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Practice Topics Exam 5 > Endocrine Pathophysiology > Flashcards

Endocrine Pathophysiology Flashcards

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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
Presentation of hypopituitarism
Presentation depends on which hormone are affected If GH affected - will see dwarfism
26
Hyperpituitarism - Gigantism and Acromegaly
Increase in release of GH
27
Hyperpituitarism - primary cause
Adenoma/Tumor | They are functioning tumors that produce and release hormones
28
S/S with Hyperpituitarism - Gigantism and Acromegaly
Excessive bony and CT growth | Impingement of nerves can result
29
Hyperpituitarism - Gigantism vs. Acromegaly
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
Prolactinoma is what
Pituitary tumor that can cause a hyper pituitary state | Benign tumor
31
Prolactinoma - what will it do/what does prolactin do
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
S/S of prolactinoma
``` Lactation Amenorrhea Hirsutism Estrogen deficit OP (estrogen helps maintain bone density) Might also see vision changes ```
33
Hyperthyroidism - disease
Graves disease
34
Hyperthyroidism - Graves disease - most common cause of
Thyrotoxicosis
35
Hyperthyroidism - Graves disease - Caused by
Stimulation of thyroid with antibodies against TSH receptors
36
Hyperthyroidism - Graves disease - S/S
``` High T3 and T4 Thyroid enlargement Opthalmopathy Tachycardia Tremor High BP Weight loss, Hot body temp/heat intolerance ```
37
Hypothyroidism - Disease
Hashimoto Disease
38
Hypothyroidism - Hashimoto Disease - is what
Autoimmune thyroiditis - Tissue specific immune response | Loss of thyroid tissue resulting in dec in T3/T4 production
39
Hypothyroidism - Hashimoto Disease - S/S
Weight gain, Cold intolerance, Lethargic, Goiter, Myxedmea, Bradycardia, low BP
40
Hyperparathyroidism
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
Hyperparathyroidism - Hypercalcemia - impact
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
Hypoparathyroidism
Parathyroid is not producing enough of the parathyroid hormone So will see hypocalcemia
43
Hypoparathyroidism - Hypocalcemia - impact
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
Hypoparathyroidism - Hypocalcemia - S/S
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
Hypercortical function - disease
Cushing Disease
46
Hypercortical function - Cushing Disease is caused by
excessive ACTH - primarily due to adrenal tumors
47
Hypercortical function - Cushing Disease - Results in
Increased circulating cortisol
48
Hypercortical function - Cushing Disease - S/S
Weight gain in characteristic pattern (abdominal, CT junction) Glucose intolerance Protein wasting Hyperpigmentation (striae - elbow, post knee, axilla) Fluid retention - moon face
49
Hypercortical function - Cushing Disease - Without treatment what happens
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
Hypocorticalism - disease
Addison Disease
51
Hypocorticalism - Addison disease
Autoimmune destruction of cortical cells | Often associated with other autoimmune diseases
52
Hypocorticalism - Addison disease - S/S
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
Endocrine pancreas
Islets of Langerhans!
54
Endocrine pancreas - Insulin is produced by
Beta cells!
55
Endocrine pancreas - Insulin does what
Facilitates glucose transport into cells Facilitates K transport into cells Facilitates lipid and protein synthesis Antihyperglycemic effect
56
Endocrine pancreas - Amylin
Secreted with insulin in response to eating Also has antihyperglycemic effect ``` Released when blood sugar is high Promotes satiety (feeling of fullness) ```
57
Endocrine pancreas - Glucagon
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
Endocrine pancreas - Somatostatin
Required for carb, fat, and protein metabolism
59
Endocrine pancreas - Pancreatic dysfunction - Diabetes Mellitus types
1 = absoulte insulin deficiency 2 = insulin resistance with insulin secretion deficit Other Gestational
60
Endocrine pancreas - Pancreatic dysfunction - DM - Diagnostic criteria
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
Endocrine pancreas - Pancreatic dysfunction - Type 1
10% Autoimmune destruction of pancreatic cells Multifactorial inheritance Ketoacidosis
62
Endocrine pancreas - Pancreatic dysfunction - Type 1 - Ketoacidosis
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
Endocrine pancreas - Pancreatic dysfunction - Type II Risk Factors S/S
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
Endocrine pancreas - Pancreatic dysfunction - Gestational Diabetes Risk Factors
``` Family hx Race Advanced maternal age Polycystic ovarian syndrome High BMI ```
65
Endocrine pancreas - Pancreatic dysfunction - Acute complications of DM
Hypoglycemia Diabetic ketoacidosis Hyperglycemia Dawn phenomenon
66
Endocrine pancreas - Pancreatic dysfunction - Acute complications of DM - Signs of hypoglycemia
Light headed, can go into diabetic coma, clammy cold sweating, difficulty thinking, shakiness, tingling around mouth, weak
67
Endocrine pancreas - Pancreatic dysfunction - Chronic complications of DM -
``` 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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