT

A

Anterior pituitary

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35
Q

What releases T3 and T4

A

Thyroid

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36
Q

Which is more potent? T3 or T4

A

T3

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37
Q

HPT axis

A

Production of thyroid hormone (T3/T4)

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38
Q

What are the master metabolic hormones

A

T3/T4

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39
Q

How does TS3/T4 work

A
  • signals through a steroid pathway
  • bone growth and maturation
  • CNS maturation
  • increases BMR and heat production
  • increases all body metabolism
  • increases CO
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40
Q

Why is different about T3/T4?

A

It is a peptide hormone, but acts like a steroid

  • carried by binding proteins
  • activates intracellular receptor
  • directly initiates transcriptional changes
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41
Q

Disease of thyroid

A

Hyperthyroidism

Hypothyroidism

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42
Q

Too much T3/T4

A

Hyperthyroidism

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43
Q

Graves’ disease

A

Hyperthyroidism

-Ab bind to activate TSH receptor on thyroid

44
Q

Problems with hyperthyroidism

A 
Weight loss, increased appetite 
Heat intolerance, sweating 
Increased CO
Exopthalmos (overactive SNS to lids)
Goiter
45
Q

How is hyperthyroidism Dx

A

Measuring serum TSH and T3/T4 levels

46
Q

TX of hyperthyroidism

A

Remove the thyroid/tumor

-appears as a goiter

47
Q

Not enough T3/T4

A

Hypothyroidism

48
Q

Hashimotos

A

Hypothyroidism

-most common

49
Q

What are the tow most common types of hypothyroidism

A

Hashimotos

Iodine deficiency

50
Q

Most common hypothyroidism in underdeveloped countries

A

Iodine deficiency

51
Q

Symptoms of hypothyroidism

A
  • weight gain, cold intolerance
  • low CO
  • mental slowness, lack of energy
  • myxedema: swollen puffy skin
52
Q

Dx of hypothyroidism

A

Requires TSH serum levels

53
Q

Treatment of hypothyroidism

A

Give them exogenous T3/T4 or iodine

54
Q

Cretinism

A

Congenital hypothyroidism due to poor diet of mother

55
Q

Symptoms of cretinism

A

Learning disabilities
Growth inhibited
Protruding tongue
Umbilical hernia

56
Q

Hashimotos

A
  • 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
Q

First signs of hypothyroidism (hashimotos)

A

Goiter

58
Q

Enlarged thyroid gland, most often caused by low iodine, also by too much cabbage

A

Goiter

59
Q

When do you get a goiter

A

Hyper or hypothyroidism

60
Q

What can a goiter lead to

A

Tumors due to increased cellular proliferation, hypertrophy, and stress

61
Q

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

A

Low serum TSH levels

62
Q

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

A

Low dietary iodine

63
Q

4 glands under the thyroid

A

Parathyroid glands

64
Q

What do parathyroid glands release

A

PTH from chief cells

65
Q

What does PTH respond to

A

Serum ionized calcium levels

  • release in response to low levels
  • works to raise blood calcium levels
66
Q

Actions of PTH

A
  • 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
Q

Primary hyperparathyroidism

A

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
Q

Secondary hyperparathyroidism

A
  • 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
Q

Hypoparathyroidism

A

-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
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

A

Hypercalcemia

71
Q

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

A

Loss of bone strength

72
Q

Anterior posterior pituitary release

A

A lot of stimulating hormones as well as growth hormone

73
Q

Non-functioning tumor, congenital, due to ischemic, or radiation damage

A

Hypopituitarism

74
Q

What can hypopituitarism result in

A

Slow loss of most downstream glandular function

  • FSH and LH are usually lost first
  • GH is second
  • thyroid and ACTH are usually lost
75
Q

What hormone axis can hypopituitarism affect

A

Can affect only a single hormone axis or many

-secondary hypo-whatever-ism

76
Q

Usually due to a tumor in the pituitary gland, most are one cell type and will produce too much of only one hormone

A

Hyperpituitarism

77
Q

What hormone does not have a downstream gland from the pituitary

A

GH

78
Q

Mechanism of GH

A

JAK STAT

-alter transcription and translation

79
Q

Regulates blood levels of all energy sources, causes protein synthesis and organ growth, causes linear bone growth

A

GH

80
Q

What does GH produce

A

Somatomedins which function like GH in some target tissues

81
Q

GH deficiency

A

Usually due to pituitary damage

82
Q

Congenital GH deficiency

A

Failure to grow and develop normally in first months

Must give GH allow to catchup growth

83
Q

Children-acquired GH deficiency

A
  • short stature, possible dwarfism if not corrected
  • underdeveloped features
  • poor bone density
  • low muscle mass
  • late to puberty
84
Q

Adults-acquired GH defiance

A
  • loss of lean muscle, obesity
  • poor bone density
  • increased risk of cardiovascular disease
85
Q

GH excess

A

Due to tumor

-syomtpsm Demond on time of excess

86
Q

Newborns and children GH excess

A
  • pituitary gigantism
  • rare
  • increases linear growth, very tall
  • usually early death due to overgrowth if organs
  • predisposition to DM, HTN, osteoporosis
87
Q

GH excess in adults

A
  • 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
Q

Paired organs on top of kidneys

A

Adrenal glands

89
Q

What do adrenal glands produce

A

Glucocorticoids (cortisol)
NE and Epi
Mineralocorticoids (aldosterone)
-under control of RAAS and K

90
Q

Stress hormone that increases protein catabolism, FA utilization and maintaineence of blood glucose levels

A

Cortisol

91
Q

Starvation hormone

A

Cortisol

92
Q

Stimulates gluconeogensis by liver

A

Cortisol

  • liver produces glucose from other sources like fat, and proteins
  • causes muscle breakdown to provide AA to liver
93
Q

Anti-inflammatory and immunosuppression in cortisol

A
  • inhibits production of inflammatory molecules
  • inhibits proliferation of lymphocytes
  • inhibits platelets activation
94
Q

Hypercortioslim

A

Monst common cause is taking glucocorticoids (cortisol)

95
Q

Cushings

A
  • 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
Q

What is hypocortisolism due to

A

Autoimmune destruction of adrenal cortex

-also common after TB

97
Q

Addison’s diseases

A

Hypocortisolim

  • adrenals dont produce enough cortical hormones
  • hypoglycemia and weight loss, muscle weakness
  • Hypotension, hyperkalemia, metabolic acidosis
  • hyperpigmentation
98
Q

Hyperpigmentation from Addison’s

A

Course due to overproduction of ACTH

  • ACTH and MSH come from same protein
  • bronze skin and dark gums
99
Q

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

A

Tuberculosis

100
Q

Tumors of chromaffin cells

A

Pheochromocytoma

101
Q

What do chromoffin cells make

A

NE and epi

102
Q

Where are chromaffin cells reside

A

Adrenal medulla

-can come from any neural crest derived cell

103
Q

Predominant symptom of pheochromocytoma

A

HTN

  • usually episodic with tachycardia, sweating, HA, and apprehension
  • increases risk of sudden MI and cardiac arrest
104
Q

Dx of pheochromocytoma

A

Imaging and serum levels of Ne and EPi metabolites

105
Q

How do you five pheochromocytoma

A

Remove the tumor

Pathology Block 11 (8 decks)

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