Chapter 10 Flashcards
What are the 4 hypofunction dysfunctions of the endocrine system?
- 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
What are the 3 hyperfunction dysfunctions of the endocrine system?
- Excessive stimulation
- Hyperplasia
- Ectopic source i.e.. Hormone producing tumors
What do releasing hormones of the hypothalamus do?
Releasing hormones from hypothalamus tell the pituitary what to release into the blood
What do trophic hormones of the hypothalamus do?
Trophic hormones from the pituitary tell specific peripheral glands to grow and produce their hormones
Where is growth hormone produced?
anterior pituitary
What are the actions of growth hormone?
Bone & muscle growth
Protein synthesis
Fat metabolism
CHO metabolism
What is growth hormone stimulated by?
- Hypoglycemia, fasting, starvation
- Stress
What is growth hormone inhibited by?
- Increased glucose levels, free fatty acid release, and obesity
- Cortisol
What disease occurs with a deficiency of growth hormone?
Dwarfism
What diseases occur with an excess of growth hormone?
In childhood: gigantism
In adulthood: acromegaly
What causes growth hormone deficiency in children?
- Idiopathic
- Pituitary tumors
What are the clinical manifestations of GH and IGF deficiency in children?
- Decreased birth length
- Decreased growth rate
- Normal intelligence
- Short stature
- Obesity
- Immature facial features
What are the clinical manifestations of GH deficiency in adults?
-Change in body composition with decreased overall lean body mass
-↑ Cardiovascular risk factors Increased body fat ↑ LDL ↓ HDL Insulin resistance
-↓ bone mineral density
What are the clinical manifestations of adult GH excess?
-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
What are the actions of thyroid hormones (t3 & t4)?
- ↑ metabolic rate
- ↑ O2 consumption
- ↑ heart rate, contractility, cardiac output
- ↑ ventilation
- ↑ peristalsis and production of gastric secretions
- Enhance skeletal muscle reactivity
- Interaction with the SNS
What are 3 thyroid function disorders?
- Goiter
- Hypothyroidism
- Hyperthyroidism
What is a goiter?
Enlargement of the thyroid gland
What is the cause of goiter?
Usually compensatory hyperplasia (increase in size) and hypertrophy (increase in number)
When is the goiter toxic and when is it nontoxic?
toxic = hyper non = hypo
What is hypothryoidism?
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
What is myxedema?
Accumulation of hydrophilic mucopolysaccharide substance (Myxedematous fluid) in the connective tissues of the body
What are the clinical manifestations in hypothyroidism?
-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
What are the clinical manifestations of myxedema?
- Puffy face
- Enlarged tongue
- Hoarse, husky voice
- Pericardial and pleural effusions
What is another name for hyperthyroidism?
Thyrotoxicosis
What does graves disease come from?
secondary hyperthyroidism
What is graves disease?
Autoimmune disorder of unknown etiology
Thyroid stimulating antibodies (TSAbs)
What is Exophtalmos?
Protrusion of the eyeballs
-Prone to corneal
ulcerations → blindness
-Extraocular muscle
paralysis
-Involvement of the optic
nerveWhat are the clinical manifestations of hyperthryoidism?
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
What are the adrenal cortical hormones?
Aldosterone (Mineralocorticoid)
Cortisol (Glucocorticoid)
Androgens (Adrenal sex hormones)
Catecholamines (epinephrine, norepinephrine and dopamine
What are the actions of aldosterone?
Regulation of Na+, K+ & H2O
What are the actions of cortisol?
Glucose metabolism Protein metabolism Fat metabolism Anti-inflammatory Psychic effects Facilitates tissue response to humoral and neural influences
What are the actions of androgens?
Secondary sex characteristics
What are the clinical manifestations of addisons disease/
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
What is adrenal crisis?
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
What are the manifestations of adrenal crisis?
Nausea & vomiting Muscular weakness Severe hypotension Dehydration Vascular collapse
What is cushing syndrome?
Cushing Syndrome”
Benign or malignant adrenal
tumor
“Cushing’s disease”
Pituitary tumor → ↑ ACTH
Other
Long term glucocorticoid therapy “Iatrogenic Cushing’s Syndrome”
What are the clinical manifestations of cushings?
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
What is diabetes insipidus?
Deficiency of or decreased response to ADH
Neurologic (brain)
Defective synthesis or release of ADH
Nephrogenic (kidney)
Loss of renal response to ADH
What is the cause of neurogenic?
Head trauma
Surgery near the hypothalamic-posterior stalk
What is the cause of nephrogenic?
Acquired
Genetic
Lithium, hyperkalemia, hypercalcemia
Interfere with the action of ADH in the collecting tubules
What are the clinical manifestations of diabetes insipidus?
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
what is syndrome of inappropriate adh?
too much adh
what are the causes of siadh
Brain tumors
Hydrocephalus
Head injury
Can occur with cancer
What are the clinical manifestations of siadh
Decreased serum osmolality
Fluid volume excess w/ dilutional hyponatremia (low sodium)
Decreased urine output
↓ Hematocrit related to dilution
*Need fluid restriction or sodium replacement
What is the function of glucagon?
causes cells to release stored energy into the blood
What is the function of insulin?
allows cells to take up glucose from the blood; the key that opens the door
What is the function of amylin?
slows glucose absorption in small intestine; suppresses glucagon secretion
what is the function of somatostatin?
decreases GI activity; suppresses glucagon and insulin secretion
How much glucose absorbed after a meal is removed from the blood and converted into glycogen in the liver for storage?
2/3
What is done with unused glucose?
converted to fat for storage
What is glycogenesis?
the formation of glycogen from glucose.
What is gluconeogenesis?
when the liver converts amino acids, glycerol and lactic acid into glucose that is stored as glycogen or released directly into the blood stream.
What is glycogenolysis?
when the liver breaks down stored glycogen via glucagon back to glucose.
What should the glucose be after a 2 hour oral glucose tolerance test?
< 140 mg/dl
What is diabetes mellitus?
1. Deficiency of insulin secreted by the beta cells of the islets of Langerhans
OR
2. Defective insulin receptors
OR
3. Early destruction of insulinWhat is type 1 diabetes mellitus?
pancreatic beta cell destruction predominantly by an autoimmune process w/ absolute insulin deficiency
What is type 2 diabetes mellitus?
a combination of beta cell dysfunction and insulin resistance
What is the pathogenesis of type 1 diabetes?
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.
Is type 2 heredity?
yes
What is the pathogenesis of type 2?
Impaired release of insulin
Inadequate or defective insulin receptors
Increased hepatic glucose production
What are the risk factors of central obesity?
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)
What happens with metabolic syndrome?
Elevated triglyceride levels Low HDL lipoproteins Hypertension Elevated C-reactive protein (inflammation) Vascular disease Peripheral Cerebral Coronary
What is gestational diabetes?
Glucose intolerance during pregnancy
What are the risk factors of developing gestational diabetes?
Family history of DM
Heavy for date babies
5 or more pregnancies
History of stillbirth or fetal anomalies
How do you diagnose gestational diabetes?
: FPG >126mg/dl or OGTT > 140 mg/dl
What is the pathogenesis of gestational diabetes?
Hormonal changes of pregnancy changes in metabolism which result in impaired glucose tolerance
What are the risks of fetus with gestational diabetes?
Increased risk of maternal and/or fetal demise
Increased risk of fetal abnormalities
macrosomia, hypoglycemia, polycythemia, hypocalcemia, hyperbilirubinemia
What are the clinical manifestations of diabetes mellitus?
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
What are the acute complications of diabetes?
Diabetic ketoacidosis
Hyperglycemic hyperosmolar state
Hypoglycemia
What are the chronic complications of diabetes?
Macroangiopathy
Microangiopathy
Neuropathy
Nephropathy
What is diabetic ketoacidosis (DKA)?
- Characterized by hyperglycemia, ketosis and acidosis
- Fat & protein breakdown in absence of insulin ketoacidosis (ketones made from this process and pH of blood decreases)
Is DKA life threatening?
yes
What are the causes of DKA?
Severe stress (release of counter regulatory hormones)
cortisol, epinephrine, glucagon)
Infection
Non-compliance with insulin injections
What are the clinical manifestations of DKA?
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
What is hyperglycemic (hyperosmolar state)?
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
What is the cause of HHS?
Increased resistance to insulin, elderly, dehydration
What are the clinical manifestations of HHS?
Severe dehydration Elevated serum osmolality > 320 mOsm/L Decrease in sensorium → coma Hyperthermia Seizures
What are the acute complications of hypoglycemia?
Relative excess insulin in the blood
Blood glucose below normal (< 50-60 mg/dl)
What are the neurological complications of hypoglycemia?
Headache
Vague feeling of abnormal mental state
Difficulty with problem solving
What happens with SNS activation with hypogylcemia?
Sweating
Shaking
Palpitations
Tachycardia
What is microangiopathy?
Thickening of the capillary basement membrane
Chronic Hyperglycemia proliferation of basement membrane cells ↓ tissue perfusion
What are the clinical manifestations of neuropathy?
Pain
Paresthesia (numbness & tingling)
Loss of sensation
Diminished reflexes
What does hyperglycemia lead to?
leads to nerve cell damage. Loss of sensation increases diabetic foot ulcers because of increased risk of injury.
What is the path of retinopathy?
Microaneurysms in the retinal arterioles hemorrhage scarring blindness
What is nephropathy?
most common cause of end stage renal disease (ESRD) aka kidney failure
-Hyperglycemia along with hypertension –> destruction of nephrons
What is macroangiopathy?
- Peripheral vascular disease and CAD
- Hyperglycemia is accumulation of glucose bound end products attach to vessel walls and Lipids deposit (hyperlipidemia)
