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BIOL 2200 > module 8: endocrine system disorders > Flashcards

module 8: endocrine system disorders Flashcards

1
Q

What 3 general causes lie behind endocrine disorders?

A
  1. the target tissue receives too much or too little hormone
  2. hormone arrives at the target tissue but finds abnormal cell receptor function
  3. altered intracellular response to the hormone-receptor complex
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2
Q

Describe the 6 ways by which the target tissue can receive the wrong amount of hormone

A
  • over/under production of hormone from the gland
  • feedback system isn’t working correctly = release of hormone isn’t correct
  • inadequate blood supply to tissues = delivery of hormone is inadequate
  • inadequate levels of serum carrier protein
    • ex: lipid-based proteins does not have a carrier to bring it over
  • hormone being inactivated too quickly/slowly
  • abnormal production of hormone by uncontrolled ectopic sources
    • tumor that affects hormones
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3
Q

Describe the 3 ways in which the receptor function can be abnormal

A
  • decrease in number of receptors
  • impaired receptor function
    • does not recognize hormone
  • presence of antibodies that act as competitive inhibitors or mimic hormone action
    • block the hormone from binding to the receptor

**only target tissue has. receptor… if there is a problem, it does not have to do with the hormone itself

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4
Q

explain the altered intracellular response to the hormone-receptor complex

A
  • the series of reactions inside the cell that allows the hormone to have an effect on the metabolic pathways do not work correctly
  • while the hormone activates the receptor, the internal reactions are disrupted
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5
Q

Explain the hypothalamic-pituitary-target gland axis

A

hormone cascade from hypothalamus → pituitary → target gland

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6
Q

Explain primary (with examples), secondary, and tertiary disorders involving the hypothalamus-pituitary-target gland axis of control.

A
  • primary: there is a problem with the final target gland responsible for producing a hormone
    • the problem at the end of the cascade
  • secondary: problem with the pituitary gland
    • problem in the middle of the cascade
    • normally should activate hormone, but doesn’t
  • tertiary: problem with hormone production from the hypothalamus
    • problem at the beginning of the cascade
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7
Q

Describe the most common cause of hypothalamic dysfunction. What would be the outcome of this condition?

A
  • interruption of the pituitary stalk = the physical connection between the hypothalamus and the anterior pituitary
  • cause:
    • destructive lesions
    • rupture after head injury
    • tumor
  • outcome = lose function of releasing hormones from the hypothalamus = no corresponding pituitary hormones
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8
Q

Describe hypopituitarism (including panhypopituitarism)

A
  • under-producing hormones from the pituitary
  • the result from either an inadequate supply of hypothalamic-releasing hormones or inability of the pituitary gland to produce its hormones
  • also brought on through head trauma, infections, etc
  • panhypopituitarism = depleting all hormone production from anterior pituitary
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9
Q

what is panhypopituitarism

A

depleting all hormone production from anterior pituitary

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10
Q

describe hyperpituitarism

A

when excess pituitary hormone is produced

  • usually caused by a tumor causing excessive production
    • excess hormone produced, leading to tumor
    • leads to under secretion of other hormones from tissues surrounding the tumor
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11
Q

what is optic chiasm?

A

disturbance in vision due to a tumor

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12
Q

Describe two possible causes for diabetes insipidus. What are two clinical manifestations?

A

disruption in ADH = not reabsorbing enough water = excessive loss in urination

  1. insufficient production/transport/release of ADH
  2. inadequate response of the renal tubules to ADH

clinical manifestations:

  • thirst from dehydration
  • polyuria from the failure to reabsorb water
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13
Q

What does SIADH stand for and what hormone is involved? Are levels of this hormone too high or low?

A
  • SIADH= syndrome of inappropriate antidiuretic hormone secretion
  • hormone = high levels of ADH
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14
Q

What is the most common cause of SIADH?

A

medications

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15
Q

How does hyponatremia occur in SIADH? Which system is noticeably affected by extreme drops in sodium levels?

A
  • anorexia fatigue that can progress to confusion, lethargy, convulsions with extreme drops in sodium levels due to ADH problems = urinate more sodium
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16
Q

Describe thyrotoxicosis, including common signs and symptoms of disease

A

hyperthyroidism

  • thyrotoxicosis = the clinical syndrome that results from increased levels of thyroid hormones
  • signs & symptoms:
    • excessive sympathetic nervous system activity
    • weight loss
    • heat sensitivity
    • increased metabolic rate
    • goiter
    • exophthalmos (bulging of the eyes)
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17
Q

describe an example of a primary disorder that would result in thyrotoxicosis

A

thyroid is functioning abnormally

  • ex: Grave’s disease
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18
Q

describe an example of a secondary disorder that would result in thyrotoxicosis

A

the pituitary is the problem,

ex: thyroid stimulating hormone (TSH) secreting pituitary adenoma

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19
Q

Name and explain the mechanism of the cause of Graves disease.

A

because the thyroid is an end target tissue in the “hypothalamus-pituitary-target axis”, there can be a primary disorder when the thyroid is functioning abnormally

  • caused by type 2 hypersensitivity reaction
  • onset is 20-40 years old
  • 10x more frequent in females
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20
Q

Name and describe the most common cause for primary hypothyroidism

A

the thyroid itself

  • can result from an autoimmune reaction (ex: Hashimoto disease), drugs, radiation therapy, etc.
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21
Q

Describe a cause for a secondary hypothyroid disorder.

A

the pituitary is the problem

  • may result from a pituitary tumor compressing surrounding pituitary cells reducing hormone secretion
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22
Q

Name 4 signs/symptoms for hypothyroidism.

A
  1. low metabolic rate
  2. cold intolerance
  3. lethargy
  4. myxedema
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23
Q

Describe the basis of Cushing’s syndrome

A

adrenal glands secrete excess glucocorticoids

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24
Q

describe the 3 forms that contribute to Cushing’s syndrome

A
  • primary = disease of the adrenal cortex
  • secondary = hyperfunction of the anterior pituitary
  • tertiary = hypothalamic dysfunction or injury
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25
Q

which are the most common causes of Cushing’s syndrome?

A
  • an overproduction of adrenocorticotropic (corticotropin) hormone
    • either through hypersecretion at the anterior pituitary or as a paraneoplastic effect
    • in 70% of patients
26
Q

Describe the manifestations and complications associated with Cushing’s syndrome.

A

manifestations:

  • weight gain
  • buffalo hump
  • thinning extremities with muscle wasting
  • muscle weakness
  • thin, fragile skin and scalp hair
  • bruising
  • impaired wound healing

complications:

  • excess cortisol
  • could include osteoporosis and pathologic fractures
  • peptic ulcers
  • lipidosis
  • impaired glucose tolerance
27
Q

Describe the basis of Addison’s disease

A
  • adrenal hypofunction or adrenal insufficiency
28
Q

describe the primary form that contributes to the development of Addison’s disease

A

primary disorders:

  • most common
  • originate with the adrenal gland where more than 90% of tissue is destroyed
  • usually due to an autoimmune reaction
  • can also be caused by hemorrhaging into the adrenal glands, infection, or neoplasms
29
Q

describe the secondary form that contributes to the development of Addison’s disease

A

there is hypopituitarism (decreased adrenocorticotropic hormone)

  • may result from pituitary damage or a tumor compressing surrounding pituitary cells = less hormone secretion
  • disorders in hypothalamic-pituitary function may also cause reduced ACTH production
30
Q

What is adrenal crisis and who is at risk for this complication?

A

adrenal crisis = serious complications of Addison’s disease

those at risk:

  • unresponsive to hormone replacement therapy
  • undergo trauma
  • undergo extreme stress without glucocorticoid replacement
  • develop gland thrombosis after a severe infection
31
Q

Which two hormones contribute to adrenal crisis?

A
  • absent/low cortisol
  • absent/low aldosterone
32
Q

How can a decrease or absence of the two hormones lead to shock with the possibly of coma or death in Addison’s?

A
  • absent/low cortisol →
    • LIVER: lower glucose output = hypoglycemia
    • STOMACH: lower digestive enzymes, vomiting, and diarrhea = hypotension
  • absent or low aldosterone →
    • KIDNEY: Na+/K+ imbalance → water loss = hypotension
    • HEART ARRHYTHMIAS: lower cardiac output = hypotension

ALL OPTIONS CAN LEAD TO SHOCK, COMA, DEATH

33
Q

Describe how Cushing’s syndrome and Addison’s disease are treated

A

cushing’s:

  • radiation
  • drug therapy
  • surgery depending on the cause

Addison’s:

  • hormone replacement therapy
34
Q

Explain how the endocrine response to stress can affect the immune system

A
  • catecholamines (epinephrine and noepinephrine)
    • increases blood sugar and breaks down protein and fat
    • increases HR, vasoconstriction, and bronchodilation
  • corticotropin-releasing hormone (CRH) from the hypothalamus
    • stimulates adrenocorticotrpoic (ACTH) from the anterior pituitary
    • leads to glucocorticoids (cortisol) from the adrenal glands
      • inhibits reproductive system, digestive system, inflammation, and immune system
  • mineralcortocoids (aldosterone), and ADH
    • aldosterone increases sdium reabsorption (blood volume)
    • ADH increases water reabsorption (blood volume), and vasoconstriction (increased BP to get O2 and nutrients to muscles)
35
Q

Describe how the relationship between endocrine and stress response relates to the manifestations seen with chronic stress

A
  • can depress the immune system
  • some of the messenger molecules and cell receptors are the same in the endocrine and the immune system
    • ex: receptors for glucocorticoids, insulin, etc. have been found on lymphocytes and IL1, 6, and TNF could activate the hypothalamus-pituitary-adrenal gland axis
  • chronic stress has been linked to diseases of the cardiovascular, gastrointestinal, immune, and neurologic systems
  • cortisol, and the catecholamines can increase the production of pro-inflammatory compounds = contributors to these diseases
36
Q

Define prediabetes and outline how insulin imbalances may arise that produce this condition.

A
  • prediabetes = impaired fasting plasma glucise and impaired glucose tolerance
  • insulin imbalances arise from:
    • an absolute insulin deficiency
    • impaired release of insulin by the pancreatic beta cells
    • inadequate or defective insulin receptors
    • production of inactive insulin or insulin that is destroyed before it can carry out its action
37
Q

Define the three key clinical manifestations of diabetes mellitus – the “three Ps”.

A
  • polyuria = excessive urination
  • polydipsia = excessive thirst, from dehydration
  • polyphagia = excessive hunger
    • cells in a starvation state, so person feels hungry despite eating huge amounts of food
38
Q

Describe type 1 diabetes

A
  • previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-onset diabetes
  • developed when the body’s immune system destroys pancreatic beta cells
    • the only cells in the body that make the hormone insulin that regulates blood glucose
  • usually strikes children and young adults, although disease onset can occur at any age
  • may account for 5-10% of all diagnosed cases of diabetes
  • risk factors:
    • autoimmune
    • genetic
    • environmental factors
39
Q

describe the pathogenesis of type 1 diabetes

A
  • slow, progressive autoimmune T cell-mediated disease that destroys beta cells of the pancreas
  • autoantigens develop on the surface of pancreatic beta cells and then circulate in blood and lymph
  • autoantigens stimulate cellular and humoral immune responses that result in beta cell destruction leading to hypoinsulinemia (too little insulin)
  • hyperglycemia (high blood sugar) develops
40
Q

Describe the clinical manifestations of type 1 diabetes

A
  • glucose accumulates in the blood → hyperglycemia (high blood sugar levels)
  • glucose appears in the urine as it exceeds “renal threshold” for glucose = glycosuria
  • the 3 P’s- cardinal features of diabetes mellitus
  • wide fluctuations in blood glucose occur
  • protein and fat breakdown = weight loss
  • diabetic ketoacidosis (DKA) due to starvation state
41
Q

define type 2 diabetes

A

a condition characterized by hyperglycaemia resulting from the impaired utilization of insulin

  • insulin is being produced, but cells are not stimulated
  • could be because the cell receptors are not responding to insulin
  • may account for 90-95% of all diagnosed diabetes
  • usually begins as insulin resistance = a disorder where the cells do not use insulin properly
  • as insulin rises, the pancreas initially increases insulin production
    • as it becomes overworked, it gradually produces its ability to produce insulin
42
Q

what are the risk factors of type 2 diabetes?

A
  • older age
  • obesity
  • family history of diabetes
  • history of gestational diabetes
  • impaired glucose metabolism
  • physical inactivity
  • race/ethnicity
43
Q

Define insulin resistance

A

below optimal response of insulin-sensitive tissues (liver, muscle, and adipose tissue) to insulin

  • cells fail to response to the normal acions of the hormone insulin
44
Q

explain the mechanisms that insulin resistance is related to obesity that underlie its development

A
  1. adipose tissue produces hormones (adipokines) that are associated with decreased insulin sensitivity
  2. intracellular deposits of cholesterol and triglycerides found in obese individuals interfere with intracellular insulin signalling
  3. adipose tissue releases inflammatory cytokines which are toxic to beta cells and induce insulin resistance
45
Q

Describe the development of Type 2 diabetes

A
  • insulin resistance occurs
  • compensatory hyperinsulinemia results and prevents the clinical appearance of diabetes (hyperglycemia and its effects), possibly for many years
  • eventually, beta-cell dysfunction develops and leads to both a decrease in the number of beta-cells and a reduction of normal beta-cell function
    • remaining cells undergo “exhaustion” from increased demand for insulin biosynthesis
  • loss of insulin = hyperglycemia
    • after meals and due to increased glucose production by the liver
46
Q

Describe the clinical manifestations of type 2 diabetes

A
  • individual often overweight, but may have recent unexplained weight loss
  • hyperglycemia (high blood glucose) and glycosuria (high urine glucose)
  • often has diagnostic features of metabolic syndrome
  • class symptoms:
    • polyuria
    • polydipsia
  • nonspecific symptoms:
    • fatigue
    • pruritus (itching)
    • recurrent infections
    • visual changes
47
Q

Describe metabolic syndrome

A

a collection of disorders that confer a high risk of developing type 2 diabetes

  • central obesity
  • dyslipidemia
  • prehypertension
  • elevated fasting blood glucose level
48
Q

What is gestational diabetes mellitus?

A

any degree of glucose intolerance with onset or first recognition during pregnancy

  • higher risk for complications
  • women who have gestational diabetes mellitus have a 60-70% chance of developing diabetes mellitus within 5-15 years
49
Q

Describe the following acute complication of diabetes mellitus, including underlying causation, clinical manifestations and treatment (if appropriate): hypoglycemia

A
  • “insulin shock/reaction” due to mismatching insulin need with supply
  • pallor, tremor, tachycardia, palpitations, dizziness, confusion, seizures, coma
  • more so in type 1 than type 2 since T2DM still have mechanisms to increase blood glucose levels
  • requires immediate replacement of glucose
    • eating or drinking something with sugar
50
Q

Describe the following acute complication of diabetes mellitus, including underlying causation, clinical manifestations and treatment (if appropriate): diabetoc ketoacidosis (DKA)

A
  • with insulin deficiency (more with type 1), lipolysis (breakdown of triglycerides) is enhanced = more fatty acids delivered to liver
  • gluconeogenesis is also occurring = production of more ketones that can be used in the body
    • buildup = metabolic acidosis
  • hyperventilation
  • dizziness
  • nausea
  • CNS depression
51
Q

Describe the following acute complication of diabetes mellitus, including underlying causation, clinical manifestations and treatment (if appropriate): somogyi effect

A

characterized by alternating episodes of hypoglycemia and hyperglycemia

  • insulin induced hypoglycemia occurs = release of epinephrine, growth hormone, and corticosteroids (cortisol)
  • hormones stimulate glucogenesis = hyperglycemia = “rebound hyperglycemia”
  • worse effect if combined with dawn phenomenon
52
Q

Describe the following acute complication of diabetes mellitus, including underlying causation, clinical manifestations and treatment (if appropriate): dawn phenomenon

A
  • early morning rise in blood glucose levels
  • related to an increased release of growth hormone, epinephrine, and cortisol in early morning = increased blood sugar
  • idea is to increase glucose levels for energy production o prepare the body for daily activity
53
Q

Describe the following acute complication of diabetes mellitus, including underlying causation, clinical manifestations and treatment (if appropriate): HHS (hyperosmolar hyperglycemic syndrome)

A
  • complication of type 2- can be fatal
  • high glucose levels and plasma osmolarity and dehydration = no ketoacidosis)
  • if blood glucose is high, the kidneys excrete more fluid
    • if fluid is not replaced, dehydration occurs
  • excessive dehydration pulls water out of cells, including brain cells
  • weakness, dehydration, polyuria, neurological signs and symptoms
  • more common in elderly people
    • onset can be very gradual - may be mistaken for a stroke
54
Q

Name and describe the molecular pathological effects of chronic hyperglycemia

A
  • advanced glycation end products (AGEs)
    • long term excess of glucose can result in glucose permanently binding to proteins inside/outside cells (AKA glycation) = interference with cell metabolism, produces endothelial changes, or microvascular damage
  • polyol pathway:
    • tissues that do not require insulin to import glucose (kideys, RBCs, blood vessels, eye lens, and nerves) cannot down-regulate the uptake
    • excess glucose is converted into sorbitol, which is osmotically active
    • buildup of sorbitol may damage schwann cells producing neuropathies, and damage the eye lens from swelling due to osmotic pressure
  • altered hemoglobin-o2 binding affinity:
    • due to glycation of the hemoglobin molecule
    • causes impaired oxygen release to tissues
  • inappropriate protein kinase C (PKC) activation:
    • KC = an intracellular messenger controlling various cell functions including permeability and dilation of blood vessels
    • inappropriate activation is linked to vascular damage in the retina, nerves, and kidneys
55
Q

Describe the following chronic complications of diabetes mellitus, including the underlying pathological effects of chronic hyperglycemia and its clinical manifestations: diabetic retinopathy (vision problems)

A
  • a leading cause of blindness in diabetes mellitus
  • results from increased capillary permeability and ischemia of the retinal blood supply
  • leaking macular capillaries can lead to macular edema = severe loss of central vision
56
Q

Describe the following chronic complications of diabetes mellitus, including the underlying pathological effects of chronic hyperglycemia and its clinical manifestations: diabetic nephropathy (kidney problems)

A
  • the glomeruli are progressively injured by glycation and high renal blood flow in response to hyperglycemia
  • characterised by nephrotic syndrome, proteinuria, edema, and high blood cholesterol
  • most common cause of end stage renal disease (complete loss of kidney function)
57
Q

Describe the following chronic complications of diabetes mellitus, including the underlying pathological effects of chronic hyperglycemia and its clinical manifestations: diabetic neuropathy (nervous system problems)

A
  • due to metabolic factors (including build up of sorbitol in neurons) and vascular effects (ischemia)
  • sensory deficits are more common than motor and often involved extremities
  • loss of sensation in toes/fingers means minor injuries go unnotices, may become infected and gangrenous
58
Q

Describe the following chronic complications of diabetes mellitus, including the underlying pathological effects of chronic hyperglycemia and its clinical manifestations: infection

A
  • those with diabetes mellitus are at an increased risk of infection due to:
    • impaired senses
    • impairment of the immune system
    • increase in pathogen growth due to higher level of glucose in body fluids
59
Q

To what are macrovascular disorders due?

A

advanced glycation end products (AGEs) and poor tissue oxygenation

60
Q

Name and be able to describe 4 macrovascular disorders that can be caused by long-term diabetes mellitus.

A
  • accelerated atherosclerotic disease
  • coronary artery disease
    • most common cause of morbidity and mortality in people with diabetes mellitus
  • stroke
    • twice as common in those with diabetes mellitus
  • peripheral vascular disease
    • narrowing or obstruction of peripheral arteries, usually below the knee as a result of atherosclerosis and inflammation
    • occulsions of small arteries can lead to neuropathy, diabetic foot ulcers and dry and sometimes wet gangrene

BIOL 2200 (12 decks)

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