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MCPHS PA Pathophys Exam 3 Endocrine Flashcards

1
Q

What are the two classes of Hormones?

A

Protein and steroid hormones

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2
Q

Where do each class of Hormone bind?

A

Protein derived hormones bind on the cell surface.

Steroid derived Hormones diffuse accross the cell membrane and interact with intracellular receptors.

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3
Q

What are the two primary causes of Endocrine disorders?

A

Hormone imbalance (over or under production)

Mass / Lesion that can be non-functional (no hormone production) or Functional (abnormal hormone production)

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4
Q

What problems can develop with the Pituitary Gland?

A

Hyper/Hypopituitarism

Posterior Pituitary Syndromes

  • Central Diabetes Insipidus
  • SIADH
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5
Q

What is the basic structure of the Pituitary Gland?

A

The Pituitary is made of an Anterior Lobe (adenohypophysis populated with a portal vascular system to transport the hormones produced by the hypothalamus)

and

the Posterior Lobe (neurohypophyis, a collection of glial cells and axonal processes extending from the hypothalamus)

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6
Q

What hormones are released by the Pituitary Gland?

A

The Anterior releases FLAT PEG (FSH. LH, ACTH, TSH, PRL, Endorphins, GH)

and

the Posterior releases Oxytocin and ADH.

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7
Q

What is the Hypothalamus - Pituitary - ETC Axis?

A

An axis of control and feedback starting with the Hypothalamus extending through the Anterior Pituitary and ending at whatever the Hypothalamus is trying to control (ex. Adrenal gland, Thyroid gland). Hormones selected will refelct the end goal. Also once hormone levels rise enough they will negatively inhibit the Hypothalamus and pituitary.

Hypothalmus can use stimulating or inhibatory hormones.

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8
Q

What is a Sellar Mass?

A

A benign growth presenting on the Sella Turcica. 90% of these are Pituitary Adenomas.

Have the possibility of causing Hyperpituitarism if functional.

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9
Q

What are the main concerns with a Sellar Mass?

A

These benign growths can have pressure effects on thier surroundings.

They can cause visual disturbances by pressuring the Optic Chiasm

They may be functional and produce hormone abnormalities.

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10
Q

What are the classes of functional (Hormone releasing) pituitary adenomas?

A

Gonadotroph (LH or FSH / Most Common)

Thyrotroph (increased TSH)

Corticotroph (Cortisol / Cushing’s disease)

Lactotroph (Prolactin / hyperprolactemia)

Somatotroph (Growth Hormone / acromegaly)

Lactotroph / Somatotroph combos (Prolactin and GH)

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11
Q

What is Hypopituitarism?

A

Decreased secretion of hormones due to diseases of hypothalamus or pituitary.

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12
Q

What are the causes of Hypopituitarism?

A

Hypothalamic

Tumors (benign and metastic from lung, breast)

Radiation

Infection (Meningitis)

Pituitary

Mass (non-functional pituitary adenomas)

Pituitary Surgery / Radiation

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13
Q

What are the clinical features of Hypopituitarism?

A

Growth Failure (GH deficiency)

Amenorrhea / Infertility (women)

Decreased Libido / Impotence / Pubic and axillary hair loss (men) (LH & FSH deficiency)

Hypo thyroidism/adrenalism (TSH / ACTH deficiency)

Failure of Postpartum Lactation (Prolactin deficiency)

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14
Q

What are the Posterior Pituitary Syndromes?

A

Central Diabetes Insipidus

SIADH

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15
Q

What is Central Diabetes Insipidus?

A

Polyuria due to inability of Kidney to reabsorb water from Urine. Caused by ADH deficiency

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16
Q

What is the Etiology of Central Diabetes Insipidus?

A

Idiopathic

Head Trauma

Tumor

Inflammatory disorders of the hypothalamus/Pituitary

Surgical Complications

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17
Q

What is SIADH?

A

Syndrome of Inappropriate ADH secretion - Caused by excessive amounts of ADH leading to excessive amount of free water reabsoption resulting in hyponatremia.

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18
Q

What Causes SIADH?

A

Malignant neoplasm (ectopic ADH secretion)

Drug that increases ADH secretion.

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19
Q

What are the Diseases of Hyperthyroidism we went over in class?

A

Graves Disease

Goiter

Thyroiditis

Thyroid Storm

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20
Q

What types of Cells are found in the thyroid?

A

Follicular Cells

Parafollicular Cells (C Cells)

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21
Q

What is the function of Follicular Cells in the Thyroid?

A

These cells convert thyroglobulin into Throxine (T4) and lesser amount of Triiodothyronine (T3)

Cannot be produced in the absence of Iodine.

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22
Q

What is the function of Parathyroid (C) Cells?

A

They Synthesize and secrete Calcitonin (tones down blood calcium) which lowers blood Calcium levels by promoting absorption of calcium by the skeletal system, and inhibits reabsorption of bone by osteoclasts.

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23
Q

What regulates T3 and T4 production?

A

TRH is released from the hypothalamus to the Anterior Pituitary which releases TSH to the Thyroid which releases T3 and T4.

The liver may convert some T4 to T3 depending on the situation, and T3 and T4 in the circulatory system form a negative feedback loop with the Hypothalamus.

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24
Q

What is Hyperthyroidism?

A

A hypermetabolic state caused by elevated circulating levels of T3 and T4.

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25
In a radioactive iodine uptake test what does a normal or high radioiodine uptake indicate?
De novo synthesis of hormone.
26
In a radioactive iodine uptake test what does a near absent radioiodine uptake indicate?
Inflammation and destruction of thyroid tissue with release of preformed hormone into circulation An extrathyroidal source of thyroid hormone (medication etc)
27
What Hyperthyroid diseases have a normal or High radioiodine uptake?
Autoimmune (Graves disease or Hashitoxicosis) Autonomous Thyroid Tissue (Toxic Multinodular Goiter)
28
What Hyperthyroid diseases have a near absent radioiodine uptake?
Thyroiditis Exogenous Thyroid Hormone Intake Ectopic Hyperthyroidism
29
What is Graves Disease?
A syndrome that may consist of hyperthyroidism, goiter, eye disease (orbitopathy) and occasional dermopathy (scaley orangepeel / thick skin around the shins) Hyperthyroidism most common indication.
30
What is the cause of Graves Disease?
autoantibodies called TRAb that activate the TSH receptor. This stimulates thyroid hormone synthesis and secretion. May also cause thyroid growth (a goiter).
31
What are the three types of TRAb in Graves disease?
stimulating (most common in graves) blocking neutral
32
How does the type of TRAb in Graves disease effect presentation of symptoms?
Patients have a mix of Stimulating (most common), Blocking, and Neutral autoantibodies, symptoms will reflect whatever the current make-up is.
33
What do thyroid cells from PT's with autoimmune thyroid disease express?
MHC Class II molecules
34
What is the clinical significance of MHC class II molecules?
Class II molecules activate autoreactive T Cells, with the Potential for **Persistence** of thyroid disese.
35
What are the predisposing factors to graves disease?
Genetic susceptability Thyroid injury (Infection, Radiation, Drugs) Stress Sex Steroids Pregnancy
36
What is the Pathophysiology of Graves Opthalmopathy?
Autoantibodies stimulate the TSH receptors on orbital Fibroblasts which leads to increase hyaluronic acid production and new fat cells from adipocyte precursors. This leads to accumulation of HA and edema within the orbit and expansion of orbital muscle and fat volume.
37
What is the pathophysiology of skin in Graves disease?
Skin is warm and smooth, increased sweating, onycholysis (nail softening).
38
What is the cadiovascular effect of Graves Disease?
T3 is similar to beta adrenergic stimulation. increased HR and Contractility Increased LVEF and CO
39
What is an Autonomously-functioning thyroid adenoma?
A benign tumor that produces Thyroid Hormone (local increase in size of thyroid) Clinically present as a single nodule that is hyperfunctioning on radioisotope scan. Caused by muitations in TSH receptor stimulating thyroid cell division and hormone production.
40
What is a Toxic multinodular Goiter?
The most common benign thyroid Tumor. Need to determine - If it is Cancer - If it is cancer is it lethal? - Is it functional?
41
What is a Goiter?
Abnormal growth of the thyroid gland. Can be diffuse or nodular.
42
What are the main concerns about a Goiter?
Is it non-Toxic (makes normal amounts of TH) or Toxic (makes higher than normal amounts of TH leading to suppressed TSH).
43
What is the etiology of a goiter?
Iodine deficiency is the most common cause, other causes relate to a complex mix of genetic and environmental factors.
44
What forms a Goiter?
Increased TSH (with Iodine deficiency or Chronic autoimminue thyroiditis (Hashimoto's)) Increased growth factors (In Nontoxic multinodular goiters with normal TSH levels) TRAbs stimulating the TSH receptor (In Grave's) Genetic Factors
45
What is Thyroiditis?
A group of heterogeneous disorders that are characterized by some form of thyroid inflammation.
46
What is the course of Thyroiditis?
Hyperthyroid phase (characterized by damaged follicles and initial drop of T3/T4) Eurothyroid phase (no new hormone synthesis, but start of TSH release) Transient hypothyroid phase (peak of TSH and initiation of T3/T4 synthesis) Recovery Phase (Regen of thyroid Follicles)
47
What is a Thyroid storm?
A rare complication of hyperthyroidism characterized by severe clinical symptoms of thyrotoxicosis (Potentially fatal)
48
What is the Cause of thyroid storm?
Surgery / Infection / trauma in a OT with untreated or only partially treated thyrotoxicosis.
49
What is Hypothyroidism?
A structural or functional disorder anywhere in the hypothalamic / pituitary / thyroid axis that interferes with production of Thyroid Hormone.
50
What are the major causes of Hypothyroidism?
**Primary (in the thyroid)** Decreased T3 and T4 Increased TSH **Central (Hypothalamus or Oituitary)** Decreased TSH / TRH
51
What are the Major symptoms / signs of Hypothyroidism?
Slowing of metabolic processes Increased confusion / decreased mental status Lower cardiac function
52
What is Myxedema Coma?
Severe hypothyroidism causing the Function of multiple Organs to slow down. It is a medical emergency.
53
What are the hallmarks of Myxedema Coma?
Decreased mental status. Hypothermia High Mortality rate
54
What is Hashimoto's Thyroiditis?
Chronic autoimmune thyroiditis. Most common cause of hypothroidism in _iodine-sufficient_ areas of the world.
55
What causes Hashimoto's Thyroiditis?
A combination of genetic susceptability and environmental factors.
56
What are the clinical Characteristics of Hashimoto's Thyroiditis?
Gradual Thyroid Failure (with or without Goiter formation) High Serum concentrations of antibodies against thyroid antigens **Follicular destruction** (Antagonist antibodies perform cellular blockade on TSH receptors)
57
What Thyroid antigens are affected by Hashimoto's Thyroiditis?
Thyroglobulin (Tg) Thyroid Peroxidase (TPO) TSH Receptor
58
What is the role of B cells in Hashimoto's Thyroiditis?
They are the origin of the autoantibodies PT's have high serum concentrations of Tg and TPO TSH receptor antibodies block the TSH receptor
59
What is the role of T cells in Hashimoto's Thyroiditis?
Apoptic destruction of thyroid cells by activating Cytotoxic T cells Regulation of local Immune response
60
What is Thyroid Carcinoma?
A thyroid follicular epithelial-derived Cancer.
61
What are the 3 catagories of Thyroid Carcinoma?
Papillary (most common 85%) Follicular (12%) Anaplastic (\<3%)
62
What causes Thyroid Carcinoma?
Accumulation of multiple genetic alterations and progressive instability in signaling pathways. Genetic and epigenetic alterationc cause cell proliferation MAPK netwrok breakdown allowing proliferation differentiation and cell survival.
63
What are the primary risk factors of Papillary Carcinoma?
Thyroid radiation exposure during childhood Family history of Thyroid Cancer in 1st degree relative
64
What are the Clinical features of thyroid carcinoma?
Asymptomatic Thyroid Nodule May present with Hoarsness, dysphagia, cough, dyspnea (which suggest advanced state of disease)
65
What are the Parathyroid glands made out of?
Chief Cells (Create Parathyroid hormone) Oxyphil Cells
66
What is the relationship between calcium and phosphate ions in the blood?
They are inversely related.
67
What are the functions of the Calcium ion in the blood?
Bone minerlization Muscle contraction A co-factor in blood coagulation
68
What are the functions of Phosphate ion in the blood?
Formation of ATP Important cellular anion Major component of DNA/RNA and membrane bilayer Formation of hydroxyapatite crystals (bone mineralization)
69
How does Parathyroid Hormone increase blood Calcium Level?
**Minute to Minute** Stimulation of renal tubular calcium reabsorption Increaseing bone reabsorption **Chronically** Calcidiol -\> calcitriol in kidney - Stim Intestinal Calcium reabsorption - Increase Bone Reabsorption - Decrease renal calcium and phosphate excretion
70
What inhibits PTH?
Calcitriol FGF23 (also increases phosphate excretion)
71
What is Hyperparathyroidism?
**Primary** Autonomous overproduction of PTH (ususlly caused by Adenoma 85-95% most common clinical presentation asymptomaric hypercalcemia) **Secondary** Compensatory hypersecretion of PTH in response to prolonged hypocalcemia from Renal Failure **Tertiary** Persistant hypersecretion of PTH even after Renal Transplant.
72
What is CaSR?
An extremely sensative calcium sensing receptor (they are located on the Parathyroid cells, and throughout the body.
73
What type of CaSR mutations are possible?
Activating (meaning increased sensitivity to Ca) Inactivating (decreased sensetivity to Ca)
74
What is the cellular basis of Primary Hyperparathyroidism?
Decresed sensativity of the CaSR which leads to Hypercalcemia as well
75
What is the Etiology of Primary Hyperparathyroidism?
Radiation exposure Chronically low calcium intake Genetic Defect -Abnormalities in key proto-oncogenes or tumor supperssor genes
76
What are the Causes of Hypercalcemia?
Primary Secondary, and Tertiary Hyperparathyroidism Hypercalcemia of Malignancy
77
What is Hypercalcemia?
A condition in which the entry of Calcium into the blood excedds the excretion of Ca into urine or depostion in bone.
78
What is the etiology of Hypercalcemia?
Accelerated bone reabsorption Excessive GI absorption Decreased Renal excretion of calcium
79
What are the most common tumors causing Hypercalcemia in hypercalcemia of malignancy?
Breast Cancer, multiple myeloma, lymphoma, and squamous cell cancer.
80
What are the 3 major mechanisms of Hypercalcemia of malignancy?
Tumor secretion of parathyroid hormone-related protein (PTHrP) Osteolytic metastases with local release of cytokines Tumor production of 1, 25-dihydroxy Vitamin D (calcitrol)
81
What is the clinical course of Hyperparathyrpidism?
Asymptomatic until identified during routine blood work.
82
When symptomatic what are the most common clinical manifestations of Hyperparathyroidism?
Painful bones, Renal Stones, abdominal groans, and psychic moans. Excessive bone reabsorption can lead to osteopenia Increased excretion of Ca in urine can lead to Renal Stones (Nephrolithiasis)
83
What can Cause Hypoparathyroidism?
Destruction of Parathyroid glands (autoimmune, surgical) Abnormal Parathyroid Development Changed regulation of PTH production or decreased PTH function.
84
What is the Etiology of Hypoparathyroidism?
Most often through surgical or autoimmune damage. In adults most common cause is surgical
85
What are the Clinical Features of hypoparathyroidism?
THe Hallmark Feature of Hypoparathyroidism is **_Hypocalcemia_** which presents as Tetany when below 50% of normal.
86
What two tests can be done during Physical exam to test for hypocalcemia?
Chvostek (direct mechanical stimulation of motor fibers in Facial nerve) Trousseau (arm muscles contract in ischemic conditions caused by BP cuff)
87
What are the 5 functions of Cortisol we discussed in Lecture?
Adipose tissue (promote Breakdown of fat) Bone (Reduction of Bone formation) Liver (Glucose generation) Muscle (Decreased Amino Acid uptake by muscle) Pancreas (Cortisol counteracts insulin)
88
What is the Cause of Cushing's Syndrome?
Excess Cortisol.
89
What is Adrenogenital or Virilizing syndrom?
An excess of Androgens
90
What are the syndromes of Hyperadrenalism?
Cushing's Syndrome Hyperaldosteronism Adrenogenital or Virilizing Syndrome
91
What does the circadian clock consist of?
**A Central Master Clock** in the SuperChiasmatic Nucleus (SCN) in the Hypothalamus An **Adrenal Peripheral Clock** in virtually all organs and tissues
92
What regulates the Circadian Clock?
The Central Clock controls the HPA axis with diurnal oscillations of adenocorticotropic and cortisol. HPA axis adjusts daily rythms of glucocorticoids and syncronizes Peripheral clocks
93
What can happen if the Clock systems and HPA axis are Dysregulated?
Pathologic manifestations such as Obesity, metabolic syndrome, and CV disease as it reduces the tissue sensitivity to glucocorticoids.
94
What are the two types of Cushings Syndrome?
**ACTH-dependent** (Cushings disease or Ectopic ACTH secretion by non pituitary tumor) **ACTH-independent** (drug induced)
95
What is the hallmark feature of ACTH-Dependent Cushing Syndrome?
Elevated ACTH level throughout day.
96
What is the most common cause of Cushing's Disease?
Pituitary Adenoma
97
What is the Result of the increased plasma ACTH concentrations in Cushing's Disease?
Adrenocortical Hyperplasia and hypersecretion of Cortisol lead to breaking of the normal circadian rythm and cortisol serum concentrations on par with the morning throughout the day.
98
What can you say about ACTH if you are able to suppress it with Dexometazone?
It is coming from the Pituitary Gland.
99
What is one of the side effects of POMC stimulation in Cushing's Disease?
Hyperpigmentation via overproduction of melanocytes
100
If someone is on Prednisone for more than 3 weeks what is the result?
The HPA axis is suppressed and you have non ACTH dependent Cushing's Syndrome.
101
What are the Clinical Symptoms of Cushing's Syndrome?
Buffalo-Hump Moon Face Weight Gain Red Stretch Marks
102
Why is diabetes common in Cushing Syndrome?
Chronic exposure to glucocorticoid excess (eityher endogenous or exogenous) can trigger an insulin resistant state or impaired insulin secretion.
103
What are the Hallmark signs of Primary Hyperaldosteronism (Hyperadrenalism)?
HTN and Hypokalemia
104
What is Adrenal Insufficiency (Hypoadrenalism)?
Destruction of the Adrenal cortex and subsequent reduction of adrenal hormones.
105
What is the Cause of Primary Adrenal Insufficiency (Hypoadrenalism)?
Caused by an inability of the Adrenal gland to produce enough steroid hormones, typically caused by autoimmune adrenalitis (Addison's disease).
106
What is the cause of Secondary Adrenal Insufficiency (Hypoadrenalism)?
There is inadequate pituitary or Hypothalamic stimulation of the Adrenal Glands.
107
What antigen triggers the Autoimmune response in Addisons that triggers the destruction of Adrenocortical cells?
21-hydroxylase
108
What are the Clinical symptoms of Addison's Disease?
Hyperpigmentation Hypotension
109
What is Adrenal Crisis?
A sudden and severe worsening of Adrenal Insufficiency symptoms
110
In what settings can an Adrenal Crisis occur?
PT W/ _undiagnosed Primary Adrenal Insufficiency_ who is **experiencing serious infection or other acute& serious stress**. PT W/ _known Primary Adrenal Insufficiency_ who **does not take more glucocorticoid during an infection or other major illness**. After **Bilateral Adrenal infarction** PT _abruptly withdrawn_ from glucocorticoids that **cause secondary adrenal insufficiency**.
111
What is the Major Hormonal precipitating Factor for Adrenal Crisis?
Mineralcorticoid
112
What is the main feature of Adrenal Crisis?
Shock
113
What is the Adrenal Medulla composed of?
Neural Crest cells called Chromaffin Cells, and thier supporting cells.
114
What are Catecholamines?
Tyrosine derived hormones produced by Chromaffin cells and the Sympathetic nervous system. Epinephrine Norepinephrine Dopamine
115
What is a Pheochromocytoma?
A tumor that is overproducing Catecholamines originating from Chromaffin cells and sympathetic ganglia (catecholamine secreting paraganglioma).
116
What are the clinical features of a Pheochromocytoma?
Headaches Palpations Sweating (a Life-Threatening acute hypertensive emergency)
117
What are the three types of HTN we talked about in Pheochromocytoma?
**Sustained HTN** Caused by excess Norepi causing continous vasoconstriction With elevated Epinephrine levels PT may experience Orthostatic HTN **Paroxysmal HTN** High-levels of Plasma Epinephrine Sudden release of Catecholamines by tumors induced by physical activity, smoking, abdominal pressure, postural changes and anxiety. **Normotension** Familial Pheochromcytoma -Tumorsmay be to small to secrete high levels of Catecholamines or dopamine secreting only
118
What is Multiple Endocrine Neoplasia (MEN) Syndrome?
A group of inherited diseases causing proliferative lesions (hyperplasia, adenomas, and carcinomas) of multiple endocrine organs either Synchrnously or metachronously (at different times).
119
What are the main health problems associated with MEN 1?
**_Parathyroid Tumors_**, Pancreatic tumors, and Pituitary Tumors.
120
What are the main health problems associated with MEN 2a?
**_Medullary Thyroid Cancers_**, Pheochromocytoma, and Parathyroid Tumors.
121
What are the main health problems associated with MEN 2b?
Medullary Thyroid Cancers, Pheochromocytoma, and neuromas.
122
What essential info about the Pineal gland did we learn?
It is composed entirely of Pineocytes (cells with photosensory and neuroendocrine functions) It's principle secretory product is Melatonin.
123
What does Mealtonin do?
Screted into blood and CSF it conveys signals to distant organs, but mainly the brain and affects sleep and circadian rhythms.
124
What happens to the Melatonin metabolism during daylight hours?
The serotonin in pinealocyctes is stored and unavailable to MAO enzyme.
125
What happens to the Melatonin metabolism with the onset of darkness?
The release of Norepi onto pinealocytes causes stored serotonin to become accessible for metabolism. Norepi activates enzyme that converts serotonin to melatonin. Melatonin then diffuses into bloos and CSF and crosses the blood brain Barrier
126
What is the link between melatonin and the Circadian Cycle?
Melatonin follows the Circadian rythm indicating management by the SCN.

Pathophys (4 decks)

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