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w7 quiz - endocrine Flashcards

1
Q

Chemical structure: steroid

A

lipids that enter the cell nucleus to initiate transcription directly

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2
Q

chemical structure: nonsteroid

A

needs secondary messanger system to activate transcription in nucleus

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3
Q

What do the endocrine and nervous systems do?

A

regulate metabolic activites

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4
Q

positive feedback system

A

g

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5
Q

negative feedback system

A

g

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6
Q

what is an antogonist to calcitonin

A

parathyroid hormone

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7
Q

what is an antagonist for insulin

A

glucagon

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8
Q

Describe how hormone release is most often controlled by negative feedback mechanisms

A

Endocrine and nervous system work together to regulate metabolic activities

  • complex system for some hormones
  • secretion of hormones may be controlled by more than one mechanism
  • rate and timing of secretion may vary (cyclic patterns)
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9
Q

endocrine disorders reflect what

A

impaired control or feedback

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10
Q

excess hormone levels are caused by what

A

a. tumor producing high levels
b. excretion by liver or kidney impaired
c. congenital condition produces excess hormones

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11
Q

Deficit of hormone or reduced effects are due to what

A

a. Tumor produced too little hormone caused by inadequate tissue receptors present
- antagonist hormone production is increased
- malnutrition
- atrophy, surgical removal of gland
- congential deficit

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12
Q

Endocrine system: diagnostic test

A

Blood tests (check hormone levels, radioimmunoassay, immunochemical methods)

urine tests

stimulation or suppression tests

scanning, ultrasound, MRI

Biopsy

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13
Q

Endocrine system treatments

A

Replacement therapy (hormone deficit)

medication, surgery, radiation (hormone excess)

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14
Q

diabetes mellitus results in

A

abnormal carb, protein and fat metabolism

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15
Q

some tissue can transport glucose in the absense of insulin such as

A

CNS, kidney, mycardium, gut, skeletal muscle

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16
Q

Type 1 diabetes

A

Autoimmune destruction of beta cells in pancreas

  • insulin replacement requires
  • not linked to obesity
  • genetic factors
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17
Q

what type of diabetes has acute onset in children and adolescents

A

type 1

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18
Q

type 1 diabetes: metabolic changes

A

Catabolism of fats and proteins

    • excess fatty acids and metabolites
    • ketones in blood
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19
Q

What type of diabetes has decompensated metabolic acidosis

A

type 1

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20
Q

Type 2 diabetes

A

non-insulin dependent; caused by decrease production of insulin / decreased resistance by body cells to insulin

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21
Q

type 2 diabetes onset

A

slow and insideoous, unsually in those older than 50

- associated with obesity

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22
Q

what diabetes is associated with a component of metabolic syndrome?

A

2

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23
Q

Control of type 2 diabetes

A

diet, increase bodys use of glucose by exercise, reducing insulin resistance, stimulate beta cells of pancreas to produce more insulin

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24
Q

initial stage of diabetes

A

Insulin deficit
BG rise
excess glucose in urine (large urine vol.)
dehydration –> thirst

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25
manifestations of diabetes
polyphagia, fatigue, hyperglycemia, glucosuria, dehydration, polyuria, polydipsia
26
diabetes diagnostics
``` fasting BG level glucose tolerance test glycosylated hemoglobin test -- clinical and subclinincal diabetes -- monitor glucose levels over several months ```
27
Diabetes treatment
Keep BG in normal range diet and exercise (exercise lowers BG as skeletal muscle uses glucose) oral medications (incurease insulin secretions, reduce BG levels) insulin replacement
28
Complications of diabetes
Directly related to duration and extent of abnormal BG levels Complications can be acute or chronic
29
What factors may lead to fluctuations in serum glucose levels
Variations in diet and alcohol use Change in PA Infection Vomiting
30
Acute complication of diabetes: hypoglycemia (insulin shock)
more common with insulin replacement treatment; can occur because excess oral hypoglycemic drugs
31
What may cause an excess of insulin in ciruclation
``` Glucose deficit in blood strenuous exercise dosage error vomiting skipping meal after taking insulin ```
32
Hypoglycemic shock: s/s
``` disoriented / behavior change anxiety / decrease responsiveness decreased BP, increase HR may appear impaired decreased BG level Decrease level of consciousness ``` IMMIDIATE ADMIN. OF GLUCOSE IS REQUIRED TO PREVENT BRAIN DAMAGE
33
hypoglycemic shock: emergency treatment
If conscious, immidiately give sweet fruit juice, honey, candy, sugar If unconscious, give nothing PO; IV glucose 50% required
34
Emergent treatment for diabetic ketoacidosis:
Insulin, fluid, and sodium bicarbonate.
35
Diabetic ketoacidosis (DKA)
Occurs in insulin dependent clients; more commonly in type 1 results of insufficient insulin in blood high BG levels
36
What results in the production of ketoacids
Mobilization and use of lipids to meet cellular needs
37
what may DKA be initiated by?
infection or stress
38
what might DKA result from
dose error, infection, change in diet, alcohol, exercise
39
DKA s/s
``` Thirst Dry, rough oral mucosa Rapid pulse, but weak and thready BP low Oliguria Rapid, deep respirations Acetone breath (fruity) Lethargy and decreased responsiveness indicates depression of CNS, owing to acidosis and decreased blood flow ```
40
Metabolic acidosis
decrease serum bicarbonate levels and decreased serum pH
41
Metabolic acidosis s.s
dehydration progresses, renal compensation reduced, acidosis becomes decompensated LOC
42
Hyperosmolar Hypoglycemic Nonketotic Coma (HHNK)
Type 2 Diagnosis often missed Occurs in older pt. and assumed to be cognitive impairment results in severe dehydration and electrolye imbalances
43
Manifestations of Hyperosmolar HypoglycemicNonketotic Coma (HHNK)
hyperglycemia severe dehydration - increased hemotocrit, loss of turgor, increase HR and resp.
44
Hyperosmolar HypoglycemicNonketotic Coma (HHNK) - electrolyte imbalances result in what
neurological deficits, muscle weakness, difficulties with speech, abnormal reflexes
45
Chronic complications of diabetes: vascular
atherosclerosis in small and large arteries
46
Chronic complications of diabetes: microangiopathy (changes in microcirculation)
Obstruction/rupture of small capillaries and arteries - tissue necrosis and loss of function - neuropathy and loss of sensation - retinopathy (leading cause of blindness) - chronic renal failure (degeneration of glomeruli in kidney)
47
Chronic complications of diabetes: macroangiopathy - affects large arteries
Result of abnormal lipid levels - high incidence of MI, strokes, PVD - may result in ulcers on legs and feet (slow healing) - frequent infections and gangrenous ulcers - amputation may be necessary
48
chronic complications of diabetes - peripheral neuropathy
Caused by ischemis and microcirculation to peripheral nerves impair sensations, numbness, tingling, weakness, muscle wasting
49
Neuropathy leads to
impaired sensation, numbness, tingling, weakness, muscle weakness
50
chronic complications of diabetes: infections
infection in feet and legs caused by neurologic impairment fungal infections common (candidica) UTI dental caries gingivitis and periodontitis
51
chronic complications of diabetes: cataracts
Related to abnormal metabolism of glucose
52
chronic complications of diabetes - pregnancy
Both mother and fetus may experience complications | - spontaneous abortions
53
Infants born to diabetic mothers can experience what
increase size and weigh | hypoglycemia in first hours after birth
54
Hypoparathyroidism leads to
hypocalcemia - weak cardiac muscle contractions - increased excitability of nerves (spontaneous contraction of skeletal muscle)
55
causes of hypoparathyroidism
Congenital lack of parathyroid Surgery or radiation in neck area Autoimmune disease
56
hyperparathyroidism results in what
hypercalcemia - forceful cardiac contractions - osteoporosis - predisposition to kidney stones
57
caused of hyperparathyroidism
tumor secondary to renal failure enlargement (hyperplasia) of glands
58
What are the most common cause of pituitary hormones
adenomas
59
Pituitary adenomas: effect of mass
May cause pressure in skull | -- headaches, siezures, drowsiness, visual deficits
60
How to adenomas effect pituitary hormone secretion
Dependent on cells and location involved May cause excessive or decreased release of hormones
61
Growth hormone (GH): Dwarfism
Deficit in growth hormone production and release
62
GH: gigantism
excess GH prior to puberty anf fusion of epiphysis
63
GH: Acromegaly
Excess GH secretion in adults - associtated with adenoma - bones: broader and heavy - soft tissue grows (hands and feet, change in facial features)
64
How does diabetes insipidus is what
Deficit of ADH
65
What is Diabetes insipidus often associated with
adenoma
66
Diabetes insipidus may originate in the neurohypopysis, meaning what
Head injury or surgery Possible genetic problem Replacement treatment required
67
Inappropriate AHD syndrome
Excess ADH (temporary from stress, secreted from ectopic source such as tumor)
68
Innappropriate ADH syndrome Treatment
diuretics | Na supplements
69
Goiter: Endemic goiter
Hypothyroid condition in regions with low iodine levels in soil and food
70
Goiter: goitrogens
Foods that contain elements to block synthesis of T3 and T4
71
What are T3 and T4 (names)
triiodothyronine (t3) and thyroxine (t4)
72
goiter: toxic goiter
results from hyperactivity of thyroid glans
73
hyperthyroidism
Related to autoimmune factor Hypermetabolism and increased stimulation of SNS toxic goiter Exophthalamos
74
Exophthalamos
Presense of protruding, staring eyes, decreased blind and eye movement result of increased tissue mass in orbit may result in visual impairment
75
Hypothyroidism
Iodine deficit
76
Hypothyroidism: hasmimoto thyroiditis
autoimmune disorder
77
hypothyroidism: tumor
surgical removal or treatment of gland
78
hypothyroidism: cretinism
Results in short statue and severe cognitive deficits Untreated congenital hypothyroidism May be related to iodine deficiency during pregnancy
79
Hypothyroidism manifestations
Goiter (if caused by iodine deficit) intolerance to cold increased BMI lethargy and fatige decrease appetite Myxedema
80
myxedema
nonpitting edema in face, thickened tongue
81
myxedema coma
acute hypotension, hypoglycemia, and hypothermia result in loss of consciousness; life threatening if untreated
82
diseases of adrenal medulla
Pheochromocytoma
83
diseases of adrenal cortex
cushing syndrome | addisons disease
84
Pheochromocytoma
Benign tumor of adrenal medulla - secretes epinephrine, norepinephrine and possible other substances occassionally many tumors
85
Pheochromocytoma s/s
HA, palpitation, sweating, intermittent or constant anxiety
86
Cushing syndrome
caused by excessive level of glucocorticoids
87
Cushing syndrome is a possible result of what
adrenal adenoma, pituitary adenoma, ectopic carcinoma, iatrogenic conditions, substance abuse
88
changes assiciated with Cushing syndrome (appearance)
round face with ruddy color, truncal obesity with fat between scalpulae, thin limbs, think hair, fragile skin, striae
89
What are systemic changes with Cushing disease
a. retention of Na and H2O b. suppression of immune system c. erythrocyte production d. emotional lability and euphoria e. increase catabolism of bone and protein f. slowed healing g. increase insulin resistance and possible glucose intolerance
90
Addison's disease
Deficiency of adrenocorticoid secretions; autoimmune reason is a common cause adrenal gland may be destroyed by hemorrhage or infection
91
Addisons disease s.s
``` decreased BG levels inadequate stress response fatigue weight loss infections lower serum Na concetration decrease BV hypotension high K+ levels ```

Pathophysiology (11 decks)

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