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hlsc 222 - pathophysiology across the lifespan > Chapter 19 - Alterations in Hormonal Regulation > Flashcards

Chapter 19 - Alterations in Hormonal Regulation Flashcards

1
Q

Abnormal secretion of ADH is a disorder of the ___________ gland

A

posterior pituitary

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2
Q

ADH is aka ___________

A

vasopressin, hormone that signals water reabsorption

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3
Q

Reduced ADH secretion leads to water __________ and ECF ____________

A

secretion; hyperosmolarity

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4
Q

Excess ADH secretion leads to water ________ and ECF _____________

A

reabsorption; hypo-osmolarity

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5
Q

Disease of the posterior pituitary can also lead to insufficient hormonal _______ proteins in plasma

A

carrier

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6
Q

What does SIADH stand for?

A

syndrome of inappropriate (EXCESSIVE) antidiuretic hormone

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7
Q

When does SIADH occur?

A

when high ADH levels are present in the absence of normal stimuli for its release

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8
Q

SIADH can be caused by: (3)

A

-ectopic ADH secretion via tumour
-surgery
-medications

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9
Q

Cancers of the _______, duodenum, and ______ as well as lymphomas and sarcomas can lead to SIADH

A

stomach; pancreas

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10
Q

SIADH can be caused by CNS disorders such as: (2)

A

encephalitis and meningitis

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11
Q

Surgery can result in increased ADH for __-__ days

A

5-7

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12
Q

Why does surgery lead to SIADH?

A

fluid and volume changes occur after surgery

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13
Q

How is ADH released following pituitary surgery?

A

unregulated

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14
Q

____________ medications for diabetes mellitus, along with opioids, antidepressants, and anti___________ may lead to SIADH

A

Hypo-glycemic; inflammatories

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15
Q

SIADH’s key feature is increased water ________ by the kidneys to the peritubular capillaries

A

reabsorption

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16
Q

Increased ADH secretion leads to an increase in which protein being inserted into the luminal membrane?

A

water channel proteins

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17
Q

Na+ = H20 is _______ osmolarity

A

normal

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18
Q

more Na+ than H20 = _____osmolarity

A

hyper

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19
Q

less Na+ than H2- = ______-osmolarity

A

hypo

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20
Q

Hyponatremia causes the symptoms of _______-

A

SIADH

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21
Q

Hyponatremia occurs when _____ in the blood is low

A

Na+

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22
Q

The effects of SIADH depend on how fast and ________ onset is

A

severe

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23
Q

What is a normal serum sodium level?

A

140-130 mmol/L

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24
Q

What serum sodium level signifies vomiting, abdominal cramps, and weight gain?

A

130-120 mmol/L

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25
Q

What serum sodium level involves confusion, lethargy, muscle twitches, and convulsions?

A

below 110 mmol/L

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26
Q

Correction of hyponatremia…

A

resolves symptoms

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27
Q

Diabetes insipidus is an ______ insufficiency

A

ADH

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28
Q

DI leads to polyuria and poly______

A

polydipsia

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29
Q

Polyuria

A

frequent urination

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30
Q

Polydipsia

A

frequent drinking

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31
Q

DI can be _______ (central) or nephrogenic

A

neurogenic

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32
Q

Neurogenic DI is caused by: insufficient ____ secretion, lesions on the ________, interference with ADH transport/________, brain tumours, aneurysms, TBI

A

ADH; hypothalamus; release

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33
Q

Nephrogenic DI can be ________ or genetic

A

acquired

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34
Q

Acquired DI is related to medication disorders that damage ______ ______

A

renal tubules

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35
Q

What are the two disorders that cause acquired DI?

A

-pyelonephritis
-polycystic kidney disease

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36
Q

Pyelonephritis

A

urinary tract infection

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37
Q

Polycystic Kidney Disease

A

genetic disorder that causes many fluid-filled cysts to grow in your kidneys

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38
Q

Genetic DI occurs from a mutation of the gene coding for _________-__

A

aquaporon-2 (water channel)

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39
Q

DI associated with pregnancy is ______

A

rare

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40
Q

Gestational DI involves an increase in ____________

A

vasopressinase (vasopressin-degrading enzyme)

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41
Q

Gestational DI is usually ______ and doesn’t require treatment

A

mild

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42
Q

DI leads to a large volume of ________ urine

A

dilute

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43
Q

DI _________ plasma osmolarity

A

increases

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44
Q

What are the clinical signs of DI?

A

-polyuria
-nocturia (waking at night to pee)
-polydipsia

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45
Q

What is a normal urinary output?

A

1-2 L/day

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46
Q

DI can cause urine output to be as high as __-___ L/day (may be higher than daily fluid intake!)

A

8-12

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47
Q

Longstanding DI leads to an enlarged _______ _______ and hydronephrosis

A

bladder capacity

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48
Q

Hydronephrosis

A

swelling of one or both kidneys

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49
Q

Neurogenic DI has a _______ onset

A

sudden

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50
Q

Nephrogenic DI has a ________ onset

A

gradual

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51
Q

How is DI diagnosed?

A

-dilute urine
-hyperosmolarity
-hypernatremia

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52
Q

Continued diuresis despite high serum osmolarity is abnormal because normally there is only extra urine when….

A

the body needs to get rid of something

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53
Q

How is DI treated?

A

-ADH replacement
-oral/intravenous fluid replacement
-reversing aquaporing-2 dysfunction (new!)
-medications that increase ADH (carbamazepine/Tegretol)

54
Q

Primary thyroid disorder is due to dysfunction of the…

A

thyroid gland

55
Q

Secondary thyroid disorder is due to dysfunction of the…

A

pituitary gland or hypothalamus

56
Q

What is subclinical thyroid disease?

A

thyroid disease with no symptoms but abnormal lab values

57
Q

Thyrotoxicosis

A

a condition resulting from any cause of increased thyroid levels

58
Q

Hyperthyroidism

A

excess secretion of thyroid hormone from the thyroid gland

59
Q

Graves disease and toxica mutinodular goiter are _____thyroid diseases

A

hyper

60
Q

Thyrotoxicosis symptoms are caused by the metabolic effects of increased serum _______ _______

A

thyroid hormones

61
Q

Increased metabolic rate leads to _______ heat INtolerance and increased tissue sensitivity to __________ stimulation

A

increased; sympathetic

62
Q

Periorbital edema, smaller thyroid, bradycardia, constipation, and edema of the extremeties are symptoms of…

A

hypothyroidism

63
Q

Periorbital edema

A

swelling around the eyes

64
Q

Exophthalmos, elarged thyroid, tachycardia, diarrhea, and pretibial edema are symptoms of…

A

hyperthyroidism

65
Q

Exophthalmos

A

bulging, protruding eyeballs

66
Q

Pretibial Edema

A

anterior skin lesions of tibial region

67
Q

___________ is the underlying cause of up to 80% of hyperthyroidism

A

Graves’ disease

68
Q

Graves’ disease is more common in ________

A

women

69
Q

Graves’ disease is an ____________ disorder with an unknown (but likely genetic) cause

A

autoimmune

70
Q

With Graves’ disease, autoantibodies called ________________ (TSIs) override normal mechanisms

A

thyroid-stimulating immunogolbulins

71
Q

TSI leads to _________ of the thyroid gland and increased secretion of TH (especially ____!)

A

hyperplasia; T3

72
Q

TSI accounts for abnormalities of the __________ NS and ________ muscles

A

sympathetic; orbital

73
Q

Diplopia (_______ vision) and decreased acuity also results from Graves’

A

double

74
Q

Pretibial Myxedema: subcutaneous swelling of anterior portion of the legs from recruited __ cells which stimulate _____ acid production

A

T; hyaluronic

75
Q

Where is hyaluronic acid naturally found?

A

eyes and joints

76
Q

Normally after enlarging to respond to TH demand, the thyroid…

A

returns to normal size

77
Q

Nodular thyroid disease causes irreversible changes in _______ cells causing them to produce excess TH

A

follicular

78
Q

Thyroid multinodular goitre results from…

A

enlarged cells from an increased TH output

79
Q

Thyrotoxic crisis is aka…

A

the thyroid storm

80
Q

Death can occur within ___ hours without treatment with a thyrotoxic crisis

A

24

81
Q

Thyrotoxic Crisis may result from:

A

-Graves’ disease (esp. those subject to infection, pulmonary, or CV) disorder
-Thyroid surgery

82
Q

Which type (primary or central) accounts for most cases of hypothyroidism?

A

primary

83
Q

Which type (primary or central) is related to pituitary or hypothalamic failure?

A

central aka secondary

84
Q

What are 2 alternative names for autoimmune thyroiditis?

A

-Hashimoto’s disease
-Chronic Lymphocytic Thyroiditis

85
Q

What is the most common cause of primary hypothyroidism in Canada?

A

autoimmune thyroiditis

86
Q

What causes autoimmune thyroiditis?

A

auto-reactive T cells, NK cells and induction of apoptosis

87
Q

Congenital hypothyroidism occurs when a) thyroid tissue is _____ or with b) ___ synthesis defects

A

absent; TH

88
Q

How long is the fetus dependent on maternal T4?

A

first 20 weeks of gestation

89
Q

Insufficient T4 from mom to baby may lead to _______ defects

A

cognitive

90
Q

Symptoms of Congenital Hypothyroidism:

A

-high birth weight
-hypothermia
-neonatal jaundice
-difficulty eating
-horse cry
-protruding tongue
-excessive sleeping

91
Q

An examination of ______________ tells about T4 and TSH levels

A

umbilical cord

92
Q

___________ treatment will lead to normal growth and intellectual function if administered before 4 months of age

A

levothyroxine

93
Q

Without screening, congenital hypothyroidism may be difficult to determine before ___ months

A

4

94
Q

What is the most common pediatric chronic disease?

A

Type I Diabetes Mellitus

95
Q

___% of Canadians have type I diabetes mellitus

A

10

96
Q

Type I DM has a strong ______ link

A

genetic (can also be due to medications or virus)

97
Q

Is T1D fast or slow progressing?

A

slow

98
Q

T1D is an _________ __-cell-mediated disease

A

autoimmune T-cell

99
Q

What cells do the T1D T cells destroy?

A

pancreatic

100
Q

Where do T1D autoantigens express?

A

pancreatic beta cells

101
Q

Autoantigens detach and circulate to activate __-________ cells and macrophages to produce ________

A

T-cytotoxic; autoantibodies

102
Q

Autoantibodie production destroys beta cells and reduces ________ secretions

A

insulin

103
Q

Hyperglycemia results from insulin declining from __-__% of beta cells are destroyed

A

80-90%

104
Q

Why does T1D have glucose in urine?

A

glucose builds up in the blood and must be eliminated

105
Q

Diuresis is a T1D symptoms because…

A

there is a dramatic increase in thirst

106
Q

Diuresis

A

excessive urination

107
Q

Diabetic Ketoacidosis (life-threatening)

A

when proteins and fat are utilized due to insulin deficiency and cause high levels of circulating ketones

108
Q

Type II Diabetes Mellitus accounts for ___% of all diabetes in Canada

A

90

109
Q

What are the risk factors for T2D?

A

-age
-obesity
-hypertension
-physical activity
-family history

110
Q

T2D is linked to more than ___ genes that code for beta cell mass and functionality

A

60

111
Q

T2D results from insulin resistance and…

A

decreased insulin secretion by beta cells

112
Q

T2D is a _____-_______ response of insulin sensitive tissue

A

sub-optimal

113
Q

What are some examples of insulin sensitive tissue?

A

liver, muscle, adipose tissue

114
Q

The sub-optimal response of these tissues leads to insulin ____________

A

resistance

115
Q

Insulin Resistance

A

cell dysfunction of insulin receptors

116
Q

With T2D, ________ results in increased serum levels of ________ and decreased levels of _________

A

obesity; leptin; adiponectin

117
Q

With T2D, elevated levels of serum ____-____-acids lead to intracellular deposits of _____________ which decrease tissue response to insulin and lead to insulin resistance

A

free-fatty; triglycerides

118
Q

T2D - obesity is linked to ______insulinemia and decreased insulin receptor ________

A

hyper; density

119
Q

What is the effect of T2D?

A

beta-cell exhaustion - a decrease in beta cell mass and dysfunction

120
Q

Cushing’s syndrome occurs from chronic exposure to excess ________

A

cortisol

121
Q

Cushing’s disease results from excess ______ secretion or an ectopic-secreting ______________ tumour

A

ACTH; nonpituitary

122
Q

With hypercortisolism, normal dinural secretion patterns of ______ and _______ are lost and there is no increased ACTH or cortisol secretion in response to stress

A

ACTCH and cortisol

123
Q

Hypercortisolism results in _______ ACTH secretion with no _________________ control

A

excess; negative-feedback

124
Q

Cushing’s Disease Manifestations

A

-weight gain
-cravings
-increased glucose release
-osteoporosis
-muscle wasting
-vertebral compression fractures
-kyphosis
-reduced height
-stretched skin
-immunosuppression

125
Q

With Cushing’s disease, where does the weight gain occur?

A

-face
-trunk
-buffalo hump (upper back/neck area)

126
Q

Why do cravings happen with Cushing’s?

A

to increase fats and carbs available for fuel

127
Q

Why does Cushing’s involve glucose intolerance?

A

because of cortisol-induced insulin resistance

128
Q

What leads to osteoporosis?

A

reabsorption of bone components

129
Q

What leads to muscle wasting?

A

cortisol promotes protein breakdown for amino acid release

130
Q

Kyphosis

A

outward curvature of the spine “humpback”

131
Q

What leads to stretched skin?

A

weakened integumentary tissue

hlsc 222 - pathophysiology across the lifespan (17 decks)

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