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Pathophysiology > Chapter 19 - Alteration In Hormonal Regulation > Flashcards

Chapter 19 - Alteration In Hormonal Regulation Flashcards

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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
Medication disorders in acquired nephrogenic Diabetes insipidus
-pyelonephritis (UTI) -polycystic kidney disease (genetic disorder many fluid filed cysts grow in your kidneys)
26
Genetic neophrogenic Diabetes insipidus
Mutation of gene coding for aquaporon 2 (water channel)
27
Rare case of Diabetes insipidus
Associated with pregnancy -usually mild and doesn’t require treatment
28
What is associated with the rare Diabetes insipidus
An increase in level of vasopressin degrading enzyme vasopressin are
29
Pathophysiology of Diabetes insipidus
Total inability to alter concentration of urine -insufficient ADH causing large volume of dilute urine, increased plasma osmolarity -serum hypernatremia and hyper osmolarity
30
Clinical signs of Diabetes insipidus
Polyuria, nocturia (waking up at night to urinate), polydispia
31
Normal urinary output vs Diabetes insipidus output
Normal: 1-2L/day Diabetes insipidus: 8-12L/day
32
Long standing Diabetes insipidus
Enlarged bladder capacity and hydro nephronsis (swelling of one or both kidneys
33
Onset of neurogenic Diabetes insipidus and nephrogenic Diabetes insipidus
Neurogenic: sudden Nephrogenic: gradual
34
Diagnosis of Diabetes insipidus
Dilute urine -hyper osmolarity, hypernatremia -continued diuresis despite high serum osmolarity (normally there is extra urine when body needs to get rid of something)
35
TX for Diabetes insipidus
-ADH replacement -oral/intravenous fluid replacement -carbamazepine (tegretol) -revering acquaporing-2 dysfunction
36
Thyroid function disorder generally due to
Primary dysfunction of thyroid gland
37
Secondary thyroid dysfunction occurs because of
Pituitary or hypothalamic alterations
38
Subclinical thyroid disease
Thyroid disease with no symptoms but abnormal laboratory values
39
Thyrotoxicosis
Condition resulting from any cause of inc thyroid hormone levels -metabolic effects of inc serum thyroid hormones
40
Hyperthyroidism
Excess secretion of thyroid hormone from thyroid gland
41
Hypothyroidism
-Loss of hair, coarse, brittle hair -puffy face -normal/small thyroid -bradycardia heart failure -constipation -cold intolerance -Edelman of extremities
42
Hyperthyroidism
-thin hair -exophthalmos -enlarged thyroid (warm on palpitation, nodular) -tachycardia heart failure -weight loss -diarrhea -warm skin, sweaty palms -hyper reflexia -pertibial deems
43
Exopathalmos
Building protruding eyeballs -hyperthyroidism
44
What disease makes up 80% of hyperthyroidism
Graves’ disease
45
Graves’ disease
Autoimmune -more common in women -exact cause unknown -genetic with environmental aspects
46
Graves’ disease results in
Autoantibodies stimulate receptors on thyroid gland
47
Antibodies in Graves’ disease
Thyroid stimulating immunoglobulins override normal regulatory mechanisms
48
TSI stimulation causes
Hyperplasia of gland and inc secretion of TH (T3)
49
TSIs contribute to two distinguishing manifestations of Graves’ disease:
1. Abnormalities from hyperactivity of sympathatic nervous system 2. Changes to orbital contents with enlargement of orbital muscles
50
Graves’ disease results in
Exophthalmos, diplopia (double vision), decreased visual acuity -pretibial myxedema: swelling of anterior portion of legs
51
Swelling of pretibial myxedema is a result of
Recruited T cells that stimulate excessive amounts of hyaluronic acid production
52
Hyaluronic acid
Natural substance found in fluids in eyes and joints
53
Normal thyroid
Thyroid enlarges in response to increased demand for TH, when condition subsides, thyroid returns to normal size
54
Abnormal thyroid
Irreversible changes in some follicular cells causing production of excess TH
55
Toxic multinodular goitre
Several nodules increase in size and increase TH output = increased size of thyroid gland
56
Thyrotoxic crisis
Rare and dangerously worsening state = death occurring within 24 hours without treatment -can occur due to thyroid surgery
57
Hypothyroidism results from
Deficient TH production by thyroid gland
58
Primary vs central hypothyroidism
Primary: accounts for most cases Central: related to pituitary or hypothalamic failure
59
Autoimmune thyroiditis examples
Hashimotos disease, chromic lymphocytic thyroiditis
60
Most common cause of primary hypothyroidism in Canada
Autoimmune thyroiditis
61
Autoimmune thyroiditis results in
Gradual inflammatory destruction of thyroid tissue
62
Causes of Autoimmune thyroiditis
Infiltration of auto reactive T cells, NK cells, and induction of apoptosis
63
Congenital hypothyroidism
Occurs in infants when thyroid tissue is absent or with hereditary defects in TH synthesis
64
TH is essential for
Embryonic growth (brain tissue) -depend upon maternal T4 for first 20 weeks of gestation, and lack of it results in cognitive defects
65
Symptoms of congenital hypothyroidism
-high brith weight, hypothermia, neonatal jaundice -umbilical cord blood examination can provide T4 and TSH levels
66
Normal growth and intellectual function can occur with
Treatment of levothyroxine before child is 4 months old
67
Without ___, hypothyroidism may be difficult to determine before 4 months
Screening
68
Symptoms that may be missed without screening
Difficulty eating, horse cry, protruding tongue, excessive sleeping
69
Hormones of endocrine pancreas
-somatostatin -glucagon -insulin
70
Most common paediatric chronic disease, and 10% of Canadians have this form
Type 1 diabetes mellitus
71
Pathophysiology of Type 1 diabetes mellitus
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
Autoantigens and result in Type 1 diabetes mellitus
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
In order for insulin secretion to decline and Jane hyperglycaemia develop
80-90% of beta cells must be destroyed
74
Manifestations of type 1 diabetes mellitus
Insulin deficiency and hyperglycaemia -glucose builds up in blood and urine, glucose in urine exceeds renal threshold
75
Result of glucose in urine exceeding renal threshold
Diuresis (excessive urination) causing dramatic inc in thirst
76
Due to lack of insulin
Proteins and fat become utilized leading to high levels of circulating ketones causing diabetic ketoacidosis -which can be life threatening
77
What type of diabetes accounts for 90% of all diabetes in Canada
type 2 diabetes mellitus
78
Risk factors for type 2 diabetes mellitus
Age, obesity, hypertension, physical activity, family history
79
Occurrence of type 2 diabetes mellitus is linked to
More than 60 genes which code for beta cell mass and functionality
80
Result of type 2 diabetes mellitus
Two mechanisms: insulin resistance and decreased insulin secretion by beta cells
81
Metabolic syndrome
A list of disorders predict a high risk of type 2 diabetes mellitus
82
Criteria fro diagnosis of metabolic syndrome
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
Pathophysiology of type 2 diabetes mellitus
A sub optimal response of insulin sensitive tissue (mainly liver, muscle, adipose tissue) = condition of insulin resistance (cell dysfunction of insulin receptors)
84
Mechanisms involved in type 2 diabetes mellitus
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
Result of type 2 diabetes mellitus mechanisms
Hyperinsulinemia
86
Beta cell exhaustion
Decrease in beta cell mass and dysfunction of normal beta cell function
87
Cushing syndrome
Chronic exposure to excess cortisol
88
Cushing disease is a result of
Excess secretion of ACTH by anterior pituitary or an ectopic secreting non pituitary tumour
89
Two observations apply with hypercortisolism
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
Result of hypercortisolism
-excess ACTH secretion but a loss of negative feedback controls on ACTH -symptoms of hypercortisolism develops
91
Cortisol will…
-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
Cortisol = break down of
Proteins for amino acid release = muscle wasting
93
Manifestations of Cushings disease
-weight gain -vertebral compression fractures, kyphosis and reduced height -weakened integumentary tissue -suppression of immune system
94
Kyphosis
Outward curvature of spine -humpback

Pathophysiology (20 decks)

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