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Pathophysiology > Chapter 10 > Flashcards

Chapter 10 Flashcards

1
Q

What are the 4 hypofunction dysfunctions of the endocrine system?

A
  • Congenital defects (absence or impaired development of the gland or hormone synthesis).
  • Gland destruction (disruption of blood flow, infection, inflammation, autoimmune, neoplasm or drug therapy).
  • Aging
  • Receptor defects
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2
Q

What are the 3 hyperfunction dysfunctions of the endocrine system?

A
  • Excessive stimulation
  • Hyperplasia
  • Ectopic source i.e.. Hormone producing tumors
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3
Q

What do releasing hormones of the hypothalamus do?

A

Releasing hormones from hypothalamus tell the pituitary what to release into the blood

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4
Q

What do trophic hormones of the hypothalamus do?

A

Trophic hormones from the pituitary tell specific peripheral glands to grow and produce their hormones

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5
Q

Where is growth hormone produced?

A

anterior pituitary

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6
Q

What are the actions of growth hormone?

A

Bone & muscle growth
Protein synthesis
Fat metabolism
CHO metabolism

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7
Q

What is growth hormone stimulated by?

A
  • Hypoglycemia, fasting, starvation

- Stress

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8
Q

What is growth hormone inhibited by?

A
  • Increased glucose levels, free fatty acid release, and obesity
  • Cortisol
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9
Q

What disease occurs with a deficiency of growth hormone?

A

Dwarfism

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10
Q

What diseases occur with an excess of growth hormone?

A

In childhood: gigantism

In adulthood: acromegaly

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11
Q

What causes growth hormone deficiency in children?

A
  • Idiopathic

- Pituitary tumors

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12
Q

What are the clinical manifestations of GH and IGF deficiency in children?

A
  • Decreased birth length
  • Decreased growth rate
  • Normal intelligence
  • Short stature
  • Obesity
  • Immature facial features
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13
Q

What are the clinical manifestations of GH deficiency in adults?

A

-Change in body composition with decreased overall lean body mass

-↑ Cardiovascular risk factors
Increased body fat
↑ LDL
↓ HDL
Insulin resistance

-↓ bone mineral density

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14
Q

What are the clinical manifestations of adult GH excess?

A

-Slow onset
-Bone overgrowth
*Enlargement of the small
bones of the hands and
feet
*Enlargement of facial
features
Bulbous nose, slanted
forehead, protruding lower
jaw
-Splayed teeth
-Kyphosis
-Joint pain
-Cartilage growth
-Deepening voice (enlargement of larynx)
-Bronchitis
-Enlargement of the heart
-Accelerated atherosclerosis
50-70% develop diabetes mellitus
-Sleep apnea (90% of people

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15
Q

What are the actions of thyroid hormones (t3 & t4)?

A
  • ↑ metabolic rate
  • ↑ O2 consumption
  • ↑ heart rate, contractility, cardiac output
  • ↑ ventilation
  • ↑ peristalsis and production of gastric secretions
  • Enhance skeletal muscle reactivity
  • Interaction with the SNS
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16
Q

What are 3 thyroid function disorders?

A
  • Goiter
  • Hypothyroidism
  • Hyperthyroidism
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17
Q

What is a goiter?

A

Enlargement of the thyroid gland

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18
Q

What is the cause of goiter?

A

Usually compensatory hyperplasia (increase in size) and hypertrophy (increase in number)

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19
Q

When is the goiter toxic and when is it nontoxic?

A 
toxic = hyper
non = hypo
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20
Q

What is hypothryoidism?

A

Thyroid dysfunction
Thyroid dysfunction
↓ T3 & T4

Inadequate stimulation of thyroid
Anterior pituitary dysfunction
↓ Thyroid stimulating hormone (TSH) →↓ T3 & T4
Hypothalamic dysfunction
↓ Thyroid releasing hormone (TRH) → ↓ TSH →↓ T3 & T4

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21
Q

What is myxedema?

A

Accumulation of hydrophilic mucopolysaccharide substance (Myxedematous fluid) in the connective tissues of the body

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22
Q

What are the clinical manifestations in hypothyroidism?

A

-Weakness & fatigue
-Weight gain w/ loss of appetite
-Cold intolerance
-Dry rough skin
-Coarse brittle hair
-↓ GI motility
-Constipation, flatulence & abdominal distention
-Nervous System
-Lethargy, mental dullness & impaired memory
-Myxedema Coma
end-stage hypothyroidism

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23
Q

What are the clinical manifestations of myxedema?

A
  • Puffy face
  • Enlarged tongue
  • Hoarse, husky voice
  • Pericardial and pleural effusions
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24
Q

What is another name for hyperthyroidism?

A

Thyrotoxicosis

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25
Q

What does graves disease come from?

A

secondary hyperthyroidism

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26
Q

What is graves disease?

A

Autoimmune disorder of unknown etiology

Thyroid stimulating antibodies (TSAbs)

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27
Q

What is Exophtalmos?

A 
Protrusion of the eyeballs
    -Prone to corneal 
     ulcerations → blindness
    -Extraocular muscle 
     paralysis
    -Involvement of the optic 
     nerve
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28
Q

What are the clinical manifestations of hyperthryoidism?

A

Increased O2 consumption
Shortness of breath

Hypermetabolism
Weight loss w/ large appetite, fatigue, muscle cramps, heat intolerance, excessive sweating

Excessive SNS activity
Nervousness, irritability, tachycardia, palpitations

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29
Q

What are the adrenal cortical hormones?

A

Aldosterone (Mineralocorticoid)

Cortisol (Glucocorticoid)

Androgens (Adrenal sex hormones)

Catecholamines (epinephrine, norepinephrine and dopamine

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30
Q

What are the actions of aldosterone?

A

Regulation of Na+, K+ & H2O

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31
Q

What are the actions of cortisol?

A 
Glucose metabolism
Protein metabolism
Fat metabolism
Anti-inflammatory
Psychic effects
Facilitates tissue response to humoral and neural influences
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32
Q

What are the actions of androgens?

A

Secondary sex characteristics

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33
Q

What are the clinical manifestations of addisons disease/

A

Aldosterone deficiency
Hyponatremia, hyperkalemia, ECF deficits, ↓ CO
Orthostatic hypotension, dehydration, weakness & fatigue

Glucocorticoid deficiency
Poor tolerance of stress
Hypoglycemia
Lethargy
Gastrointestinal symptoms
Anorexia, nausea, vomiting & diarrhea

↑ ACTH (adrenalcorticotropic hormone)
Hyperpigmentation
Exposed and unexposed skin

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34
Q

What is adrenal crisis?

A

Insufficient adrenal function to respond to stressors
Etiology
Minor illness or injury abrupt withdrawal of long term supplemental steroids such as prednisone
Pathogenesis
Unable to increase the secretion of hormones in response to stress

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35
Q

What are the manifestations of adrenal crisis?

A 
Nausea & vomiting
Muscular weakness
Severe hypotension
Dehydration
Vascular collapse
36
Q

What is cushing syndrome?

A

Cushing Syndrome”
Benign or malignant adrenal
tumor

“Cushing’s disease”
Pituitary tumor → ↑ ACTH

Other
Long term glucocorticoid therapy “Iatrogenic Cushing’s Syndrome”

37
Q

What are the clinical manifestations of cushings?

A

Exaggeration of the effects of cortisol

Glucose intolerance

Altered fat metabolism
Buffalo hump, protruding abdomen, moon face

Protein breakdown and muscle wasting

Osteoporosis

Purple striate

38
Q

What is diabetes insipidus?

A

Deficiency of or decreased response to ADH

Neurologic (brain)
Defective synthesis or release of ADH

Nephrogenic (kidney)
Loss of renal response to ADH

39
Q

What is the cause of neurogenic?

A

Head trauma

Surgery near the hypothalamic-posterior stalk

40
Q

What is the cause of nephrogenic?

A

Acquired
Genetic
Lithium, hyperkalemia, hypercalcemia
Interfere with the action of ADH in the collecting tubules

41
Q

What are the clinical manifestations of diabetes insipidus?

A 
Polyuria (up to 20 L/day)
Polydipsia (abnormal thirst)
Hypernatremia
Inadequate access to water
Hypertonic dehydration and increased serum osmolality
  • Need synthetic anti-diuretic hormone
42
Q

what is syndrome of inappropriate adh?

A

too much adh

43
Q

what are the causes of siadh

A

Brain tumors
Hydrocephalus
Head injury
Can occur with cancer

44
Q

What are the clinical manifestations of siadh

A

Decreased serum osmolality

Fluid volume excess w/ dilutional hyponatremia (low sodium)

Decreased urine output

↓ Hematocrit related to dilution

*Need fluid restriction or sodium replacement

45
Q

What is the function of glucagon?

A

causes cells to release stored energy into the blood

46
Q

What is the function of insulin?

A

allows cells to take up glucose from the blood; the key that opens the door

47
Q

What is the function of amylin?

A

slows glucose absorption in small intestine; suppresses glucagon secretion

48
Q

what is the function of somatostatin?

A

decreases GI activity; suppresses glucagon and insulin secretion

49
Q

How much glucose absorbed after a meal is removed from the blood and converted into glycogen in the liver for storage?

A

2/3

50
Q

What is done with unused glucose?

A

converted to fat for storage

51
Q

What is glycogenesis?

A

the formation of glycogen from glucose.

52
Q

What is gluconeogenesis?

A

when the liver converts amino acids, glycerol and lactic acid into glucose that is stored as glycogen or released directly into the blood stream.

53
Q

What is glycogenolysis?

A

when the liver breaks down stored glycogen via glucagon back to glucose.

54
Q

What should the glucose be after a 2 hour oral glucose tolerance test?

A

< 140 mg/dl

55
Q

What is diabetes mellitus?

A 
1. Deficiency of insulin       secreted by the beta cells of the islets of Langerhans
OR
2. Defective insulin receptors
     OR	
3. Early destruction of insulin
56
Q

What is type 1 diabetes mellitus?

A

pancreatic beta cell destruction predominantly by an autoimmune process w/ absolute insulin deficiency

57
Q

What is type 2 diabetes mellitus?

A

a combination of beta cell dysfunction and insulin resistance

58
Q

What is the pathogenesis of type 1 diabetes?

A

Destruction of Beta cells (90 %) lack of insulin hyperglycemia

Glucose cannot get into cells without insulin. Fats and proteins broken down in liver to provide energy to cells. Cells need insulin for glucose to enter cell.

59
Q

Is type 2 heredity?

A

yes

60
Q

What is the pathogenesis of type 2?

A

Impaired release of insulin
Inadequate or defective insulin receptors
Increased hepatic glucose production

61
Q

What are the risk factors of central obesity?

A

Greater risk for developing type 2 diabetes

↑ resistance to the action of insulin

impaired suppression of glucose production in the liver

Increased circulating free fatty acids (FFA’s)

62
Q

What happens with metabolic syndrome?

A 
Elevated triglyceride levels
Low HDL lipoproteins
Hypertension
Elevated C-reactive protein (inflammation) 
Vascular disease
Peripheral
Cerebral
Coronary
63
Q

What is gestational diabetes?

A

Glucose intolerance during pregnancy

64
Q

What are the risk factors of developing gestational diabetes?

A

Family history of DM
Heavy for date babies
5 or more pregnancies
History of stillbirth or fetal anomalies

65
Q

How do you diagnose gestational diabetes?

A

: FPG >126mg/dl or OGTT > 140 mg/dl

66
Q

What is the pathogenesis of gestational diabetes?

A

Hormonal changes of pregnancy changes in metabolism which result in impaired glucose tolerance

67
Q

What are the risks of fetus with gestational diabetes?

A

Increased risk of maternal and/or fetal demise
Increased risk of fetal abnormalities
macrosomia, hypoglycemia, polycythemia, hypocalcemia, hyperbilirubinemia

68
Q

What are the clinical manifestations of diabetes mellitus?

A

Onset
Type 1 rapid
Type 2 slow
Hyperglycemia (fasting plasma glucose [FPG] > 126 mg/dl)
Normal 80-90 mg/dl
Polydypsia (excessive or extreme thirst)
Polyphagia (excessive or extreme hunger)
Much less common in Type 2
Polyuria (excessive or extreme urination)
Weight loss except in type 2, Somnolence, Fatigue, Blurred vision

69
Q

What are the acute complications of diabetes?

A

Diabetic ketoacidosis

Hyperglycemic hyperosmolar state

Hypoglycemia

70
Q

What are the chronic complications of diabetes?

A

Macroangiopathy

Microangiopathy

Neuropathy

Nephropathy

71
Q

What is diabetic ketoacidosis (DKA)?

A
  • Characterized by hyperglycemia, ketosis and acidosis
  • Fat & protein breakdown in absence of insulin ketoacidosis (ketones made from this process and pH of blood decreases)
72
Q

Is DKA life threatening?

A

yes

73
Q

What are the causes of DKA?

A

Severe stress (release of counter regulatory hormones)
cortisol, epinephrine, glucagon)
Infection
Non-compliance with insulin injections

74
Q

What are the clinical manifestations of DKA?

A 
Hyperglycemia > 250 mg/dl
Metabolic acidosis
Low serum bicarbonate and Low pH
Osmotic diuresis 
dehydration
Electrolyte loss of Sodium and Potassium through urination and vomiting
Glucosuria
Ketonuria
Fruity breath, deep and labored breathing
75
Q

What is hyperglycemic (hyperosmolar state)?

A 
Type 2 DM
Severe hyperglycemia > 600 mg/dl
Hyper serum osmolarity >320 mOsm/L
Severe Dehydration with neurologic signs (decreased mental state)
Absence of ketoacidosis
Potassium depletion from diuresis
76
Q

What is the cause of HHS?

A

Increased resistance to insulin, elderly, dehydration

77
Q

What are the clinical manifestations of HHS?

A 
Severe dehydration
Elevated serum osmolality > 320 mOsm/L
Decrease in sensorium → coma
Hyperthermia
Seizures
78
Q

What are the acute complications of hypoglycemia?

A

Relative excess insulin in the blood

Blood glucose below normal (< 50-60 mg/dl)

79
Q

What are the neurological complications of hypoglycemia?

A

Headache
Vague feeling of abnormal mental state
Difficulty with problem solving

80
Q

What happens with SNS activation with hypogylcemia?

A

Sweating
Shaking
Palpitations
Tachycardia

81
Q

What is microangiopathy?

A

Thickening of the capillary basement membrane

Chronic Hyperglycemia proliferation of basement membrane cells ↓ tissue perfusion

82
Q

What are the clinical manifestations of neuropathy?

A

Pain
Paresthesia (numbness & tingling)
Loss of sensation
Diminished reflexes

83
Q

What does hyperglycemia lead to?

A

leads to nerve cell damage. Loss of sensation increases diabetic foot ulcers because of increased risk of injury.

84
Q

What is the path of retinopathy?

A

Microaneurysms in the retinal arterioles hemorrhage scarring blindness

85
Q

What is nephropathy?

A

most common cause of end stage renal disease (ESRD) aka kidney failure
-Hyperglycemia along with hypertension –> destruction of nephrons

86
Q

What is macroangiopathy?

A
  • Peripheral vascular disease and CAD
  • Hyperglycemia is accumulation of glucose bound end products attach to vessel walls and Lipids deposit (hyperlipidemia)

Pathophysiology (11 decks)

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