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Pathophysiology > Chapter 19 - Alteration In Hormonal Regulation > Flashcards

Chapter 19 - Alteration In Hormonal Regulation Flashcards

1
Q

Reduced secretion from PP

A

water excretion and ECF hyper osmolarity

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2
Q

Diseases of posterior pituitary

A
  1. Abnormal secretion of antidiuretic hormone
  2. Insufficient hormonal carrier proteins in plasma
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3
Q

Excess secretion from pp

A

water reabsorption and hypo osmolarity

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4
Q

Syndrome of inappropriate anitdiuretic hormone

A

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

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5
Q

Common causes of Syndrome of inappropriate anitdiuretic hormone

A
  1. Ectopic secretion of ADH by tumours
  2. Surgery
  3. Medications
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6
Q

Ectopic secretion of ADH by tumours

A

-Cancers of stomach and duodenum, pancreas
-lymphomas, sarcomas (cancer in bone)
-CNS disorders: encephalitis and meningitis

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7
Q

Surgery causing Syndrome of inappropriate anitdiuretic hormone

A

Any surgery can result in inc ADH, up to 5-7 days
-mechanism likely related to fluid and volume changes following surgery
-following pituitary surgery ADH is released in an unregulated manner

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8
Q

Medications causing Syndrome of inappropriate anitdiuretic hormone

A

Hypoglycaemic medications (diabetes mellitus), opioids, antidepressants, anti inflammatory

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9
Q

Key feature of Syndrome of inappropriate anitdiuretic hormone

A

Increased kidney water reabsorption to peritubular capillaries

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10
Q

Mechanism in Syndrome of inappropriate anitdiuretic hormone

A

Increased ADH secretion = inc water channel proteins inserted into tubular luminal membrane

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11
Q

Result of Syndrome of inappropriate anitdiuretic hormone

A

Inc water reabsorption into ECF = hypo osmolarity

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12
Q

Normal osmolarity

A

Match between Na and H2O

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13
Q

Hyper osmolarity

A

Na>H2O

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14
Q

Hypoosmolarity

A

Na<H2O

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15
Q

Manifestations of Syndrome of inappropriate anitdiuretic hormone

A

=hyponatremia (Na in blood is low) = inc H2O reabsorbed from kidney

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16
Q

Effects of Syndrome of inappropriate anitdiuretic hormone

A

Dependent upon severity and rapidity of onset

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17
Q

Serum sodium levels decrease rapidly from

A

140 to 130 mmol/L

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18
Q

130-120 mmol/L

A

Vomiting, abdominal cramps, weight gain

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19
Q

Below 110 mmol/L

A

Confusion, lethargy, muscle twitches and convulsions

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20
Q

Symptoms resolve in Syndrome of inappropriate anitdiuretic hormone with

A

Correction of hyponatremia

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21
Q

Diabetes insipidus

A

Insufficiency of ADH activity, leading to polyuria (frequent urination) and polydipsia (frequent drinking)

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22
Q

Neurogenic or central Diabetes insipidus is caused by

A

-Insufficient secretion of ADH from posterior pituitary
-lesions on hypothalamus
-PP interference with transport/release of ADH
-brain tumours, aneurysms
-TBI complication

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23
Q

Nephrogenic Diabetes insipidus

A

Acquired or genetic

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24
Q

Acquired nephrogenic Diabetes insipidus

A

Related to medication disorders that damage renal tubules

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25
Q

Medication disorders in acquired nephrogenic Diabetes insipidus

A

-pyelonephritis (UTI)
-polycystic kidney disease (genetic disorder many fluid filed cysts grow in your kidneys)

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26
Q

Genetic neophrogenic Diabetes insipidus

A

Mutation of gene coding for aquaporon 2 (water channel)

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27
Q

Rare case of Diabetes insipidus

A

Associated with pregnancy
-usually mild and doesn’t require treatment

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28
Q

What is associated with the rare Diabetes insipidus

A

An increase in level of vasopressin degrading enzyme vasopressin are

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29
Q

Pathophysiology of Diabetes insipidus

A

Total inability to alter concentration of urine
-insufficient ADH causing large volume of dilute urine, increased plasma osmolarity
-serum hypernatremia and hyper osmolarity

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30
Q

Clinical signs of Diabetes insipidus

A

Polyuria, nocturia (waking up at night to urinate), polydispia

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31
Q

Normal urinary output vs Diabetes insipidus output

A

Normal: 1-2L/day

Diabetes insipidus: 8-12L/day

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32
Q

Long standing Diabetes insipidus

A

Enlarged bladder capacity and hydro nephronsis (swelling of one or both kidneys

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33
Q

Onset of neurogenic Diabetes insipidus and nephrogenic Diabetes insipidus

A

Neurogenic: sudden

Nephrogenic: gradual

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34
Q

Diagnosis of Diabetes insipidus

A

Dilute urine
-hyper osmolarity, hypernatremia
-continued diuresis despite high serum osmolarity (normally there is extra urine when body needs to get rid of something)

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35
Q

TX for Diabetes insipidus

A

-ADH replacement
-oral/intravenous fluid replacement
-carbamazepine (tegretol)
-revering acquaporing-2 dysfunction

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36
Q

Thyroid function disorder generally due to

A

Primary dysfunction of thyroid gland

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37
Q

Secondary thyroid dysfunction occurs because of

A

Pituitary or hypothalamic alterations

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38
Q

Subclinical thyroid disease

A

Thyroid disease with no symptoms but abnormal laboratory values

39
Q

Thyrotoxicosis

A

Condition resulting from any cause of inc thyroid hormone levels
-metabolic effects of inc serum thyroid hormones

40
Q

Hyperthyroidism

A

Excess secretion of thyroid hormone from thyroid gland

41
Q

Hypothyroidism

A

-Loss of hair, coarse, brittle hair
-puffy face
-normal/small thyroid
-bradycardia heart failure
-constipation
-cold intolerance
-Edelman of extremities

42
Q

Hyperthyroidism

A

-thin hair
-exophthalmos
-enlarged thyroid (warm on palpitation, nodular)
-tachycardia heart failure
-weight loss
-diarrhea
-warm skin, sweaty palms
-hyper reflexia
-pertibial deems

43
Q

Exopathalmos

A

Building protruding eyeballs
-hyperthyroidism

44
Q

What disease makes up 80% of hyperthyroidism

A

Graves’ disease

45
Q

Graves’ disease

A

Autoimmune
-more common in women
-exact cause unknown
-genetic with environmental aspects

46
Q

Graves’ disease results in

A

Autoantibodies stimulate receptors on thyroid gland

47
Q

Antibodies in Graves’ disease

A

Thyroid stimulating immunoglobulins override normal regulatory mechanisms

48
Q

TSI stimulation causes

A

Hyperplasia of gland and inc secretion of TH (T3)

49
Q

TSIs contribute to two distinguishing manifestations of Graves’ disease:

A
  1. Abnormalities from hyperactivity of sympathatic nervous system
  2. Changes to orbital contents with enlargement of orbital muscles
50
Q

Graves’ disease results in

A

Exophthalmos, diplopia (double vision), decreased visual acuity
-pretibial myxedema: swelling of anterior portion of legs

51
Q

Swelling of pretibial myxedema is a result of

A

Recruited T cells that stimulate excessive amounts of hyaluronic acid production

52
Q

Hyaluronic acid

A

Natural substance found in fluids in eyes and joints

53
Q

Normal thyroid

A

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

54
Q

Abnormal thyroid

A

Irreversible changes in some follicular cells causing production of excess TH

55
Q

Toxic multinodular goitre

A

Several nodules increase in size and increase TH output = increased size of thyroid gland

56
Q

Thyrotoxic crisis

A

Rare and dangerously worsening state = death occurring within 24 hours without treatment
-can occur due to thyroid surgery

57
Q

Hypothyroidism results from

A

Deficient TH production by thyroid gland

58
Q

Primary vs central hypothyroidism

A

Primary: accounts for most cases
Central: related to pituitary or hypothalamic failure

59
Q

Autoimmune thyroiditis examples

A

Hashimotos disease, chromic lymphocytic thyroiditis

60
Q

Most common cause of primary hypothyroidism in Canada

A

Autoimmune thyroiditis

61
Q

Autoimmune thyroiditis results in

A

Gradual inflammatory destruction of thyroid tissue

62
Q

Causes of Autoimmune thyroiditis

A

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

63
Q

Congenital hypothyroidism

A

Occurs in infants when thyroid tissue is absent or with hereditary defects in TH synthesis

64
Q

TH is essential for

A

Embryonic growth (brain tissue)
-depend upon maternal T4 for first 20 weeks of gestation, and lack of it results in cognitive defects

65
Q

Symptoms of congenital hypothyroidism

A

-high brith weight, hypothermia, neonatal jaundice
-umbilical cord blood examination can provide T4 and TSH levels

66
Q

Normal growth and intellectual function can occur with

A

Treatment of levothyroxine before child is 4 months old

67
Q

Without ___, hypothyroidism may be difficult to determine before 4 months

68
Q

Symptoms that may be missed without screening

A

Difficulty eating, horse cry, protruding tongue, excessive sleeping

69
Q

Hormones of endocrine pancreas

A

-somatostatin
-glucagon
-insulin

70
Q

Most common paediatric chronic disease, and 10% of Canadians have this form

A

Type 1 diabetes mellitus

71
Q

Pathophysiology of Type 1 diabetes mellitus

A

Strong genetic link as well as environmental
-slow progressing autoimmune T cell mediated disease destroying pancreatic cells

Gene environmental interactions = formation of autoantigens expressed on pancreatic beta cells

72
Q

Autoantigens and result in Type 1 diabetes mellitus

A

Autoantigens detach and circulate in bloodstream and lymphatics
-activation of T cytotoxic cells and macrophages and production of autoantibodies occurs
-result in pancreas beta cell destruction reducing insulin secretion

73
Q

In order for insulin secretion to decline and Jane hyperglycaemia develop

A

80-90% of beta cells must be destroyed

74
Q

Manifestations of type 1 diabetes mellitus

A

Insulin deficiency and hyperglycaemia
-glucose builds up in blood and urine, glucose in urine exceeds renal threshold

75
Q

Result of glucose in urine exceeding renal threshold

A

Diuresis (excessive urination) causing dramatic inc in thirst

76
Q

Due to lack of insulin

A

Proteins and fat become utilized leading to high levels of circulating ketones causing diabetic ketoacidosis
-which can be life threatening

77
Q

What type of diabetes accounts for 90% of all diabetes in Canada

A

type 2 diabetes mellitus

78
Q

Risk factors for type 2 diabetes mellitus

A

Age, obesity, hypertension, physical activity, family history

79
Q

Occurrence of type 2 diabetes mellitus is linked to

A

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

80
Q

Result of type 2 diabetes mellitus

A

Two mechanisms: insulin resistance and decreased insulin secretion by beta cells

81
Q

Metabolic syndrome

A

A list of disorders predict a high risk of type 2 diabetes mellitus

82
Q

Criteria fro diagnosis of metabolic syndrome

A
  1. Inc waist circumference
  2. Plasmas triglycerides >1.7 or medication related
  3. Plasma high density lipoprotein cholesterol
  4. Blood pressure systolic >130/85
  5. Fasting plasma glucose >5.6
83
Q

Pathophysiology of type 2 diabetes mellitus

A

A sub optimal response of insulin sensitive tissue (mainly liver, muscle, adipose tissue) = condition of insulin resistance (cell dysfunction of insulin receptors)

84
Q

Mechanisms involved in type 2 diabetes mellitus

A
  1. Obesity (inc serum levels of lepton and Dec levels of adiponectin)
  2. Elevated levels of serum free fatty acids = intracellular deposits of triglycerides= Dec response to insulin
  3. Obesity linked to hyperinsulinemia and Dec insulin receptor density
85
Q

Result of type 2 diabetes mellitus mechanisms

A

Hyperinsulinemia

86
Q

Beta cell exhaustion

A

Decrease in beta cell mass and dysfunction of normal beta cell function

87
Q

Cushing syndrome

A

Chronic exposure to excess cortisol

88
Q

Cushing disease is a result of

A

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

89
Q

Two observations apply with hypercortisolism

A
  1. Normal diurnal secretion patterns of ACTH and cortisol are lost
  2. There is no inc ACTH and cortisol secretion in response to stress
90
Q

Result of hypercortisolism

A

-excess ACTH secretion but a loss of negative feedback controls on ACTH
-symptoms of hypercortisolism develops

91
Q

Cortisol will…

A

-inc craving to inc fats and carbohydrates available for fuel which causes weight gain (face, trunk, buffalo hump)
-inc release of glucose
-glucose intolerance occurs because of cortisol induced insulin resistance
-reabsorption of bone components causes osteoporosis

92
Q

Cortisol = break down of

A

Proteins for amino acid release = muscle wasting

93
Q

Manifestations of Cushings disease

A

-weight gain
-vertebral compression fractures, kyphosis and reduced height
-weakened integumentary tissue
-suppression of immune system

94
Q

Kyphosis

A

Outward curvature of spine
-humpback

Pathophysiology (20 decks)

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