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rrd 11 Flashcards

endocrine disorders

1
Q

endocrine is dependent on?

A

negative feedback systems

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2
Q

negative feedback systems of endocrine

A
  • HIGH blood level of circulating hormone will suppress gland that secreted it and/or other glands in the feedback loop
  • result: more hormone in circulation
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3
Q

most endocrine disorders are problems of either?

A
  • hyposecretion
  • hypersecretion
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4
Q

pituitary gland

A
  • hypophysis
  • located in brain near base of skull
  • master gland bc secretes many hormones that govern other glands
  • ADH (antidiuretic), TSH (thyroid-stimulating), ACTH (adrenocorticotropic)
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5
Q

diabetes insipidus (DI)

A

under secretion of ADH

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6
Q

nomenclature of DI

A
  • diabetes: too much urine
  • insipidus: flavorless, no color
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7
Q

renal-related etiology of DI

A

sick kidneys often have decreased response of renal tubules to ADH

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8
Q

CNS-related etiologies of DI

A
  • a lesion (ex: pituitary tumor) causes gland to diminish its secretion of ADH
  • acute abnorm in brain (ex: head injury) or other causes of cerebral edema + IICP in brain put pressure on pit gland -> diminish ADH secretion
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9
Q

w/o influence of ADH, you ____ hold onto water effectively. what does this mean?

A
  • won’t
  • H2O will indiscriminately flow from peritubular capillaries of kidneys into tubules -> very dilute urine
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10
Q

ADH secretion is a norm process that the body uses to ______ for ____ fluid volume: when the pituitary detects circulating fluid vol is _____, it secretes ADH -> ADH tells kidney to hang onto water by ______ urine output -> fluids are ____ and fluid volume in body goes ____.

A
  • compensate
  • low
  • low
  • decreasing
  • conserved
  • up
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11
Q

S/S DI

A
  • polyuria (void huge amts of dilute urine)
  • thirsty bc H2O flows right thru pt
  • blood less water -> conc increase -> higher serum osmolality -> T-to-B fluid shift -> tissue cells dehydrated + shrunken
  • dehydration: poor skin turgor + dry mucus membranes
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12
Q

syndrome of inappropriate antidiuretic hormone (SIADH)

A

over secretion of ADH

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13
Q

events that trigger SIADH

A
  • ectopically-produced ADH (ex: from small-cell bronchogenic cancer)
  • drugs that affect brain, esp gen anesthetics (seen in post-op recovery)
  • trauma to brain (swelling of brain -> pressure on pit gland -> over secretion)
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14
Q

mechanism of action of SIADH

A
  1. hold onto water 2 much by decrease urination
  2. increased vascular fluid volume
  3. water added to blood
  4. diluted plasma department
  5. lower serum osmolality
  6. small amts highly conc urine
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15
Q

S/S SIADH

A
  • oliguria (decreased urine output bc body hold onto water inappropriately in vascular space)
  • B-to-T shift -> edema
  • peripheral + pulmonary edema
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16
Q

thyroid gland and TSH pathway

A
  1. pit gland secrete TSH (thyroid stim hormone)
  2. TSH stims thyroid
  3. thyroid produce, release, and/or store 3 thyroid hormones
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17
Q

thyroid hormones from thyroid gland

A
  • thyroxine (T4)
  • triiodothyronine (T3)
    ^ reg metabolic activities
  • calcitonin: increase Ca2+ movement from blood into bone
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18
Q

T3 + T4 is very dependent on _____ uptake from blood — _____ is consumed in our diet from _______.

A
  • iodide
  • iodide
  • seafood and iodized salt
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19
Q

T3 and T4 act on receptor cells of many diff organs and affect body’s:

A
  • metabolic rate
  • caloric requirements
  • oxygen consumption
  • carbohydrate + lipid metabolism
  • growth and development
  • brain + nervous system fxns
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20
Q

negative feedback system of thyroid fxn

A
  1. drop in T3 + T4 in bloodstream
  2. pituitary stimulated
  3. increase TSH secretion
  4. thyroid stim to release more T3 + T4
  5. norm levels T3 + T4 reestablished
  6. norm levels suppress TSH secretion from pituitary
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21
Q

the positive feedback loop occurs with _____ levels of thyroid hormones.

A

inccreased

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22
Q

calcitonin is also regulated by _____ feedback.

A

negative

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23
Q

hyperthyroidism

A
  • state of having excess T3 + T4 production + release
  • Graves disease
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24
Q

Graves disease

A
  • an autoimmune disorder in which autoantibodies attack/stim TSH receptors on the thyroid
  • autoantibodies mimic TSH -> thyroid secrete more T3 + T3
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25
Q

lab work for hyperthyroidism

A
  • serum T4 higher
  • serum TSH lower
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26
Q

other features of hyperthyroidism included is one of _____ S/S due to the ______ processes caused by high levels _____

A
  • overactive
  • hypermetabolic
  • T3, T4
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27
Q

psych/CNS S/S hyperthyroidism

A
  • nervous
  • irritable
  • tremors
  • insomnia
  • emotionally labile
  • sometimes psychosis (hallucinations, paranoia)
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28
Q

cardiovascular S/S hyperthyroidism

A
  • tachycardia
  • increased afterload
  • sometimes HF due to increased heart workload
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29
Q

GI S/S hyperthyroidism

A
  • increased appetite
  • diarrhea
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30
Q

hair changes S/S hyperthyroidism

A
  • hair follicles sensitive to metabolic state -> stressed by 2 much thyroid hormone -> hair thins or falls out -> alopecia
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31
Q

other S/S hyperthyroidism

A
  • exophtalmus
  • goiter
  • fatigue + weight loss (overdrive state use energy)
  • increased body temp + heat intolerance
  • skin flushed, warm, damp from excessive sweating
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32
Q

exopthalmus

A

bulging eyes from deposits of excess tissue behind eyes

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33
Q

goiter

A

an enlargement of the thyroid gland that can sometimes be easily visualized w/ hyperthyroidism AND hypothyroidism

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34
Q

causes of goiter in hyperthyroidism

A

cells pathologically stimulated by autoantibodies to increase their thyroid hormone output (overdrive = increased size of cell)

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35
Q

thyrotoxic crisis

A
  • thyroid storm
  • extreme state of hyperthyroidism
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36
Q

thyrotoxic crisis is a ____ emergency triggered by some stressor such as _____.

A
  • hyperthyroid
  • infection, trauma, surgery, etc.
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37
Q

neuro S/S thyrotoxic crisis

A
  • extreme restlessness and agitation
  • delirium
  • seizures
  • coma
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38
Q

circulatory S/S thyrotoxic crisis

A
  • severe tachycardia
  • heart failure
  • shock
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39
Q

other S/S thyrotoxic crisis

A
  • diaphoresis
  • hyperthermia (103-105 F)
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40
Q

tx hyperthyroidism

A
  • antithyroid meds: inhibit synthesis of thyroid hormones
  • thyroidectomy (usually 90% removed)
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41
Q

hypothyroidism

A

state of deficient T3/T4 production + release

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42
Q

hypothyroidism is caused by:

A
  • congenital defects
  • direct removal of tissue (tumor) or direct destruction of tissue (radiation)
  • autoimmune thyroiditis
  • endemic iodine deficiency
  • overactivity of antithyroid drugs
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43
Q

what is the autoimmune thyroiditis disorder that cause hypothyroidism?

A

Hashimoto’s thyroiditis

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44
Q

Hashimoto’s thyroiditis

A
  • autoantibodies actually destroy tissue
  • insidious onset w/ thyroid tissue slowly replaced by lymphocytes + scar tissue
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45
Q

endemic iodide deficiency

A
  • lack of iodide in diet -> thyroid hormone synthesis drops
  • significant in children
  • pregnant mom not enuf iodide in diet -> baby have congenital hypothy w/ stunted mental + physical growth (cretinism)
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46
Q

overactivity of antithyroid drugs

A

pts start w/ being treated for hyperthyroidism but goes too far

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47
Q

lab work for hypothyroidism

A
  • serum T4 lower
  • serum TSH higher
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48
Q

psych/CNS S/S hypothyroidism

A
  • confusion
  • slow speech and thinking
  • sluggish
  • memory loss
  • depression
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49
Q

circulatory S/S hypothyroidism

A
  • anemia
  • bradycardia
  • decreased CO
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50
Q

pulmonary S/S hypothyroidism

A
  • dyspnea
  • hypoventilation
  • CO2 retention
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51
Q

GI S/S hypothyroidism

A
  • decreased appetite
  • constipation
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52
Q

hair w/ hypothyroidism

A
  • dry and brittle
  • may fall out (alopecia)
  • not having enuf thyroid hormone to support metabolic needs of follicles
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53
Q

skin S/S hypothyroidism

A
  • myxedema: changes in dermis that cause water to be trapped under skin over time -> pt has overall puffy lewk
  • skin coarse + dry
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54
Q

goiter in hypothyroidism

A
  • hyperplasia + hypertrophy of tissue compensatory response
    to increase thyroid hormone secretion
  • inflammation + scar tissue from autoimmune attack
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55
Q

other body changes bc hypothyroidism

A
  • weight gain despite decreased appetite
  • decreased body temp + cold-intolerance
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56
Q

myxedema coma or crisis

A

extreme state of hypothyroidism

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57
Q

myxedema coma is precipitated by stressor such as?

A
  • infection
  • drug
  • exposure to cold
  • trauma
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58
Q

myxedema coma is manifested by?

A
  • progression of hypothyroid sluggishness + drowsiness
  • into gradual or sudden impaired consciousness
  • often hypotension and hypoventilation
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59
Q

tx hypothyroidism

A
  • synthetic thyroid hormone
  • levothyroxine (Synthroid)
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60
Q

calcium needed for what fxns?

A
  • building + maintenance of appropriate bone density
  • cell electrical activity
  • clotting
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61
Q

____ is the biggest storage area for calcium and there is always movement from _____ to ______ and back again.

A
  • bone
  • bone
  • blood
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62
Q

when the serum calcium is lower than normal, _________. when higher than normal, _______.

A
  • hypocalcemia
  • hypercalcemia
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63
Q

chief regulators of calcium movement

A
  • calcitonin
  • PTH (parathyroid hormone)
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64
Q

calcitonin is secreted by the ______ and enhances movement of calcium from ______.

A
  • thyroid gland
  • blood into bone
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65
Q

PTH is secreted by _______ and stimulates ______.

A
  • parathyroid gland
  • resorption: movement of substance back into circulation from somewhere else; from bone to blood
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66
Q

PTH enhances movement of calcium from _____ to _____ by ____________.

A
  • bone
  • bloodstream
  • increasing osteoclastic activity
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67
Q

osteoclasts

A
  • cells that migrate along the walls of capillaries found in bones
  • break down bone cells to free up calcium, which then can move into bloodstream
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68
Q

calcitonin + PTH work by _____ feedback and balance each other out.

A

negative

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69
Q

if there is a state of hypocalcemia or if calcium is needed in other parts of the body, PTH secretion is _____ and calcitonin secretion by thyroid is _____, resulting in _____ osteoclastic activity and bringing ___ serum calcium levels.

A
  • increased
  • suppressed
  • increased
  • up
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70
Q

if there is a state of hypercalcemia or if more calcium is needed in the bone (e.g., for building more bone matrix), calcitonin secretion by thyroid is ______ and PTH secretion is ______, resulting in _____ osteoclastic activity and bringing ____ serum calcium levels.

A
  • increased
  • suppressed
  • decreased
  • down
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71
Q

as part of the aging process and genetics, resorption will slowly _____ due to _____ osteoclastic activity - osteoclastic breakdown of bone and movement of calcium _____ bone formation that is maintained by osteocytes.

A
  • increase
  • increased
  • exceeds
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72
Q

the increase in resorption due to increased osteoclastic activity causes bone density to _____ and bone becomes more _____.

A
  • decrease
  • porous
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73
Q

which gender is more likely to have increased resorption/osteoclastic activity? why?

A
  • women
  • women’s bones significantly less dense than men’s to begin with
  • menopausal loss of estrogen
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74
Q

why does menopausal loss of estrogen contribute to low bone density and porous bones in older women?

A
  • bones have estrogen receptors: stim by estrogen -> bone-building + maintenance of density
  • during + after menopause: atrophy of ovaries -> less estrogen
  • less estrogen -> less bone building -> more osteoclastic activity -> more resorption -> less density
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75
Q

osteopenia

A

the condition of having somewhat less than normal bone density

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76
Q

osteoporosis

A

bone density that is markedly lower than normal

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77
Q

sequelae in either osteopenia or osteoporosis

A
  • bones more easily fractured, esp in hip + vertebra
  • deaths from hip frac related to med complications caused by fracture or resulting immobility
78
Q

complications from hip fracture include:

A
  • immobility
  • infection
  • DVT
  • PE
  • fat embolism
  • pneumonia
  • hemorrhage
  • shock
79
Q

____ emboli occur when a long bone (ribs, tibia, femur, pelvis) is injured and ___ is released from the ___ of the injured bone to systemic circulation. these ___ globs can lodge in small circulation of lungs, brain, or kidney, causing ______ and _____>

A
  • fat
  • fat
  • marrow
  • inflammation
  • ischemia
80
Q

tx hip fractures

A
  • surgury
  • subsequent rehabilitation/physical therapy
81
Q

tx osteopenia and osteoporosis

A
  • meds to decrease osteoclastic activity
  • nasal calcitonin and bisphosphonates (Fosamax)
82
Q

hypo or hypercalcemia can affect ___ movement in/out of cells, affecting ____ and causing certain S/S.

A
  • Na+
  • RMP
83
Q

low calcium = low _____ ability. disorder results in hypocalcemia, a pt might have easy _____, manifested by S/S such as petechiae and purpura.

A
  • clotting
  • bleeding
84
Q

____calcemia can cause kidney stones.

A

hyper

85
Q

PTH release is triggered by _____calcemia.

A

hypo

86
Q

PTH release ____ osteoclastic activity.

A

increases

87
Q

PTH release results in _____ resorption (calcium moving from _______).

A
  • increased
  • bone to blood
88
Q

PTH release is suppressed by ____calcemia

A

hyper

89
Q

calcitonin release is triggered by _____calcemia

A

hyper

90
Q

calcitonin release ___ osteoclastic activity

A

decreases

91
Q

calcitonin release results is ____ resorption so that calcium moves from ______.

A
  • decreased
  • blood to bone
92
Q

calcitonin release is suppressed by ___calcemia

A

hypo

93
Q

______: decreased PTH -> decreased resorption of calcium -> _________ -> _____polarized RMP

A
  • hypoparathyroidism
  • hypocalcemia
  • hypo
94
Q

__________: increased calcitonin -> decreased resorption of calcium -> ______ -> ____polarized RMP

A
  • calcitonin hypersecretion
  • hypocalcemia
  • hypo
95
Q

S/S hypocalcemia

A
  • muscle spasms
  • CKD tetany
  • (+) Chvostek’s sign
  • petechiae and purpura
96
Q

_______: excess PTH -> excess resorption of calcium -> ________ -> ____polarized RMP

A
  • hyperparathyroidism
  • hypercalcemia
  • hyper
97
Q

______: decreased calcitonin -> increased resorption of calcium -> ______ -> ____polarized RMP

A
  • calcitonin hyposecretion
  • hypercalcemia
  • hyper
98
Q

________: less bone-building -> more osteoclastic activity -> commonly causes _______, though not always hypercalcemia

A
  • menopause/aging
  • osteoporosis
99
Q

S/S hypercalcemia

A
  • weakness
  • lethargy
  • renal calculi
  • osteoporosis
100
Q

post-prandial (_____) process is thought as a?

A
  • after-eating
  • regulatory and anabolic
101
Q

food is initially processed in the stomach + duodenum -> capillaries in their linings absorb ____ into blood, creating transient ______.

A
  • glucose
  • hyperglycemia
102
Q

state of hyperglycemia stimulates secretion of ______ from the ______. what is the secreted substance’s fxns?

A
  • insulin
  • pancreas
  • assist glucose from blood into cells to be used as energy source
  • induce liver to store extra, unneeded glucose as glycogen (glycogenesis)
  • stims amino acids to build protein mass
  • important role in fat metabolism
103
Q

btw meals if glucose level in blood drops, that state of _______ may trigger hormone secretion _____ of insulin; these are called ______ hormones (__________).

A
  • hypoglycemia
  • opposite
  • counterregulatory
  • glucagon, epinephrine, cortisol, growth hormone
104
Q

____ and _____ are secreted from the adrenal glands -> give signals such as _____. the message is _____.

A
  • epinephrine
  • cortisol
  • shakiness, irritability, sweating, hunger pains
  • EAT
105
Q

if you don’t eat, the body must use back-up plans (_______) for energy, which are associated with what hormones?

A
  • compensatory actions
  • GH secreted from pituitary
  • Glucagon secreted from pacreas
106
Q

GH and glucagon stimulate the liver to begin ______ first, then _____ if needed. end product of these compensatory processes is that blood glucose will _______.

A
  • glycogenolysis
  • glucagon
  • increase
107
Q

the adrenal cortex secretes

A
  • cortisol
  • aldosterone
108
Q

cortisol

A
  • a glucocorticoid
  • endogenous steroidal hormone
  • exogenous steroids (made in lab) mimic this
109
Q

aldosterone

A
  • mineralocorticoid
  • directs kidneys to hold onto Na+ in blood (which then holds onto H2O) in exchange for secretion of K+ into urine
110
Q

Cushing’s syndrome two main components are?

A
  • hypercortisolism
  • hyperaldosteronism
111
Q

hypercortisolism

A

higher-than-normal levels of cortisol in body

112
Q

usually called Cushing’s syndrome when the high levels of cortisol are due to?

A
  • receiving chronic steroid treatment
113
Q

usually called Cushing’s disease when?

A
  • pathologic over secretion of adrenocorticotropic hormone (ACTH) from pit gland
    and/or
  • adrenal cortex itself has tumor or other malfxn that causes it to hypersecrete cortisol
114
Q

if pituitary malfxns, such as when there is a pit tumor, amount of ACTH is abnormally ______ -> stims _____ to secrete abnormally _____ amts of _______.

A
  • high
  • adrenal cortex
  • high
  • cortisol
115
Q

hyperaldosteronism

A

oversecretion of aldosterone by adrenal cortex

116
Q

S/S of increased cortisol and aldosterone

A
  • increased glycogenolysis + gluconeogenesis -> hyperglycemia -> type II DM
  • abnorm breakdown of adipose tissues (lipolysis) -> high levels of circulating fat products (hyperlipidemia) -> deposition
  • abnorm catabolized protein -> (-) effects on skin + muscle
  • increased osteoclastic activity
  • suppression of prostaglandin activity
117
Q

where does the circulating fate products from increased cortisol + aldosterone deposit?

A
  • trunk (truncal obesity)
  • face (moon face)
  • back (buffalo hump)
  • combo: cushinoid appearance
  • high levels LDL + increased risk for atherosclerosis
  • weight gain
118
Q

what are the negative effects on skin and muscle from abnormally catabolized protein due to increased cortisol + aldosterone?

A
  • muscle weakness + wasting (thin arms + legs)
  • children = short stature
  • weakened collagen fibers -> skin fragility -> skin bruises + tears easily
  • skin stretching -> purple striae (stretch marks) seen where skin stretched from increased fat deposits
119
Q

increased osteoclastic activity due to increased cortisol + aldosterone can lead to:

A
  • hypercalcemia (lethargy, fatigue)
  • hypercalcinuria (Ca2+ in urine) -> increased risk renal calculi
  • osteoporosis + fractures -> risk increase bc also reduced calcium absorption in gut
120
Q

suppression of prostaglandin activity from increased cortisol + aldosterone results in?

A
  • anti-clotting effects: pt bleeds more easily
  • anti-immunocyte effects: more susceptible to infection
  • decreased protection of stomach lining bc steroidal inhibit phospholipase in arachidonic pathway -> increased risk of peptic ulcers
  • increased peripheral vasocon -> HTN
121
Q

S/S of hyperaldosteronism

A
  • increased Na + H2O retention -> fluid vol overload -> weight gain, edema, HTN
  • hypokalemia
122
Q

other problems that arise due to increased cortisol + aldosterone

A
  • acne
  • hirsutism (increased hair growth, usually in inappropriate places)
123
Q

dx Cushing’s

A
  • S/S
  • obtain cortisol levels in diff times of day (cortisol secretion cyclical)
124
Q

tx Crushing’s

A
  • decrease exogenous steroids if possible
  • remove endogenous cortisol hypersecretion (tumors, enlarged adrenals, etc.) via surgery, chemo, radiation
  • drugs that black aldosterone effects (spinonolactone)
125
Q

Addison’s disease

A

state of hypocortisolism and hypoaldosteronism

126
Q

causes of Addison’s disease

A
  • pituitary malfxn - not enuf ACTH secreted
  • autoimmune: autoantibodies attack adrenal gland and cause atrophy + hypofxn
127
Q

S/S Addison’s disease based on hypocortisolism

A
  • hypoglycemia: weakness, fatigue, apathy, psychosis, mental confusion, weight loss
  • anorexia + N,V,D = weight loss
128
Q

S/S Addison’s disease based on hypoaldosteronism

A
  • less aldo = body can’t hang on water due to decreased tubular absorption of Na+ -> increased urination (polyuria) -> decreased blood vol
  • decreased blood vol -> hypotension + fluid vol deficit
129
Q

Addisonian crisis

A

severe hypotension due to fluid loss

130
Q

tx Addison’s disease

A
  • meds: daily oral steroids (predinsone) + aldosterone (Florinef)
  • lots of fluids, diet fairly high in NaCl
131
Q

diabetes mellitus literal meaning

A
  • diabetes: passing too much urine
  • mellitus: honey-flavored
132
Q

glucosuria

A

glucose in urine due to state of hyperglycemia -> glucose surpasses renal threshold

133
Q

the commonality of all DM disease is that pathologic ______ is present

A

hyperglycemia

134
Q

norm fasting serum glucose

A
  • 70-90
  • norm rises after meals, but normalizes back into range after insulin users glucose into cells
135
Q

DM diagnosed by several tests, including:

A
  • fasting blood sugar (FBS) > 126 on two separate occasions
    and/or
  • A1-C > 6.5%
136
Q

DM is monitored by _______ daily and every few months by a __________, aka ______.

A
  • finger prick blood sugar (BS)
  • glycosylated hemoglobin test
  • hemoglobin A1-C (Hgb A1c)
137
Q

the glycosylated hemoglobin test is an indirect way to measure?

A

average daily glucose levels

138
Q

the A in Hgb A1c comes from the fact that most of us have _____ as the main type of Hgb in our RBCs

A

Hgb A

139
Q

glycosylated hemoglobin

A
  • HgbA1c
  • hemoglobin molecules that pick up glucose
140
Q

the Hgb A1c test asks?

A
  • in the last 4 months or so, what average percentage of overall Hgb molecules is composed of Hgb A1C?
  • what percentage of Hgb molecules is glycosylated?
141
Q

norm range for total glycosylated Hgb molecules

A

no more than 4-6%

142
Q

in a diabetic, because there are ___ glucose molecules in the blood, hemoglobin picks up ____ glucose and the Hgb A1-C percentage is ____ than normal.

A
  • more
  • more
  • higher
143
Q

good medical therapy and diet for diabetics should keep the Hgb A1-C percentage at?

A

<7%

144
Q

if a diabetic is not controlling their diet and/or their meds aren’t therapeutic, the Hgb A1C will be?

A

higher than 7%

145
Q

DM Type I

A
  • juvenile onset
  • due to total lack of insulin secretion from beta cells of pancreas
146
Q

DM Type II

A
  • abnorm low insulin production (but there is some insulin)
  • impaired insulin utilization (insulin resistance)
147
Q

Type I DM usually beings in?

A

childhood and adolescence

148
Q

TYPE 1 DM almost always is a result of a combo of?

A
  • genetic susceptibility + possible env factors that triggers autoimmune destruction of beta cells
  • no insulin production at all
149
Q

3P of Type I diabetes

A
  • polyuria
  • polydipsia
  • polyphagia
150
Q

no insulin -> glucose?

A

cant’ get into cells, so accumulates in vlood

151
Q

glucose can’t get into cells -> ?

A

glucose can’t be used as energy source

152
Q

what happens when glucose accumulates in blood?

A
  1. hyperglycemia ( > ~200)
  2. exceeds renal threshold
  3. glucosuria
  4. increase urine osmolality
  5. draws water into urine
  6. polyuria
  7. polydipsia + S/S dehydration (dry skin, dry mucus membranes)
153
Q

what happens when glucose can’t be used as an energy source?

A
  • nutritional deficiency -> weight loss despite polyphagia + fatigue
  • gluconeogenesis -> high ketones in blood (acetone, acetoacetic acid, beta hydroxybutyric acid) -> acetone breath + ketonuria
154
Q

diabetic ketoacidosis (DKA)

A

Type I diabetes extreme state if left untreated

155
Q

S/S DKA

A
  • metabolic acidosis
  • Kussmaul resps
  • progress into diabetic coma
156
Q

Kussmaul respirations

A
  • fast, deep breathing pattern
  • compensatory response to metabolic acidosis so lungs blow off CO2
  • brings pH up to norm
157
Q

tx Type I DM

A

give insulin

158
Q

in most cases, the cause of DM II is?

A

obesity

159
Q

fat cells have ________ -> this causes ______ and the _____ ability to transport glucose inside the cells for metabolic use.

A
  • decreased # of insulin receptors in cell membranes
  • insulin resistance
  • decreased
160
Q

_____ keeps stimulating beta cells to secrete _____; pancreas is in overdrive -> causes _______

A
  • hyperglycemia
  • insulin
  • hyperinsulinemia
161
Q

pancreatic beta cell fatigue

A

pancreas tired from being in overdrive for so long -> diminished insulin secretion

162
Q

S/S of Type II DM usually more ____ than Type I bc?

A
  • subtle
  • some insulin being secreted -> some glucose is allowed into cells
163
Q

usually w/ TYPE II DM, there is __________, but sometimes the first signs (like _____) are that of chronic organ damage such as ________.

A
  • fatigue, mild polydipsia, polyuria
  • HTN
  • diabetic retinitis
164
Q

usually with Type II DM, there is no S/S of _____ because?

A
  • metabolic acidosis
  • some glucose entering cells -> don’t need gluconeogenesis -> no DKA usually
165
Q

hyperglycemic-hyperosmolar-nonketotic syndrome

A
  • HHNKS, HHNK, HHNS
  • type II diabetes extreme state
166
Q

S/S type II DM _____ and often _____ for long time, glucose can ____ reach much _____ than in Type I

A
  • insidious
  • overlooked
  • slowly
  • higher
167
Q

blood glucose of Type II usually?

A

> 400 to 900

168
Q

HHNKS characterized by?

A
  • very high serum osmolality (from high # of glucose molecules)
  • extreme polyuria
  • extreme dehydration
169
Q

if not treated, HHNKS can progress to?

A

diabetic coma

170
Q

tx Type II DM

A
  • diet/weight loss
  • oral meds that vary in how they work: some decrease cells’ insulin resistance, some act like insulin, etc.
  • insulin last resort, in combo w/ oral meds
  • HHNKS need lots of IV fluids (same, to a lesser degree, in DKA)
171
Q

large # of glucose molecules + abnorm # of fat molecules in blood are very damaging to?

A
  • linings of all arteries in the body
  • give rise to angiopathy (damaged arteries)
172
Q

macroangiopathy

A
  1. glucose toxicity
  2. damage to large and medium-sized arteries
  3. atherosclerosis in brain, heart, aorta, femoral arteries (stroke, CAD, aneurysms, PAD)
173
Q

microangiopathy

A

damage to small vessels such as:
- retinal arterioles -> retinopathy -> blurred vision, blinddness
- capillaries of kidneys -> chronic renal failure
- skin: easy bruising

174
Q

angiopathic ischemia to nerves + direct toxic effects of glucose also cause?

A

neuropathy

175
Q

peripheral neuropathy

A

burning, pain, itching, numbness of feet -> lack of feeling + increase risk of trauma and infection

176
Q

autonomic neuropathy

A

damage to nerves of the autonomic system

177
Q

examples of autonomic neuropathy

A
  • slowing of gut (gastroparesis), causing altered nutrition absorption + constipation
  • bladder control probs
  • silent MI: pain transmission during MI dysfxnal -> diabetic have MI w/o pain
178
Q

toxic effects of high glucose also impairs?

A

phagocytic fxn

179
Q

impaired phagocytic fxn

A
  • pt has increased susceptibility to infections
  • recurring UTIs, yeast infections, non-healing sores
180
Q

metabolic syndrome

A
  • 25% of US have this
  • cluster of traits that significantly increases risk for CV disease
181
Q

traits of metabolic syndrome

A
  • type II DM: hyperglycemia + insulin resistance
  • elevated triglycerides, decreased HDL
  • HTN
  • abdominal obesity
182
Q

hypoglycemia

A

blood glucose < 70 + S/S

183
Q

hypoglycemia is caused by

A
  • not eating; food not absorbed (food unavailable, malabsorption/starvation)
  • over exercising compared to food intake
  • natural hyperinsulinism (rare)
  • taking too much insulin (diabetics change doses, made mistake, don’t eat after taking insulin, etc.)
184
Q

natural hyperinsulinism

A
  • glucose in blood triggers over-secretion of insulin
  • pts must avoid simple sugars + keep carbs to minimum
185
Q

S/S hypoglycemia due to lack of energy source in cells

A
  • weakness
  • fatigue
  • mental fogginess
  • apathy
  • confusion
186
Q

S/S hypoglycemia due to effects of counterregulatory hormones

A
  • shakiness
  • irritability
  • sweating
187
Q

counterregulatory hormones include? what are their fxns?

A
  • glucagon, cortisol, GH, epinephrine
  • let you know you need to ear
  • stimulates glycogenolysis + gluconeogenesis to yield glucose
188
Q

if glucose gets low enough for brain to run out of fuel, pt can become? what is this state called? what else can happen?

A
  • unconscious
  • hypoglycemic shock or coma
  • seizures
189
Q

in medical settings, most commonly see severe hypoglycemia/coma in context of? this crisis state is often called?

A
  • taking too much insulin or taking it w/o eating
  • insulin shock or coma
190
Q

hypoglycemic situations vs diabetic ones

A
  • low BS vs high BS
  • wet S/S vs dry S/S
  • hypoglycemic crisis occurs more rapidly than diabetic ones
  • hypoglycemia more dangerous
191
Q

tx hypoglycemia

A
  • if can swallow: glucose in form of orange juice, packet of sugar, etc followed by complex carb like cracker
  • if in danger, can’t swallow, unconscious: IV glucose, glucagon IM or subQ
192
Q

glucagon is a hormone that will _____ glycogenolysis, which is a process that allows? how does this treat hypoglycemia?

A
  • increase
  • breakdown of large glycogen molecule into small glucose molecule
  • glucose from glycogen moves into blood to reverse hypoglycemia

nurs pathophysiology (13 decks)

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