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Practice Topics Exam 5 > Endocrine Pathophysiology > Flashcards

Endocrine Pathophysiology Flashcards

1
Q

Hormone Regulation

A

Chemical triggers
Endocrine factors
Neural control

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2
Q

Hormone Regulation - Chemical triggers

A 
Blood sugar levels (if high release insulin, if low release glucagon)
Calcium levels (parathyroid hormone especially - if fall too low is released)
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3
Q

Hormone Regulation - Endocrine factors

A

Hormone from one gland triggers another gland to release a hormone

Ex = Pit gland - TSH - activates thyroid gland to release T3/T4

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4
Q

Hormone Regulation - Neural control

A

Autonomic nervous system

Startled - SNS activation - hypopituitary axis says need to release adrenal hormones to adapt to stress

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5
Q

Hormone regulation - Neural control

Epinephrine vs. Cortisol

A

Epinephrine - triggered with F/F
Cortisol - also released by SNS but is more dominant in chronic stress

Initial response = protective = Epinephrine
Longer we are exposed to chronic stress = cortisol levels go up = higher risk of immune suppression

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6
Q

Mechanisms of hormone action

A

Feedback loops
Hormone receptors
Up regulation
Down regulation

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7
Q

Mechanisms of hormone action - Feedback loop examples with pathology

A

Hyper or hypothyroid issues have disruption in the feedback loops

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8
Q

Mechanisms of hormone action - Feedback loop examples with pathology - Hyperthyroidism

A

Hyper - body forms antibodies that mimic TSH - these antibodies attach to TSH receptors on thyroid and thyroid thinks it needs to kick out more T3 and T4 so it will - pit gland senses the extra T3 and T4 so it will dec TSH

So Graves for ex - High T3 and T4, Low TSH

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9
Q

Mechanisms of hormone action - Feedback loop examples with pathology - Hypothyroidism

A

Thyroid is being attacked by antibodies that kill the thyroid gland and it cannot produce - leaking out as much T3 and T4 as it can - Pituitary thinks we need more TSH so it sends a lot of TSH - Thyroid keeps trying to respond but it can’t

Hashimoto - Low T3 and T4, High TSH

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10
Q

Mechanisms of hormone action - Up regulation

A

Addition of hormone receptors to a cell membrane - would happen if certain hormones are low in blood and cells are trying to open as many receptors as they can to bring the hormone in

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11
Q

Mechanisms of hormone action - Down regulation

A

More common in pathology is down regulation
Closing or removal of receptors from a cell
When there is an excess of a hormone in the blood - they say no thank you and close their doors

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12
Q

Mechanisms of hormone action - Down regulation - Example of pathology

A

Type II diabetes
Person has high glucose levels - body normally responds with secretion of insulin - over time you get hyper insulinemia - chronic high insulin in blood so then your cells down regulate insulin (dec insulin sensitivity)
exercise can restore and reverse this!!! Metformin is common rx

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13
Q

Hypothalamic Pituitary System

A

Interaction between neurological and endocrine system
Hypothalamus is connected to the pituitary gland
Hypothalamus synthesizes and releases hormones that regulate other glands

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14
Q

Interaction between neurological and endocrine system

A

Hypothalamic pituitary system

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15
Q

Anterior and posterior pituitary secrete

A

Different hormones and have differing target tissues

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16
Q

ADH is secreted from anterior or posterior
pituitary

What is other name for ADH

A

Posterior

Vasopressin

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17
Q

Posterior pituitary - SIADH is what

A

High levels of ADH

Syndrome of inappropriate ADH

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18
Q

Posterior pituitary - what does ADH normally do

A

Targets the kidneys and tells them to keep some water stored back in the body
Retain fluid

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19
Q

Posterior pituitary - SIADH - Causes

A

Ectopic production by tumor (infection/lesion)
Brain injury (impact to pit)
Drugs (barbituates, nicotine, morphine)

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20
Q

Posterior pituitary - SIADH - s/s

A

Edema, concentrated urine, Hypertension

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21
Q

GH is secreted from anterior or posterior pituitary

A

Anterior

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22
Q

Hypopituitarism is what

A

Hypo pituitary condition where you are not secreting enough of a lot of different hormones

GH is usually what we see though

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23
Q

Hypopituitarism - Dwarfism

What is it? Primary cause?

A

Too little GH

Primary cause is pituitary infarct

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24
Q

GH targets what

A

muscle and bone

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25
Q

Presentation of hypopituitarism

A

Presentation depends on which hormone are affected

If GH affected - will see dwarfism

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26
Q

Hyperpituitarism - Gigantism and Acromegaly

A

Increase in release of GH

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27
Q

Hyperpituitarism - primary cause

A

Adenoma/Tumor

They are functioning tumors that produce and release hormones

28
Q

S/S with Hyperpituitarism - Gigantism and Acromegaly

A

Excessive bony and CT growth

Impingement of nerves can result

29
Q

Hyperpituitarism - Gigantism vs. Acromegaly

A

Gigantims - inc in GH prior to growth plates fusing (growth in height)
Acro - inc after growth plates have closed (bones become more dense and thick - jaw)

30
Q

Prolactinoma is what

A

Pituitary tumor that can cause a hyper pituitary state

Benign tumor

31
Q

Prolactinoma - what will it do/what does prolactin do

A

Prolactin stimulates milk production after having baby and suppresses estrogen (therefore suppressing fertility)

Prolactinoma is often checked for in W who are having trouble getting pregnant - Prolactinoma can lead to infertility

32
Q

S/S of prolactinoma

A 
Lactation
Amenorrhea
Hirsutism
Estrogen deficit 
OP (estrogen helps maintain bone density)
Might also see vision changes
33
Q

Hyperthyroidism - disease

A

Graves disease

34
Q

Hyperthyroidism - Graves disease - most common cause of

A

Thyrotoxicosis

35
Q

Hyperthyroidism - Graves disease - Caused by

A

Stimulation of thyroid with antibodies against TSH receptors

36
Q

Hyperthyroidism - Graves disease - S/S

A 
High T3 and T4
Thyroid enlargement
Opthalmopathy
Tachycardia
Tremor
High BP 
Weight loss, Hot body temp/heat intolerance
37
Q

Hypothyroidism - Disease

A

Hashimoto Disease

38
Q

Hypothyroidism - Hashimoto Disease - is what

A

Autoimmune thyroiditis - Tissue specific immune response

Loss of thyroid tissue resulting in dec in T3/T4 production

39
Q

Hypothyroidism - Hashimoto Disease - S/S

A

Weight gain, Cold intolerance, Lethargic, Goiter, Myxedmea, Bradycardia, low BP

40
Q

Hyperparathyroidism

A

Parathyroid gland produces parathyroid hormone
When parathyroid hormone is released it increases Ca in blood
So with hyperparathyroidism - they will be in state of hypercalcemia (too much Ca in blood)

41
Q

Hyperparathyroidism - Hypercalcemia - impact

A

Pulls Ca from bone to put it in the blood so will see OP which can contribute to fractures
Also will be in metabolic acidosis - low pH and inc RR

42
Q

Hypoparathyroidism

A

Parathyroid is not producing enough of the parathyroid hormone
So will see hypocalcemia

43
Q

Hypoparathyroidism - Hypocalcemia - impact

A

The Ca that is normally in blood is now being shifted back to store areas like bone - so you will see bone deformities, spur formations
spasms

44
Q

Hypoparathyroidism - Hypocalcemia - S/S

A

MM spasms, hyperreflexia, dry skin, hair loss, ridges on nails, BG calcification, bone deformities

Also without enough Ca in blood - might see hyperreflexia and mm

45
Q

Hypercortical function - disease

A

Cushing Disease

46
Q

Hypercortical function - Cushing Disease is caused by

A

excessive ACTH - primarily due to adrenal tumors

47
Q

Hypercortical function - Cushing Disease - Results in

A

Increased circulating cortisol

48
Q

Hypercortical function - Cushing Disease - S/S

A

Weight gain in characteristic pattern (abdominal, CT junction)
Glucose intolerance
Protein wasting
Hyperpigmentation (striae - elbow, post knee, axilla)
Fluid retention - moon face

49
Q

Hypercortical function - Cushing Disease - Without treatment what happens

A

50% die within 5 yrs wihout tx

Not very good tx for it - can do Nizoral to reduce circulating cortisol levels or surgery if can identify source
PT = relaxation techniques!

50
Q

Hypocorticalism - disease

A

Addison Disease

51
Q

Hypocorticalism - Addison disease

A

Autoimmune destruction of cortical cells

Often associated with other autoimmune diseases

52
Q

Hypocorticalism - Addison disease - S/S

A

Weight loss
Difficulty responding to stress (mainly phys)
Can end up in Addisonian crisis - can be fatal from organ failure
Addison can be tx with corticosteroids

53
Q

Endocrine pancreas

A

Islets of Langerhans!

54
Q

Endocrine pancreas - Insulin is produced by

A

Beta cells!

55
Q

Endocrine pancreas - Insulin does what

A

Facilitates glucose transport into cells
Facilitates K transport into cells
Facilitates lipid and protein synthesis
Antihyperglycemic effect

56
Q

Endocrine pancreas - Amylin

A

Secreted with insulin in response to eating
Also has antihyperglycemic effect

Released when blood sugar is high
Promotes satiety (feeling of fullness)
57
Q

Endocrine pancreas - Glucagon

A

Antagonist to insulin - released when blood sugar is low!
Stimulates liver to release glucose into blood - also causes lipolysis
If liver does not have enough - goes to mm and then fat

58
Q

Endocrine pancreas - Somatostatin

A

Required for carb, fat, and protein metabolism

59
Q

Endocrine pancreas - Pancreatic dysfunction - Diabetes Mellitus types

A

1 = absoulte insulin deficiency
2 = insulin resistance with insulin secretion deficit
Other
Gestational

60
Q

Endocrine pancreas - Pancreatic dysfunction - DM - Diagnostic criteria

A

Polyuria, polydipsia, unexplained weight loss
Glucose (nonfast) level = Greater than or equal to 200
Fasting = Greater than or equal to 126
Positive glucose tolerance test

61
Q

Endocrine pancreas - Pancreatic dysfunction - Type 1

A

10%
Autoimmune destruction of pancreatic cells
Multifactorial inheritance
Ketoacidosis

62
Q

Endocrine pancreas - Pancreatic dysfunction - Type 1 - Ketoacidosis

A

Norm = use glucose to produce energy
If type 1 - they are not producing insulin so can’t use glucose for energy - so switch to using fat and protein - Takes a lot of energy and produces more waste
Ketoacidosis - lose weight because of how much energy the less efficient and waste producing route take

Low pH and high RR and frutiy breath

63
Q

Endocrine pancreas - Pancreatic dysfunction - Type II

Risk Factors
S/S

A

Multifactorial inheritance
Risk factors - race, obesity, age, family hx, F, metabolic syndrome

Nonspecific s/s and slow onset!

Obesity, hyperlipidemia, recurrent infections, pruritis, visual changes, paresthesias

64
Q

Endocrine pancreas - Pancreatic dysfunction - Gestational Diabetes Risk Factors

A 
Family hx
Race
Advanced maternal age
Polycystic ovarian syndrome
High BMI
65
Q

Endocrine pancreas - Pancreatic dysfunction - Acute complications of DM

A

Hypoglycemia
Diabetic ketoacidosis
Hyperglycemia
Dawn phenomenon

66
Q

Endocrine pancreas - Pancreatic dysfunction - Acute complications of DM - Signs of hypoglycemia

A

Light headed, can go into diabetic coma, clammy cold sweating, difficulty thinking, shakiness, tingling around mouth, weak

67
Q

Endocrine pancreas - Pancreatic dysfunction - Chronic complications of DM -

A 
Glycosylation - Advanced glycosylation endproducts (AGEs) - associated with formation of CA
Increased protein kinase C enzyme
Diabetic neuropathies 
Microvascular disease (vision, wounds)
Macrovascular (CAD)
Infection

Practice Topics Exam 5 (13 decks)

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