rrd 11 Flashcards
endocrine disorders (192 cards)
1
Q
endocrine is dependent on?
A
negative feedback systems
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
3
Q
most endocrine disorders are problems of either?
A
- hyposecretion
- hypersecretion
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)
5
Q
diabetes insipidus (DI)
A
under secretion of ADH
6
Q
nomenclature of DI
A
- diabetes: too much urine
- insipidus: flavorless, no color
7
Q
renal-related etiology of DI
A
sick kidneys often have decreased response of renal tubules to ADH
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
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
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
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
12
Q
syndrome of inappropriate antidiuretic hormone (SIADH)
A
over secretion of ADH
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)
14
Q
mechanism of action of SIADH
A
- hold onto water 2 much by decrease urination
- increased vascular fluid volume
- water added to blood
- diluted plasma department
- lower serum osmolality
- small amts highly conc urine
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
16
Q
thyroid gland and TSH pathway
A
- pit gland secrete TSH (thyroid stim hormone)
- TSH stims thyroid
- thyroid produce, release, and/or store 3 thyroid hormones
17
Q
thyroid hormones from thyroid gland
A
- thyroxine (T4)
- triiodothyronine (T3)
^ reg metabolic activities - calcitonin: increase Ca2+ movement from blood into bone
18
Q
T3 + T4 is very dependent on _____ uptake from blood — _____ is consumed in our diet from _______.
A
- iodide
- iodide
- seafood and iodized salt
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
20
Q
negative feedback system of thyroid fxn
A
- drop in T3 + T4 in bloodstream
- pituitary stimulated
- increase TSH secretion
- thyroid stim to release more T3 + T4
- norm levels T3 + T4 reestablished
- norm levels suppress TSH secretion from pituitary
21
Q
the positive feedback loop occurs with _____ levels of thyroid hormones.
A
inccreased
22
Q
calcitonin is also regulated by _____ feedback.
A
negative
23
Q
hyperthyroidism
A
- state of having excess T3 + T4 production + release
- Graves disease
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
25
lab work for hyperthyroidism
- serum T4 higher
- serum TSH lower
26
other features of hyperthyroidism included is one of _____ S/S due to the ______ processes caused by high levels _____
- overactive
- hypermetabolic
- T3, T4
27
psych/CNS S/S hyperthyroidism
- nervous
- irritable
- tremors
- insomnia
- emotionally labile
- sometimes psychosis (hallucinations, paranoia)
28
cardiovascular S/S hyperthyroidism
- tachycardia
- increased afterload
- sometimes HF due to increased heart workload
29
GI S/S hyperthyroidism
- increased appetite
- diarrhea
30
hair changes S/S hyperthyroidism
- hair follicles sensitive to metabolic state -> stressed by 2 much thyroid hormone -> hair thins or falls out -> alopecia
31
other S/S hyperthyroidism
- exophtalmus
- goiter
- fatigue + weight loss (overdrive state use energy)
- increased body temp + heat intolerance
- skin flushed, warm, damp from excessive sweating
32
exopthalmus
bulging eyes from deposits of excess tissue behind eyes
33
goiter
an enlargement of the thyroid gland that can sometimes be easily visualized w/ hyperthyroidism AND hypothyroidism
34
causes of goiter in hyperthyroidism
cells pathologically stimulated by autoantibodies to increase their thyroid hormone output (overdrive = increased size of cell)
35
thyrotoxic crisis
- thyroid storm
- extreme state of hyperthyroidism
36
thyrotoxic crisis is a ____ emergency triggered by some stressor such as _____.
- hyperthyroid
- infection, trauma, surgery, etc.
37
neuro S/S thyrotoxic crisis
- extreme restlessness and agitation
- delirium
- seizures
- coma
38
circulatory S/S thyrotoxic crisis
- severe tachycardia
- heart failure
- shock
39
other S/S thyrotoxic crisis
- diaphoresis
- hyperthermia (103-105 F)
40
tx hyperthyroidism
- antithyroid meds: inhibit synthesis of thyroid hormones
- thyroidectomy (usually 90% removed)
41
hypothyroidism
state of deficient T3/T4 production + release
42
hypothyroidism is caused by:
- congenital defects
- direct removal of tissue (tumor) or direct destruction of tissue (radiation)
- autoimmune thyroiditis
- endemic iodine deficiency
- overactivity of antithyroid drugs
43
what is the autoimmune thyroiditis disorder that cause hypothyroidism?
Hashimoto's thyroiditis
44
Hashimoto's thyroiditis
- autoantibodies actually destroy tissue
- insidious onset w/ thyroid tissue slowly replaced by lymphocytes + scar tissue
45
endemic iodide deficiency
- 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)
46
overactivity of antithyroid drugs
pts start w/ being treated for hyperthyroidism but goes too far
47
lab work for hypothyroidism
- serum T4 lower
- serum TSH higher
48
psych/CNS S/S hypothyroidism
- confusion
- slow speech and thinking
- sluggish
- memory loss
- depression
49
circulatory S/S hypothyroidism
- anemia
- bradycardia
- decreased CO
50
pulmonary S/S hypothyroidism
- dyspnea
- hypoventilation
- CO2 retention
51
GI S/S hypothyroidism
- decreased appetite
- constipation
52
hair w/ hypothyroidism
- dry and brittle
- may fall out (alopecia)
- not having enuf thyroid hormone to support metabolic needs of follicles
53
skin S/S hypothyroidism
- myxedema: changes in dermis that cause water to be trapped under skin over time -> pt has overall puffy lewk
- skin coarse + dry
54
goiter in hypothyroidism
- hyperplasia + hypertrophy of tissue compensatory response
to increase thyroid hormone secretion
- inflammation + scar tissue from autoimmune attack
55
other body changes bc hypothyroidism
- weight gain despite decreased appetite
- decreased body temp + cold-intolerance
56
myxedema coma or crisis
extreme state of hypothyroidism
57
myxedema coma is precipitated by stressor such as?
- infection
- drug
- exposure to cold
- trauma
58
myxedema coma is manifested by?
- progression of hypothyroid sluggishness + drowsiness
- into gradual or sudden impaired consciousness
- often hypotension and hypoventilation
59
tx hypothyroidism
- synthetic thyroid hormone
- levothyroxine (Synthroid)
60
calcium needed for what fxns?
- building + maintenance of appropriate bone density
- cell electrical activity
- clotting
61
____ is the biggest storage area for calcium and there is always movement from _____ to ______ and back again.
- bone
- bone
- blood
62
when the serum calcium is lower than normal, _________. when higher than normal, _______.
- hypocalcemia
- hypercalcemia
63
chief regulators of calcium movement
- calcitonin
- PTH (parathyroid hormone)
64
calcitonin is secreted by the ______ and enhances movement of calcium from ______.
- thyroid gland
- blood into bone
65
PTH is secreted by _______ and stimulates ______.
- parathyroid gland
- resorption: movement of substance back into circulation from somewhere else; from bone to blood
66
PTH enhances movement of calcium from _____ to _____ by ____________.
- bone
- bloodstream
- increasing osteoclastic activity
67
osteoclasts
- 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
68
calcitonin + PTH work by _____ feedback and balance each other out.
negative
69
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.
- increased
- suppressed
- increased
- up
70
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.
- increased
- suppressed
- decreased
- down
71
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.
- increase
- increased
- exceeds
72
the increase in resorption due to increased osteoclastic activity causes bone density to _____ and bone becomes more _____.
- decrease
- porous
73
which gender is more likely to have increased resorption/osteoclastic activity? why?
- women
- women's bones significantly less dense than men's to begin with
- menopausal loss of estrogen
74
why does menopausal loss of estrogen contribute to low bone density and porous bones in older women?
- 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
75
osteopenia
the condition of having somewhat less than normal bone density
76
osteoporosis
bone density that is markedly lower than normal
77
sequelae in either osteopenia or osteoporosis
- bones more easily fractured, esp in hip + vertebra
- deaths from hip frac related to med complications caused by fracture or resulting immobility
78
complications from hip fracture include:
- immobility
- infection
- DVT
- PE
- fat embolism
- pneumonia
- hemorrhage
- shock
79
____ 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 _____>
- fat
- fat
- marrow
- inflammation
- ischemia
80
tx hip fractures
- surgury
- subsequent rehabilitation/physical therapy
81
tx osteopenia and osteoporosis
- meds to decrease osteoclastic activity
- nasal calcitonin and bisphosphonates (Fosamax)
82
hypo or hypercalcemia can affect ___ movement in/out of cells, affecting ____ and causing certain S/S.
- Na+
- RMP
83
low calcium = low _____ ability. disorder results in hypocalcemia, a pt might have easy _____, manifested by S/S such as petechiae and purpura.
- clotting
- bleeding
84
____calcemia can cause kidney stones.
hyper
85
PTH release is triggered by _____calcemia.
hypo
86
PTH release ____ osteoclastic activity.
increases
87
PTH release results in _____ resorption (calcium moving from _______).
- increased
- bone to blood
88
PTH release is suppressed by ____calcemia
hyper
89
calcitonin release is triggered by _____calcemia
hyper
90
calcitonin release ___ osteoclastic activity
decreases
91
calcitonin release results is ____ resorption so that calcium moves from ______.
- decreased
- blood to bone
92
calcitonin release is suppressed by ___calcemia
hypo
93
______: decreased PTH -> decreased resorption of calcium -> _________ -> _____polarized RMP
- hypoparathyroidism
- hypocalcemia
- hypo
94
__________: increased calcitonin -> decreased resorption of calcium -> ______ -> ____polarized RMP
- calcitonin hypersecretion
- hypocalcemia
- hypo
95
S/S hypocalcemia
- muscle spasms
- CKD tetany
- (+) Chvostek's sign
- petechiae and purpura
96
_______: excess PTH -> excess resorption of calcium -> ________ -> ____polarized RMP
- hyperparathyroidism
- hypercalcemia
- hyper
97
______: decreased calcitonin -> increased resorption of calcium -> ______ -> ____polarized RMP
- calcitonin hyposecretion
- hypercalcemia
- hyper
98
________: less bone-building -> more osteoclastic activity -> commonly causes _______, though not always hypercalcemia
- menopause/aging
- osteoporosis
99
S/S hypercalcemia
- weakness
- lethargy
- renal calculi
- osteoporosis
100
post-prandial (_____) process is thought as a?
- after-eating
- regulatory and anabolic
101
food is initially processed in the stomach + duodenum -> capillaries in their linings absorb ____ into blood, creating transient ______.
- glucose
- hyperglycemia
102
state of hyperglycemia stimulates secretion of ______ from the ______. what is the secreted substance's fxns?
- 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
btw meals if glucose level in blood drops, that state of _______ may trigger hormone secretion _____ of insulin; these are called ______ hormones (__________).
- hypoglycemia
- opposite
- counterregulatory
- glucagon, epinephrine, cortisol, growth hormone
104
____ and _____ are secreted from the adrenal glands -> give signals such as _____. the message is _____.
- epinephrine
- cortisol
- shakiness, irritability, sweating, hunger pains
- EAT
105
if you don't eat, the body must use back-up plans (_______) for energy, which are associated with what hormones?
- compensatory actions
- GH secreted from pituitary
- Glucagon secreted from pacreas
106
GH and glucagon stimulate the liver to begin ______ first, then _____ if needed. end product of these compensatory processes is that blood glucose will _______.
- glycogenolysis
- glucagon
- increase
107
the adrenal cortex secretes
- cortisol
- aldosterone
108
cortisol
- a glucocorticoid
- endogenous steroidal hormone
- exogenous steroids (made in lab) mimic this
109
aldosterone
- mineralocorticoid
- directs kidneys to hold onto Na+ in blood (which then holds onto H2O) in exchange for secretion of K+ into urine
110
Cushing's syndrome two main components are?
- hypercortisolism
- hyperaldosteronism
111
hypercortisolism
higher-than-normal levels of cortisol in body
112
usually called Cushing's syndrome when the high levels of cortisol are due to?
- receiving chronic steroid treatment
113
usually called Cushing's disease when?
- 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
if pituitary malfxns, such as when there is a pit tumor, amount of ACTH is abnormally ______ -> stims _____ to secrete abnormally _____ amts of _______.
- high
- adrenal cortex
- high
- cortisol
115
hyperaldosteronism
oversecretion of aldosterone by adrenal cortex
116
S/S of increased cortisol and aldosterone
- 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
where does the circulating fate products from increased cortisol + aldosterone deposit?
- trunk (truncal obesity)
- face (moon face)
- back (buffalo hump)
- combo: cushinoid appearance
- high levels LDL + increased risk for atherosclerosis
- weight gain
118
what are the negative effects on skin and muscle from abnormally catabolized protein due to increased cortisol + aldosterone?
- 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
increased osteoclastic activity due to increased cortisol + aldosterone can lead to:
- hypercalcemia (lethargy, fatigue)
- hypercalcinuria (Ca2+ in urine) -> increased risk renal calculi
- osteoporosis + fractures -> risk increase bc also reduced calcium absorption in gut
120
suppression of prostaglandin activity from increased cortisol + aldosterone results in?
- 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
S/S of hyperaldosteronism
- increased Na + H2O retention -> fluid vol overload -> weight gain, edema, HTN
- hypokalemia
122
other problems that arise due to increased cortisol + aldosterone
- acne
- hirsutism (increased hair growth, usually in inappropriate places)
123
dx Cushing's
- S/S
- obtain cortisol levels in diff times of day (cortisol secretion cyclical)
124
tx Crushing's
- decrease exogenous steroids if possible
- remove endogenous cortisol hypersecretion (tumors, enlarged adrenals, etc.) via surgery, chemo, radiation
- drugs that black aldosterone effects (spinonolactone)
125
Addison's disease
state of hypocortisolism and hypoaldosteronism
126
causes of Addison's disease
- pituitary malfxn - not enuf ACTH secreted
- autoimmune: autoantibodies attack adrenal gland and cause atrophy + hypofxn
127
S/S Addison's disease based on hypocortisolism
- hypoglycemia: weakness, fatigue, apathy, psychosis, mental confusion, weight loss
- anorexia + N,V,D = weight loss
128
S/S Addison's disease based on hypoaldosteronism
- 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
Addisonian crisis
severe hypotension due to fluid loss
130
tx Addison's disease
- meds: daily oral steroids (predinsone) + aldosterone (Florinef)
- lots of fluids, diet fairly high in NaCl
131
diabetes mellitus literal meaning
- diabetes: passing too much urine
- mellitus: honey-flavored
132
glucosuria
glucose in urine due to state of hyperglycemia -> glucose surpasses renal threshold
133
the commonality of all DM disease is that pathologic ______ is present
hyperglycemia
134
norm fasting serum glucose
- 70-90
- norm rises after meals, but normalizes back into range after insulin users glucose into cells
135
DM diagnosed by several tests, including:
- fasting blood sugar (FBS) > 126 on two separate occasions
and/or
- A1-C > 6.5%
136
DM is monitored by _______ daily and every few months by a __________, aka ______.
- finger prick blood sugar (BS)
- glycosylated hemoglobin test
- hemoglobin A1-C (Hgb A1c)
137
the glycosylated hemoglobin test is an indirect way to measure?
average daily glucose levels
138
the A in Hgb A1c comes from the fact that most of us have _____ as the main type of Hgb in our RBCs
Hgb A
139
glycosylated hemoglobin
- HgbA1c
- hemoglobin molecules that pick up glucose
140
the Hgb A1c test asks?
- 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
norm range for total glycosylated Hgb molecules
no more than 4-6%
142
in a diabetic, because there are ___ glucose molecules in the blood, hemoglobin picks up ____ glucose and the Hgb A1-C percentage is ____ than normal.
- more
- more
- higher
143
good medical therapy and diet for diabetics should keep the Hgb A1-C percentage at?
<7%
144
if a diabetic is not controlling their diet and/or their meds aren't therapeutic, the Hgb A1C will be?
higher than 7%
145
DM Type I
- juvenile onset
- due to total lack of insulin secretion from beta cells of pancreas
146
DM Type II
- abnorm low insulin production (but there is some insulin)
- impaired insulin utilization (insulin resistance)
147
Type I DM usually beings in?
childhood and adolescence
148
TYPE 1 DM almost always is a result of a combo of?
- genetic susceptibility + possible env factors that triggers autoimmune destruction of beta cells
- no insulin production at all
149
3P of Type I diabetes
- polyuria
- polydipsia
- polyphagia
150
no insulin -> glucose?
cant' get into cells, so accumulates in vlood
151
glucose can't get into cells -> ?
glucose can't be used as energy source
152
what happens when glucose accumulates in blood?
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
what happens when glucose can't be used as an energy source?
- nutritional deficiency -> weight loss despite polyphagia + fatigue
- gluconeogenesis -> high ketones in blood (acetone, acetoacetic acid, beta hydroxybutyric acid) -> acetone breath + ketonuria
154
diabetic ketoacidosis (DKA)
Type I diabetes extreme state if left untreated
155
S/S DKA
- metabolic acidosis
- Kussmaul resps
- progress into diabetic coma
156
Kussmaul respirations
- fast, deep breathing pattern
- compensatory response to metabolic acidosis so lungs blow off CO2
- brings pH up to norm
157
tx Type I DM
give insulin
158
in most cases, the cause of DM II is?
obesity
159
fat cells have ________ -> this causes ______ and the _____ ability to transport glucose inside the cells for metabolic use.
- decreased # of insulin receptors in cell membranes
- insulin resistance
- decreased
160
_____ keeps stimulating beta cells to secrete _____; pancreas is in overdrive -> causes _______
- hyperglycemia
- insulin
- hyperinsulinemia
161
pancreatic beta cell fatigue
pancreas tired from being in overdrive for so long -> diminished insulin secretion
162
S/S of Type II DM usually more ____ than Type I bc?
- subtle
- some insulin being secreted -> some glucose is allowed into cells
163
usually w/ TYPE II DM, there is __________, but sometimes the first signs (like _____) are that of chronic organ damage such as ________.
- fatigue, mild polydipsia, polyuria
- HTN
- diabetic retinitis
164
usually with Type II DM, there is no S/S of _____ because?
- metabolic acidosis
- some glucose entering cells -> don't need gluconeogenesis -> no DKA usually
165
hyperglycemic-hyperosmolar-nonketotic syndrome
- HHNKS, HHNK, HHNS
- type II diabetes extreme state
166
S/S type II DM _____ and often _____ for long time, glucose can ____ reach much _____ than in Type I
- insidious
- overlooked
- slowly
- higher
167
blood glucose of Type II usually?
> 400 to 900
168
HHNKS characterized by?
- very high serum osmolality (from high # of glucose molecules)
- extreme polyuria
- extreme dehydration
169
if not treated, HHNKS can progress to?
diabetic coma
170
tx Type II DM
- 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
large # of glucose molecules + abnorm # of fat molecules in blood are very damaging to?
- linings of all arteries in the body
- give rise to angiopathy (damaged arteries)
172
macroangiopathy
1. glucose toxicity
2. damage to large and medium-sized arteries
3. atherosclerosis in brain, heart, aorta, femoral arteries (stroke, CAD, aneurysms, PAD)
173
microangiopathy
damage to small vessels such as:
- retinal arterioles -> retinopathy -> blurred vision, blinddness
- capillaries of kidneys -> chronic renal failure
- skin: easy bruising
174
angiopathic ischemia to nerves + direct toxic effects of glucose also cause?
neuropathy
175
peripheral neuropathy
burning, pain, itching, numbness of feet -> lack of feeling + increase risk of trauma and infection
176
autonomic neuropathy
damage to nerves of the autonomic system
177
examples of autonomic neuropathy
- 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
toxic effects of high glucose also impairs?
phagocytic fxn
179
impaired phagocytic fxn
- pt has increased susceptibility to infections
- recurring UTIs, yeast infections, non-healing sores
180
metabolic syndrome
- 25% of US have this
- cluster of traits that significantly increases risk for CV disease
181
traits of metabolic syndrome
- type II DM: hyperglycemia + insulin resistance
- elevated triglycerides, decreased HDL
- HTN
- abdominal obesity
182
hypoglycemia
blood glucose < 70 + S/S
183
hypoglycemia is caused by
- 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
natural hyperinsulinism
- glucose in blood triggers over-secretion of insulin
- pts must avoid simple sugars + keep carbs to minimum
185
S/S hypoglycemia due to lack of energy source in cells
- weakness
- fatigue
- mental fogginess
- apathy
- confusion
186
S/S hypoglycemia due to effects of counterregulatory hormones
- shakiness
- irritability
- sweating
187
counterregulatory hormones include? what are their fxns?
- glucagon, cortisol, GH, epinephrine
- let you know you need to ear
- stimulates glycogenolysis + gluconeogenesis to yield glucose
188
if glucose gets low enough for brain to run out of fuel, pt can become? what is this state called? what else can happen?
- unconscious
- hypoglycemic shock or coma
- seizures
189
in medical settings, most commonly see severe hypoglycemia/coma in context of? this crisis state is often called?
- taking too much insulin or taking it w/o eating
- insulin shock or coma
190
hypoglycemic situations vs diabetic ones
- low BS vs high BS
- wet S/S vs dry S/S
- hypoglycemic crisis occurs more rapidly than diabetic ones
- hypoglycemia more dangerous
191
tx hypoglycemia
- 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
glucagon is a hormone that will _____ glycogenolysis, which is a process that allows? how does this treat hypoglycemia?
- increase
- breakdown of large glycogen molecule into small glucose molecule
- glucose from glycogen moves into blood to reverse hypoglycemia
