rrd 11 Flashcards
endocrine disorders
endocrine is dependent on?
negative feedback systems
negative feedback systems of endocrine
- 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
most endocrine disorders are problems of either?
- hyposecretion
- hypersecretion
pituitary gland
- 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)
diabetes insipidus (DI)
under secretion of ADH
nomenclature of DI
- diabetes: too much urine
- insipidus: flavorless, no color
renal-related etiology of DI
sick kidneys often have decreased response of renal tubules to ADH
CNS-related etiologies of DI
- 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
w/o influence of ADH, you ____ hold onto water effectively. what does this mean?
- won’t
- H2O will indiscriminately flow from peritubular capillaries of kidneys into tubules -> very dilute urine
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 ____.
- compensate
- low
- low
- decreasing
- conserved
- up
S/S DI
- 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
syndrome of inappropriate antidiuretic hormone (SIADH)
over secretion of ADH
events that trigger SIADH
- 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)
mechanism of action of SIADH
- 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
S/S SIADH
- oliguria (decreased urine output bc body hold onto water inappropriately in vascular space)
- B-to-T shift -> edema
- peripheral + pulmonary edema
thyroid gland and TSH pathway
- pit gland secrete TSH (thyroid stim hormone)
- TSH stims thyroid
- thyroid produce, release, and/or store 3 thyroid hormones
thyroid hormones from thyroid gland
- thyroxine (T4)
- triiodothyronine (T3)
^ reg metabolic activities - calcitonin: increase Ca2+ movement from blood into bone
T3 + T4 is very dependent on _____ uptake from blood — _____ is consumed in our diet from _______.
- iodide
- iodide
- seafood and iodized salt
T3 and T4 act on receptor cells of many diff organs and affect body’s:
- metabolic rate
- caloric requirements
- oxygen consumption
- carbohydrate + lipid metabolism
- growth and development
- brain + nervous system fxns
negative feedback system of thyroid fxn
- 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
the positive feedback loop occurs with _____ levels of thyroid hormones.
inccreased
calcitonin is also regulated by _____ feedback.
negative
hyperthyroidism
- state of having excess T3 + T4 production + release
- Graves disease
Graves disease
- an autoimmune disorder in which autoantibodies attack/stim TSH receptors on the thyroid
- autoantibodies mimic TSH -> thyroid secrete more T3 + T3
lab work for hyperthyroidism
- serum T4 higher
- serum TSH lower
other features of hyperthyroidism included is one of _____ S/S due to the ______ processes caused by high levels _____
- overactive
- hypermetabolic
- T3, T4
psych/CNS S/S hyperthyroidism
- nervous
- irritable
- tremors
- insomnia
- emotionally labile
- sometimes psychosis (hallucinations, paranoia)
cardiovascular S/S hyperthyroidism
- tachycardia
- increased afterload
- sometimes HF due to increased heart workload
GI S/S hyperthyroidism
- increased appetite
- diarrhea
hair changes S/S hyperthyroidism
- hair follicles sensitive to metabolic state -> stressed by 2 much thyroid hormone -> hair thins or falls out -> alopecia
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
exopthalmus
bulging eyes from deposits of excess tissue behind eyes
goiter
an enlargement of the thyroid gland that can sometimes be easily visualized w/ hyperthyroidism AND hypothyroidism
causes of goiter in hyperthyroidism
cells pathologically stimulated by autoantibodies to increase their thyroid hormone output (overdrive = increased size of cell)
thyrotoxic crisis
- thyroid storm
- extreme state of hyperthyroidism
thyrotoxic crisis is a ____ emergency triggered by some stressor such as _____.
- hyperthyroid
- infection, trauma, surgery, etc.
neuro S/S thyrotoxic crisis
- extreme restlessness and agitation
- delirium
- seizures
- coma
circulatory S/S thyrotoxic crisis
- severe tachycardia
- heart failure
- shock
other S/S thyrotoxic crisis
- diaphoresis
- hyperthermia (103-105 F)
tx hyperthyroidism
- antithyroid meds: inhibit synthesis of thyroid hormones
- thyroidectomy (usually 90% removed)
hypothyroidism
state of deficient T3/T4 production + release
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
what is the autoimmune thyroiditis disorder that cause hypothyroidism?
Hashimoto’s thyroiditis
Hashimoto’s thyroiditis
- autoantibodies actually destroy tissue
- insidious onset w/ thyroid tissue slowly replaced by lymphocytes + scar tissue
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)
overactivity of antithyroid drugs
pts start w/ being treated for hyperthyroidism but goes too far
lab work for hypothyroidism
- serum T4 lower
- serum TSH higher
psych/CNS S/S hypothyroidism
- confusion
- slow speech and thinking
- sluggish
- memory loss
- depression
circulatory S/S hypothyroidism
- anemia
- bradycardia
- decreased CO
pulmonary S/S hypothyroidism
- dyspnea
- hypoventilation
- CO2 retention
GI S/S hypothyroidism
- decreased appetite
- constipation
hair w/ hypothyroidism
- dry and brittle
- may fall out (alopecia)
- not having enuf thyroid hormone to support metabolic needs of follicles
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
goiter in hypothyroidism
- hyperplasia + hypertrophy of tissue compensatory response
to increase thyroid hormone secretion - inflammation + scar tissue from autoimmune attack
other body changes bc hypothyroidism
- weight gain despite decreased appetite
- decreased body temp + cold-intolerance
myxedema coma or crisis
extreme state of hypothyroidism
myxedema coma is precipitated by stressor such as?
- infection
- drug
- exposure to cold
- trauma
myxedema coma is manifested by?
- progression of hypothyroid sluggishness + drowsiness
- into gradual or sudden impaired consciousness
- often hypotension and hypoventilation
tx hypothyroidism
- synthetic thyroid hormone
- levothyroxine (Synthroid)
calcium needed for what fxns?
- building + maintenance of appropriate bone density
- cell electrical activity
- clotting
____ is the biggest storage area for calcium and there is always movement from _____ to ______ and back again.
- bone
- bone
- blood
when the serum calcium is lower than normal, _________. when higher than normal, _______.
- hypocalcemia
- hypercalcemia
chief regulators of calcium movement
- calcitonin
- PTH (parathyroid hormone)
calcitonin is secreted by the ______ and enhances movement of calcium from ______.
- thyroid gland
- blood into bone
PTH is secreted by _______ and stimulates ______.
- parathyroid gland
- resorption: movement of substance back into circulation from somewhere else; from bone to blood
PTH enhances movement of calcium from _____ to _____ by ____________.
- bone
- bloodstream
- increasing osteoclastic activity
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
calcitonin + PTH work by _____ feedback and balance each other out.
negative
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
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
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
the increase in resorption due to increased osteoclastic activity causes bone density to _____ and bone becomes more _____.
- decrease
- porous
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
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
osteopenia
the condition of having somewhat less than normal bone density
osteoporosis
bone density that is markedly lower than normal
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
complications from hip fracture include:
- immobility
- infection
- DVT
- PE
- fat embolism
- pneumonia
- hemorrhage
- shock
____ 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
tx hip fractures
- surgury
- subsequent rehabilitation/physical therapy
tx osteopenia and osteoporosis
- meds to decrease osteoclastic activity
- nasal calcitonin and bisphosphonates (Fosamax)
hypo or hypercalcemia can affect ___ movement in/out of cells, affecting ____ and causing certain S/S.
- Na+
- RMP
low calcium = low _____ ability. disorder results in hypocalcemia, a pt might have easy _____, manifested by S/S such as petechiae and purpura.
- clotting
- bleeding
____calcemia can cause kidney stones.
hyper
PTH release is triggered by _____calcemia.
hypo
PTH release ____ osteoclastic activity.
increases
PTH release results in _____ resorption (calcium moving from _______).
- increased
- bone to blood
PTH release is suppressed by ____calcemia
hyper
calcitonin release is triggered by _____calcemia
hyper
calcitonin release ___ osteoclastic activity
decreases
calcitonin release results is ____ resorption so that calcium moves from ______.
- decreased
- blood to bone
calcitonin release is suppressed by ___calcemia
hypo
______: decreased PTH -> decreased resorption of calcium -> _________ -> _____polarized RMP
- hypoparathyroidism
- hypocalcemia
- hypo
__________: increased calcitonin -> decreased resorption of calcium -> ______ -> ____polarized RMP
- calcitonin hypersecretion
- hypocalcemia
- hypo
S/S hypocalcemia
- muscle spasms
- CKD tetany
- (+) Chvostek’s sign
- petechiae and purpura
_______: excess PTH -> excess resorption of calcium -> ________ -> ____polarized RMP
- hyperparathyroidism
- hypercalcemia
- hyper
______: decreased calcitonin -> increased resorption of calcium -> ______ -> ____polarized RMP
- calcitonin hyposecretion
- hypercalcemia
- hyper
________: less bone-building -> more osteoclastic activity -> commonly causes _______, though not always hypercalcemia
- menopause/aging
- osteoporosis
S/S hypercalcemia
- weakness
- lethargy
- renal calculi
- osteoporosis
post-prandial (_____) process is thought as a?
- after-eating
- regulatory and anabolic
food is initially processed in the stomach + duodenum -> capillaries in their linings absorb ____ into blood, creating transient ______.
- glucose
- hyperglycemia
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
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
____ and _____ are secreted from the adrenal glands -> give signals such as _____. the message is _____.
- epinephrine
- cortisol
- shakiness, irritability, sweating, hunger pains
- EAT
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
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
the adrenal cortex secretes
- cortisol
- aldosterone
cortisol
- a glucocorticoid
- endogenous steroidal hormone
- exogenous steroids (made in lab) mimic this
aldosterone
- mineralocorticoid
- directs kidneys to hold onto Na+ in blood (which then holds onto H2O) in exchange for secretion of K+ into urine
Cushing’s syndrome two main components are?
- hypercortisolism
- hyperaldosteronism
hypercortisolism
higher-than-normal levels of cortisol in body
usually called Cushing’s syndrome when the high levels of cortisol are due to?
- receiving chronic steroid treatment
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
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
hyperaldosteronism
oversecretion of aldosterone by adrenal cortex
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
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
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
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
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
S/S of hyperaldosteronism
- increased Na + H2O retention -> fluid vol overload -> weight gain, edema, HTN
- hypokalemia
other problems that arise due to increased cortisol + aldosterone
- acne
- hirsutism (increased hair growth, usually in inappropriate places)
dx Cushing’s
- S/S
- obtain cortisol levels in diff times of day (cortisol secretion cyclical)
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)
Addison’s disease
state of hypocortisolism and hypoaldosteronism
causes of Addison’s disease
- pituitary malfxn - not enuf ACTH secreted
- autoimmune: autoantibodies attack adrenal gland and cause atrophy + hypofxn
S/S Addison’s disease based on hypocortisolism
- hypoglycemia: weakness, fatigue, apathy, psychosis, mental confusion, weight loss
- anorexia + N,V,D = weight loss
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
Addisonian crisis
severe hypotension due to fluid loss
tx Addison’s disease
- meds: daily oral steroids (predinsone) + aldosterone (Florinef)
- lots of fluids, diet fairly high in NaCl
diabetes mellitus literal meaning
- diabetes: passing too much urine
- mellitus: honey-flavored
glucosuria
glucose in urine due to state of hyperglycemia -> glucose surpasses renal threshold
the commonality of all DM disease is that pathologic ______ is present
hyperglycemia
norm fasting serum glucose
- 70-90
- norm rises after meals, but normalizes back into range after insulin users glucose into cells
DM diagnosed by several tests, including:
- fasting blood sugar (FBS) > 126 on two separate occasions
and/or - A1-C > 6.5%
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)
the glycosylated hemoglobin test is an indirect way to measure?
average daily glucose levels
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
glycosylated hemoglobin
- HgbA1c
- hemoglobin molecules that pick up glucose
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?
norm range for total glycosylated Hgb molecules
no more than 4-6%
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
good medical therapy and diet for diabetics should keep the Hgb A1-C percentage at?
<7%
if a diabetic is not controlling their diet and/or their meds aren’t therapeutic, the Hgb A1C will be?
higher than 7%
DM Type I
- juvenile onset
- due to total lack of insulin secretion from beta cells of pancreas
DM Type II
- abnorm low insulin production (but there is some insulin)
- impaired insulin utilization (insulin resistance)
Type I DM usually beings in?
childhood and adolescence
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
3P of Type I diabetes
- polyuria
- polydipsia
- polyphagia
no insulin -> glucose?
cant’ get into cells, so accumulates in vlood
glucose can’t get into cells -> ?
glucose can’t be used as energy source
what happens when glucose accumulates in blood?
- hyperglycemia ( > ~200)
- exceeds renal threshold
- glucosuria
- increase urine osmolality
- draws water into urine
- polyuria
- polydipsia + S/S dehydration (dry skin, dry mucus membranes)
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
diabetic ketoacidosis (DKA)
Type I diabetes extreme state if left untreated
S/S DKA
- metabolic acidosis
- Kussmaul resps
- progress into diabetic coma
Kussmaul respirations
- fast, deep breathing pattern
- compensatory response to metabolic acidosis so lungs blow off CO2
- brings pH up to norm
tx Type I DM
give insulin
in most cases, the cause of DM II is?
obesity
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
_____ keeps stimulating beta cells to secrete _____; pancreas is in overdrive -> causes _______
- hyperglycemia
- insulin
- hyperinsulinemia
pancreatic beta cell fatigue
pancreas tired from being in overdrive for so long -> diminished insulin secretion
S/S of Type II DM usually more ____ than Type I bc?
- subtle
- some insulin being secreted -> some glucose is allowed into cells
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
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
hyperglycemic-hyperosmolar-nonketotic syndrome
- HHNKS, HHNK, HHNS
- type II diabetes extreme state
S/S type II DM _____ and often _____ for long time, glucose can ____ reach much _____ than in Type I
- insidious
- overlooked
- slowly
- higher
blood glucose of Type II usually?
> 400 to 900
HHNKS characterized by?
- very high serum osmolality (from high # of glucose molecules)
- extreme polyuria
- extreme dehydration
if not treated, HHNKS can progress to?
diabetic coma
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)
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)
macroangiopathy
- glucose toxicity
- damage to large and medium-sized arteries
- atherosclerosis in brain, heart, aorta, femoral arteries (stroke, CAD, aneurysms, PAD)
microangiopathy
damage to small vessels such as:
- retinal arterioles -> retinopathy -> blurred vision, blinddness
- capillaries of kidneys -> chronic renal failure
- skin: easy bruising
angiopathic ischemia to nerves + direct toxic effects of glucose also cause?
neuropathy
peripheral neuropathy
burning, pain, itching, numbness of feet -> lack of feeling + increase risk of trauma and infection
autonomic neuropathy
damage to nerves of the autonomic system
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
toxic effects of high glucose also impairs?
phagocytic fxn
impaired phagocytic fxn
- pt has increased susceptibility to infections
- recurring UTIs, yeast infections, non-healing sores
metabolic syndrome
- 25% of US have this
- cluster of traits that significantly increases risk for CV disease
traits of metabolic syndrome
- type II DM: hyperglycemia + insulin resistance
- elevated triglycerides, decreased HDL
- HTN
- abdominal obesity
hypoglycemia
blood glucose < 70 + S/S
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.)
natural hyperinsulinism
- glucose in blood triggers over-secretion of insulin
- pts must avoid simple sugars + keep carbs to minimum
S/S hypoglycemia due to lack of energy source in cells
- weakness
- fatigue
- mental fogginess
- apathy
- confusion
S/S hypoglycemia due to effects of counterregulatory hormones
- shakiness
- irritability
- sweating
counterregulatory hormones include? what are their fxns?
- glucagon, cortisol, GH, epinephrine
- let you know you need to ear
- stimulates glycogenolysis + gluconeogenesis to yield glucose
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
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
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
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
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
