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patho exam 2 > ch 18 > Flashcards

ch 18 Flashcards

1
Q

what is syndrome of inappropriate ADH secretion (SIADH)

A

high levels of ADH without physiologic stimuli for its release

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2
Q

what must exist in SIADH for diagnosis

A

normal adrenal and thyroid function

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3
Q

clinical manifestation are related to ____,_____,___ in SIADH

A

enhanced renal water retention
hypoatremia (low Na+)
hypo-osmolality (solute loss)

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4
Q

what is the most common cause of SIADH

A

ectopic secretion of ADH by tumor cells

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5
Q

what are the clinical manifestations of SIADH

A 
thirst
dyspnea on exertion (SOB)
fatigue
dulled consciousness progressing to abdominal cramps
vomitting
confusion
seizures
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6
Q

when is SIADH seen

A

in infectious pulmonary diseases

associated with psychiatric disease after treatment with a variety of drugs

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7
Q

what is diabetes insipidus

A

insufficiency of ADH leading to polyuria and polydipsia

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8
Q

what are the 3 types of diabetes insipidus

A

neurogenic
nephrogenic
psychogenic

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9
Q

what is neurogenic of diabetes insipidus

A

-insufficient amounts of ADH

lesion on hypothalamus or posterior pituitary interferes with ADH synthesis, transport or release

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10
Q

what is nephrogenic of diabetes insipidus

A

-inadequate amounts of ADH

insensitivity of renal tubule to ADH

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11
Q

what is psychogenic of diabetes insipidus

A

caused by an extremely large volume of fluid intake which results in a partial resistance to ADH

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12
Q

what are the clinical manifestation related to with diabetes insipidus

A

water excretion
hypematremia
hyper-osmolality

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13
Q

what are the two diseases of posterior pituitary

A

SIADH

diabetes insipidus

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14
Q

what are the 3 disease of the anterior pituitary

A

hypopituitarism
hyperpituitarism
hyper secretion of growth hormone
hyper secretion of prolactin

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15
Q

what is hyperpituitarism caused by

A

a benign slow growing pituitary adenoma

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16
Q

what are the manifestations of hyperpituitarism

A

headache and fatigue
visual changes
hypo secretion of neighboring anterior pituitary hormones

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17
Q

what are the 2 types of hyper secretion of GH

A

acromegaly

gigantism

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18
Q

what is the growth hormone (somatropin)

A

enhances linear bone growth in children, enhances a.a. transport across membranes, increase protein synthesis, increases F.A mobilization and utilization, decrease glucose uptake and use

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19
Q

a deficiency of GH in children often look like and how to treat

A

normal intelligence, short stature, obesity with immature facial features, puberty often delayed

treat with GH

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20
Q

what is acromegaly

A

hyper secretion of GH during adulthood

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21
Q

what is gigantism

A

hyper secretion of GH in children and adolescents

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22
Q

what is prolactinoma

A

most common hormonally active pituitary tumors leading to hyperprolactinemia

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23
Q

increased levels of prolactin in females causes

A

amenorrhea (absence of menstration)
galactorrhea (milky discharge)
hirsutisum (excessive body hair)
osteopenia due to estrogen deficiency (bone loss)

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24
Q

increased levels of prolactin in males cause

A

**hypogonadism (a failure of testes to function properly)
**erectile dysfunction
impaired libido (sexual dysfunction)
oligospermia (low sperm count)
diminished ejaculate volume

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25
Q

what are alteration of thyroid function

A

hyperthyroidism

hypothryoidism

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26
Q

what two disease of hyperthyroidism

A

thryotoxicosis

graves disease

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27
Q

what is thyrotoxicosis

A

higher than normal levels of TH from any source

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28
Q

what is graves disease

A

autoimmune

abnormal stimulation of thyroid gland by IgG antibodies

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29
Q

what does graves disease cause

A

exophthalmos (bulging eyes)
irritability
weight loss
fatigue

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30
Q

what is congenital hypothyroidism

A

appears normal at birth due to maternal TH
common cause of preventable mental retardation
cretinism- TH essential for normal brain developments and growth

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31
Q

what is acquired hypothyroidism

A

older children and adults
slowing down of metabolic processes
myxedema- nonpitting mucous edema

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32
Q

what is primary and secondary causes of acquire hypothyroidism

A

primary cause- destruction of thyroid gland
ex: hashimotos disease -autoimmune
secondary cause- impaired pituitary

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33
Q

what are alterations of the parathyroid function

A

hyperparathyroidism

hypoparathyroidism

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34
Q

what is primary hyperparathyroidism

A

excess secretion of PTH from one or more parathyroid glands

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35
Q

what is secondary hyperparathyroidism

A

increase in PTH secondary to a chronic disease

36
Q

what are clinical manifestations of hyperparathyroidism

A

hypercalcemia: too much calcium in bone
hypercalciuria: kidney stones
fatigue
depression
anorexia

37
Q

what is the most common cause of hypoparathyroidism

A

damage to PT glands during thyroid surgery

38
Q

what are clinical manifestations of hypoparathyroidism

A 
hypocalcemia- 
muscle spasm
hyper-reflexia
asphyxiation- deprived of oxygen 
dry skin
hair loss
cataracts
cone deformities
39
Q

what is hypoparathyroidism

A

abnormally low PTH levels

40
Q

what is diabetes mellitus

A

chronic hyperglycemia along with disturbances of carbohydrates, fat and protein metabolism

41
Q

what is diagnosis of DM based on

A

more than one elevated fasting plasma glucose level
elevated BG in response to oral glucose tolerance test
polys X3
glycoslyated hemoglobin (A1C)

42
Q

what is type 1 diabetes

A

lack of insulin and relative excess of glucagon

insulin dependent

43
Q

what is the epidemiology of type 1

A

most commonly diagnosed in those younger than 18

44
Q

what is the etiology of type 1

A

beta cell destroyed due to autoantibodies

45
Q

what are the clinical manifestations of type 1

A

polys X3
weight loss
fatigue
ketoacidosis due to increased metabolism of fats and proteins

46
Q

what is type 2 diabetes

A

much more common

non insulin dependent

47
Q

what is the epidemiology of type 2

A 
native americans
hispanics
blacks
most over 40 
obesity
48
Q

what is the etiology go type 2

A

impaired beta cell function
peripheral insulin resistance
increased hepatic glucose production

49
Q

what are the clinical manifestations of type 2

A

pruritus (itching)
recurrent infections
visual changes
paresthesias (burning)

50
Q

what goes along with diabetes management type 2

A

dietary- restriction of calories for overnight individual, balance fat, protein, carbs and high fiber
exercise
oral antidiabetic agents

51
Q

what are the 3 oral anti diabetic agents for diabetes management in type 2

A

Sulfonylureas
Meglitinides
Metformin

52
Q

what is induces risk for gestational diabetes

A 
family history of diabetes
high risk ethnic group
advanced maternal age
prior history of gestational diabetes
overweight
53
Q

what are acute complications of DM

A 
hypoglycemia
diabetic ketoacidosis (type 1)
hypersmolar hyperglycemia nonketotic syndrome(type 2)
somogyi effect
dawn phenomenon
54
Q

what is hypoglycemia

A

insulin shock

BG 45-60

55
Q

what are clinical manifestations of hypoglycemia

A 
pallor
tremor
anxiety
palpitations 
diaphoresis-sweating 
tachycardia
dizziness
fatigue 
confusion
seizures
coma
56
Q

what is diabetic ketoacidosis - type 1

A

complication of insulin deficiency and increase of catecholamines, cortisol glucagon, GH
glucose production increase and usage decrease
fat is mobilized

57
Q

what is hypersomolar hyperglycemia nonketotic syndrome - type 2 and the treatment

A

high mortality due to high serum glucose (more than 600) leading to severe dehydration
treatment: manage fluid/electrolytes and glucose control

58
Q

what is somogyi effect

A

combination of hypoglycemia followed by rebound hypoglycemia

59
Q

what is dawn phenomenon

A

early morning risk in BG with no hypoglycemia during the night due to nocturnal elevations of GH

60
Q

what are chronic complications of DM

A

microvascular
marcovscular
diabetic neuropathies
infection

61
Q

what is microvascular disease

A

due to capillary basment membrane thickening, ischemia, hypoxia

62
Q

what are the 2 under microvascular disease

A

retinopathy

nephropathy

63
Q

what is retinopathy

A

due to blood vessel changes and RBC aggregation

more likely to occur in type 2 as a result of long standing hyperglycemia before diagnosis

64
Q

what is nephropathy

A

most common cause of end stage renal disease

death from renal failures more common in type 1 as a result of proteinuria

65
Q

what is marcovascular complication

A

cause morbidity and mortality especially in type 2

66
Q

what are the 3 under microvascular complications

A

CAD
stroke
peripheral vascular disease

67
Q

what is CAD

A

most common cause of death in type 2

68
Q

what is stroke

A

2 x as common with diabetics

69
Q

what is peripheral vascular disease

A

due to occlusion of small vessels which may results in gangrene of the lower extremities

70
Q

what are the 2 types of neuropathies

A

somatic

autonomic

71
Q

what are infections associated with chronic complicatons

A

increased risk due to senses impairment, hypoxia, proliferation of pathogens, decreased blood supply WBC impairment

72
Q

what are the disorders of the adrenal cortex

A

cushings syndrome
congential adrenal hyperplasia
cushing disease

73
Q

what is cushing syndrome

A

glucocorticoid hormone excess

excessive anterior pituitary secretion of ATCH

74
Q

what causes cushing syndrome

A

excess production of ACTH due to pituitary tumor
benign or malignant adrenal tumor
non pituitary ACTH secreting tumor

75
Q

what are the manifestation of cushing syndrome

A

altered fat metabolism -moon face and buffalo hump
muscle weakness due to protein breakdown
deranged glucose metabolism
susceptibility to infection

76
Q

what is the treatment for cushing syndrom

A

surgery
irradiation
medication

77
Q

what is congenital adrenal hyperplasia

A

deficient production cortisol leads to increased ACTH

78
Q

what happens with males in CAH

A

seldom diagnosed at birth unless have enlarged genitals or lose salt

79
Q

what happens with females with CAH

A

ambiguous genitalia due to increase in androgens

80
Q

what is the treatment for CAH

A

cortisol replacement

recontructive surgery

81
Q

what is primary for adrenal cortical insuffciency

A

addison disease
increased ACTH and decreased cortical hormones
lifetime replacement therapy

82
Q

what are the clinical manifestations of adrenal cortical insufficiency

A

deficiency mineral- glcocorticoids
hyperpigmentation due to increased ACTH
sparse pubic- axially hair in women

83
Q

what is secondary adrenal cortical insufficiency

A

hypopituirarism or due to removal of pituitary gland

more common due to rapid removal of glucocoritcoids and adrenal cortical atrophy

84
Q

Mr. Metzner has polyuria with a urine volume of 8 L/day. His urine specific gravity is 1.02. His serum sodium (Na+) is 150 mEq/L, and his plasma osmolality is 300 mOsm/kg. He is always asking for more cold liquids to drink. What type of hormonal alteration is Mr. Metzner exhibiting? What are some possible causes of this alteration?

A

Mr. Jones has diabetes insipidus, which has three forms: neurogenic, nephrogenic, and psychogenic. The neurogenic form is caused by a hypothalamic, infundibular stem, or posterior pituitary problem, that decreases or inhibits antidiuretic hormone (ADH) synthesis, transport, or release. This may be caused by pituitary tumors, brain tumors, infections, immunologic problems, or thrombotic problems.

  • The nephrogenic form of diabetes insipidus may be acquired, permanent, or reversible. It is caused by renal tubule insensitivity to ADH. In this form the amounts of ADH are normal but the tubules are no longer able to respond to the hormone. Examples of renal problems that can lead to diabetes insipidus include pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease. It may also be secondary to anesthetic drug use and the use of lithium carbonate.
  • The psychogenic form of diabetes insipidus is caused by compulsive water drinking by individuals with psychiatric disorders. In this form the individual has periodic polyuria, high urine volume, and plasma osmolarity of less than 285 mOsm/kg.
85
Q

Mrs. Johnson is admitted to your unit with tachycardia, fever, agitation, and diarrhea. Her medical history is nonsignificant except for a history of recent pneumonia, and she takes no regular prescription or over-the-counter medication. She also reports that she has been very upset at the recent death of her mother. Her diagnosis is thyrotoxic crisis. She asks you to explain what is happening to her.

A
86
Q

John is a 40-year-old recently diagnosed with Addison disease. He asks you to explain what happened to him and explain how he can live a normal life.

A

patho exam 2 (2 decks)

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