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HLSC 222 Pathophysiology 🧫 > Chapter 19 > Flashcards

Chapter 19 Flashcards

1
Q

What are some diseases of the Posterior pituitary?

A

Abnormal secretion of antidiuretic hormone (ADH or Vasopressin)
Insufficient hormonal carrier proteins in plasma

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2
Q

Reduced secreteion of ADH from posterior pituitary causes?

A

Water excretion and ECF hyperosmolarity

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3
Q

Excess secretion of ADH from posterior pituitary causes?

A

Water reabsorption and hypoosmolarity

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4
Q

What does ADH act on?

A

Kidneys

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5
Q

What is syndrome of inappropriate antidiuretic hormone (SIADH)?

A

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

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6
Q

What are some common causes of SIADH?

A

Ectopic secretion of ADH by tumours
Surgery
Medications

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7
Q

WHat tumours cause ectopic secretion of ADH leading to SIADH?

A

Cancers of the stomach, duodenum and pancreas
Lymphomas, sarcomas (begins in bone)
CNS disorders: Encephalitis, meningitis

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8
Q

What surgery causes SIADH?

A

ANy surgery can rsult in increased ADH secrertion for up to 5-7 days

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9
Q

Why does surgery cause increased ADH?

A

It is likely related to fluid and volume changes following surgery
Following pituitary surgery, ADH is released in an unregulated manner

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10
Q

What medications cause SIADH?

A

Hypoglycemic medications (for diabetes mellitus)
Opioids
Antidepressants
Anti-inflammatory

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11
Q

What is the key feature of SIADH?

A

Increased kidney water reabsorption to peritubular capillaries

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12
Q

What is the mechanism of SIADH?

A

Increased ADH secretion causes increased water channel proteins inserted into the tubular luminal membrane

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13
Q

What is the result of SIADH?

A

Increased water reabsorption into ECF —-> Hypoosmolarity in ECF

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14
Q

What is normal osmolarity?

A

Match between [Na+] and [H2O]

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15
Q

What is hyperosmolarity?

A

More [Na+] than [H2O]

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16
Q

What is hypoosmolarity?

A

Less [Na+] than [H2O]

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17
Q

What do symptoms of SIADH result from?

A

Hyponatremia (Low blood [Na+])

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18
Q

What causes Hyponatremia (SIADH)?

A

-Low [Na+] bc of increased H2O reabsorption from kidney without matching levels of Na+ reabsorption

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19
Q

What do the effects of SIADH depend on?

A

Severity and rapidity of onset
-Serum sodium levels decrease rapidly from 140-130 mmol/L

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20
Q

SIADH effects: 130-120 mmol/L?

A

Vomiting
Abdominal cramps
Weight gain

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21
Q

SIADH effects: below 110 mmol/L?

A

Confusion
lethargy
muscle twitches
convulsions

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22
Q

How do symptoms of SIADH normally resolve?

A

With the correction of hyponatremia

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23
Q

What is diabetes insipidus/

A

Insufficiency of ADH activity leading to polyuria and polydipsia

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24
Q

Polyuria

A

Frequent urination

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25
Q

Polydipsia

A

Frequent drinking

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26
Q

What are the two forms of diabetes insipidus?

A

Neurogenic or Central
Nephrogenic

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27
Q

What causes neurogenic or central diabetes insipidus?

A

Insufficient secretion of ADH from the posterior pituitary
Lesions of the hypothalamus
PP interference with transport/release of ADH
Brain tumours, aneurysms

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28
Q

Diabetes Insipidus is a well-recognized complication of what?

A

Traumatic Brain Injury

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29
Q

What are the two types of Nephrogenic DI?

A

Acquired
Genetic

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30
Q

What is Acquired DI?

A

Related to medication disorders that damage renal tubules

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31
Q

What disorders are included in acquired DI?

A

Pyelonephritis (UTI)
Polycystic kidney disease

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32
Q

Polycystic kidney disease

A

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

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33
Q

What is Genetic DI?

A

Mutation of gene coding for aquaporin-2 (water channel)

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34
Q

What is a rare form of DI?

A

DI associated with pregnancy

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35
Q

How can pregnancy cause diabetes insipidus?

A

Increase in level of vasopressin-degrading enzyme; Vasopressinase

-Mild, doesn’t need treatment

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36
Q

What leads to Diabetes Insipidus?

A

Total inability to alter the concentration of urine caused by insufficient ADH

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37
Q

What does insufficient ADH lead to?

A

Large volumes of dilute urine and increased plasma osmolarity

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38
Q

Serum levels associated with DI?

A

Serum hypernatremia and hyperosmolarity

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39
Q

What are the clinical signs of diabetes insipidus?

A

Polyuria
Nocturia (waking to urinate)
Polydipsia

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40
Q

What is the normal urinary output?

A

1-2 L/day

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41
Q

What is someone with DI’s urinary output?

A

As high as 8-12 L/day and can be higher than daily fluid intake

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42
Q

What are the manifestations of longstanding DI?

A

Enlarged bladder capacity and hydronephrosis (swelling on one or both kidneys)

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43
Q

What is the onset of neurogenic DI?

A

Sudden

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44
Q

What is the onset of Nephrogenic DI?

A

Gradual

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45
Q

How is diabetes insipidus diagnosed?

A

Dilute urine
Hyperosmolarity, hypernatremia
Continued diuresis despite high serum osmolarity

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46
Q

Diabetes insipidus treatment?

A

ADH replacement
Oral or IV fluid replacement
Medications that increase the action of available ADH include carbamazepine (Tegretol)
New treatments: Reversing aquaporin-2 dysfunction

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47
Q

What are thyroid function disorders generally due to?

A

Primary dysfunction of the thyroid gland

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48
Q

Secondary dysfunction (thyroid disorders) occur because of?

A

Pituitary or hypothalamic alterations

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49
Q

What is Subclinical thyroid disease?

A

Thyroid disease with no symptoms but abnormal laboratory values

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50
Q

What thyroid disorder terms are often used interchangeably but have a subtle difference?

A

Thyrotoxicosis and Hyperthyroidism

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51
Q

Thyrotoxicosis

A

A condition resulting from any cause of increased hormone levels

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52
Q

Hyperthyroidism

A

Excess secretion of thyroid hormone from thyroid gland

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53
Q

What are common diseases that cause primary hyperthyroidism?

A

Graves disease
Toxic multinodular goiter

54
Q

What are features of thyrotoxicosis caused by?

A

Metabolic effects of increased serum thyroid hormones

55
Q

How does thyrotoxicosis/hyperthyroidism manifest?

A

Increased metabolic rate
Increased heat intolerance
Increased tissue sensitivity to SNS stimulation

56
Q

Signs/symptoms of Hypothyroidism?

A

Periorbital edema (swelling around eyes)
Smaller thyroid
Bradycardia
Constipation
Edema of extremities

57
Q

Signs/syptoms of Hyperthyroidism?

A

Expothalmos (buldging, protruding eyes)
Enlarged thyroid
tachycardia
diarrhea
Pretibial edema (anterior skin lesions of tibial region)

58
Q

What is the underlying cause of 80% of hyperthyroidism?

A

Grave’s disease

59
Q

Grave’s disease is more common in which gender?

A

Females

60
Q

What is the exact cause of Grave’s disease?

A

The exact cause is unknown
-Likely genetic with environmental aspects

61
Q

What kind of disease is Grave’s disease?

A

Autoimmune

62
Q

What is the autoimmune result of Grave’s disease?

A

Autoantibodies stimulate receptors on the thyroid gland

63
Q

What are the antibodies associated with grave’s disease?

A

Thyroid-stimulating immunoglobulins (TSIs)

64
Q

What do TSIs do?

A

Override normal regulatory mechanisms

65
Q

What does TSI stimulation cause?

A

Hyperplasia of gland and increased secretion of TH (especially T3)

66
Q

What 2 manifestions of Grave’s disease do TSIs contribute to?

A
  1. Abnormalities from hyperactivity of Sympathetic Nervous System
  2. Changes to orbital contents with enlargement of orbital muscles
67
Q

What is the result of Grave’s disease/

A

Exophthalmos
Diplopia (double vision)
Decrease visual acuity
Pretibial myxedema

68
Q

Pretibial myxedema

A

Subcutaneous swelling of anterior portion of legs

69
Q

What causes pretibial myxedema swelling?

A

Recruited t cells that stimulate excessive amounts of hyaluronic acid production

70
Q

Hyaluronic acid

A

Natural substance found in fluids in eyes and joints

71
Q

What is normal nodular thyroid disease?

A

Thyroid enlarges in response to increased demand for TH, when the condition subsides, the thyroid returns to normal size

72
Q

What is Abnormal nodular thyroid disease?

A

Irreversible change sin some follicular cells causing the production of excess TH

73
Q

What is a toxic multi-nodular goitre?

A

Several nodules increase in size and increase TH output causing thyroid gland to get bigger

74
Q

What is Thyrotoxic crisus (thyroid storm)?

A

Rare/dangerously worsening state of excessive release of TH

75
Q

When can death occur bc of Thyrotoxic crisis?

A

Within 24 hours without treatment

76
Q

What individuals experience Thyrotoxic crisis?

A

Those with Grave’s disease and subject to infection, pulmonary or CV disorder

77
Q

What can a thyrotoxic crisis occur because of?

A

Thyroid surgery

78
Q

What is Hypothyroidism?

A

Results from deficient TH production by the thyroid gland

79
Q

What are the two kinds of Hypothyroidism?

A

Primary
Central (secondary)

80
Q

What kind of hypothyroidism accounts for most cases?

A

Primary

81
Q

What is secondary/central hypothyroidism related to?

A

Pituitary or hypothalamic failure

82
Q

What is Autoimmune thyroiditis?

A

aka Hashimoto’s disease
Chronic lymphocytic thyroiditis

83
Q

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

A

Autoimmune thyroiditis (Hashimoto’s)

84
Q

What does Hashimoto’s disease do?

A

Causes gradual inflammatory destruction of thyroid tissue

85
Q

What causes Autoimmune thyroiditis (Hashimoto’s)?

A

infiltration of autoreactive T cells, NK cells, and induction of apoptosis

86
Q

Who is affected by Congenital hypothyroidism?

A

Infants with thyroid tissue absent or with hereditary defects in TH synthesis

87
Q

What is TH essential for?

A

Embryonic growth, particularly brain tissue

88
Q

What is the fetus dependent upon for the first 20 weeks of gestation?

A

Maternal T4

89
Q

What can a lack of maternal T4 cause?

A

Cognitive defects

90
Q

What are the symptoms of congenital hypothyroidism?

A

High birth weight
Hypothermia
neonatal jaundice

91
Q

What kind of examination can provide T4 and TSH levels?

A

Umbilical cord blood exam

92
Q

Normal growth and intellectual function can occur with the treatment of what? (Congenital hypothyroidism)

A

Levothyroxine

93
Q

When must treatment of levothyroxine be used?

A

Before child is 4 months old

94
Q

Without screening, hypothyroidism may be difficult to determine before what age?

A

4 months

95
Q

What are the symptoms of congenital hypothyroidism before 4 months?

A

difficulty eating
horse cry
protruding tongue
excessive sleeping

96
Q

What is the most common pediatric disease?

A

Type 1 Diabetes mellitus

97
Q

What percent of Canadians have Type 1 diabetes?

A

10%

98
Q

What is Type 1 diabetes linked to?

A

Strong genetic link
Environmental factors (medications, viruses)

99
Q

What is type 1 diabetes mellitus?

A

Slow progressing autoimmune T-cell-mediated disease that destroys pancreatic cells

100
Q

How do gene-environment interactions contribute to Type 1 Diabetes Mellitus?

A

They lead to the formation of autoantigens expressed on pancreatic beta cells.

101
Q

What happens to autoantigens in Type 1 Diabetes Mellitus?

A

Autoantigens detach and circulate in the bloodstream and lymphatics.

102
Q

What cells activate in Type 1 diabetes mellitus because of autoantigens?

A

Macrophages
T-cytotoxic cells

103
Q

What results from activating T-cytotoxic cells and macrophages in Type 1 Diabetes Mellitus?

A

The production of autoantibodies occurs.

104
Q

What is the final outcome of the autoimmune response in Type 1 Diabetes Mellitus?

A

The destruction of pancreatic beta cells, leading to reduced insulin secretion.

105
Q

How many beta cells must be destroyed for insulin to decline enough, causing hyperglycemia to develop in Type 1 Diabetes Mellitus?

A

80-90% of beta cells must be destroyed

106
Q

How does type 1 diabetes manifest?

A

Insulin deficiency + hyperglycemia
-Glucose builds up in blood and urine
-Glucose concentration in urine exceeds renal threshhold

107
Q

What occurs when glucose build up in blood during Type 1 diabetes?

A

diuresis (excessive urination)
Dramatic increase in thirst

108
Q

What condition can develop because of Type 1 diabetes lack of insulin?

A

Diabetic ketoacidosis
-Can be life-threatening

109
Q

What causes diabetic ketoacidosis?

A

Proteins and fat become utilized leading to high levels of circulating ketones due to lack of insulin

110
Q

What kind of diabetes accounts for 90% of all diabetes in Canada?

A

Type 2 Diabetes Mellitus

111
Q

What are risk factors associated with Type 2 diabetes?

A

Age
Obesity
Hypertension
Physical activity
Family history

112
Q

What is Type 2 diabetes occurrence linked to?

A

More than 60 genes which code for beta cell mass and functionality

113
Q

What two mechanisms are a result of Type 2 diabetes?

A

Insulin resistance
decreased insulin secretion by beta cells

114
Q

What is Type 2 diabetes?

A

A sub-optimal response of insulin-sensitive tissue (especially liver, muscle, and adipose tissue), leading to a condition of insulin resistance due to cell dysfunction of insulin receptors.

115
Q

What is one mechanism involved in the development of insulin resistance in Type 2 Diabetes Mellitus related to obesity?

A

Obesity results in increased serum levels of leptin and decreased levels of adiponectin, which are associated with inflammation and insulin sensitivity.

116
Q

How do elevated levels of serum free fatty acids contribute to insulin resistance in Type 2 Diabetes Mellitus?

A

They cause intracellular deposits of triglycerides, which decrease tissue response to insulin, leading to insulin resistance.

117
Q

What is obesity linked to in Type 2 Diabetes Mellitus?

A

Obesity is linked to hyperinsulinemia and decreased insulin receptor density.

118
Q

What is the result of the mechanisms involved in insulin resistance in Type 2 Diabetes Mellitus?

A

Hyperinsulinemia

119
Q

What is the effect of hyperinsulinemia on beta cells in Type 2 Diabetes Mellitus?

A

Beta-cell “exhaustion,” which involves a decrease in beta-cell mass and dysfunction of normal beta-cell function.

120
Q

What is Cushing’s syndrome?

A

Chronic exposure to excess cortisol

121
Q

What is cushing’s disease of result of?

A

Excess secretion of ACTH by anterior pituitary or an ectopic-secreting nonpituitatry tumour

122
Q

What two observations apply with hypercortisolism?

A
  1. Normal diurnal secretion patterns of
    ACTH and cortisol are lost
  2. There is no increased ACTH and cortisol
    secretion in response to stress
123
Q

WHat is the result of the two observations that apply to hypercortisolism?

A

Excess ACTH secretion but a loss of negative-feedback controls on ACTH secretion
Hypercortisolism symptoms develop

124
Q

How does Cushing’s syndrome manifest?

A

Weight gain
-Face, trunk, buffalo hump

125
Q

What causes the weight gain associated with Cushing’s?

A

Cortisol increases cravings to increase fats and carbs available for fuel

126
Q

What does cortisol increase the release of?

A

Glucose

127
Q

What intolerance can develop during Cushing’s?

A

Glucose intolrance because of cortisol-induced insulin resistance

128
Q

What bone condition is a result of Cushing’s?

A

Osteoporosis
-Bone components reabsorbed

129
Q

How does Cushing’s cause muscle wasting?

A

Cortisol is use to break down proteins for a.a release

130
Q

How are the vertebrae affected by cushings?

A

Veretebral compression fractures
Kyphosis (outward curve of spine ‘humpback’)
Reduced height

131
Q

How is the skin affected by Cushing’s?

A

Weakened integumentary tissue
-stretched skin

132
Q

What is supressed because of Cushing’s?

A

Immune system

HLSC 222 Pathophysiology 🧫 (16 decks)

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