F Endocrine Flashcards
What does the endocrine system do?
When is system complete
Control and regulate metabolic processes
Endocrine system complete and present at birth:
-complete hormonal control LACKING
-cannot effectively balance fluid concentration, electrolytes, amino acids, glucose
Endocrine structures
Thyroid
Parathyroid
Adrenal
Pancreas
Thyroid: hormone helps regulate metabolism and growth
Parathyroid: regulates calcium/phosphorus
Adrenal: releases aldosterone, epi & norepi
Pancreas: release of insulin and glucagon
Endocrine structures:
Hypothalamus
Pituitary gland (anterior and posterior)
Ovaries
Testes
Hypothalamus: stimulates pituitary gland
Pituitary gland:
-anterior: GH, TSH, FSH, LH, prolactin
-posterior: ADH, Oxytocin
Ovaries: release estrogen and progesterone
Testes: release testosterone
Disorders of the pituitary:
Anterior vs posterior
Anterior:
-GH deficiency
-precocious puberty
Posterior:
DI (diabetes insipidus)
SIADH (syndrome of inappropriate antidiuretic hormone)
Posterior pituitary: FOR ATI NOT EXAM
DI vs SIADH
DI:
-increased UOP), Na, thirst
-low specific gravity
SIADH:
-decreased UOP, Na
-high specific gravity
-fluid overloaded,
Hypopituitarism:
GH deficiency
AKA
What is it
Dwarfism
Failure of anterior pituitary OR hypothalamic stimulation to produce sufficient GH
Hypopituitarism:
GH deficiency
Causes
Causes:
-idiopathic
-tumors of the pituitary
-chemo/radiation
-head/brain trauma
-infection
Hypopituitarism:
GH deficiency
Diagnostics
IGF-1, IGFBP-3 (serum)
GH stimulation test (serum)
Xray (to determine skeletal maturity)
CT
Hypopituitarism:
GH deficiency
S/s
-normal birth wt and length (at birth)
-within a few years less than 3rd percentile
-higher wt to ht ratio
-prominent sub-Q deposits of abdominal fat
-decreased muscle mass
Delayed: dentition, sexual/skeletal maturation
Hypopituitarism:
GH deficiency
Tx
Biosynthetic GH: (subQ injections daily)
-can grow 3-5in in 1st year, regular ht measurements
Tx stops when epiphyseal growth plate fuses and/or child grows less than 1 inch per year:
Girls: 13-15y/o
Boys: 15-17 y/o
Precocious puberty
What is it
More common in who
Other causes
Defined as sexual development before:
Girls: 8 y/o
Boys: 9y/o
-Premature activition of the hypothalamic pituitary axis
-Gonadotropin releasing hormone (GnRH) stimulates LH, FSH
(More common in females)
Other causes:
-External sources of hormones
-Tumors of: ovary, testes, adrenal gland, pituitary
Precocious puberty
S/s
Accelerated growth
Isolated sexual development signs:
-breast development, menarche (menses)
-facial hair: boys
-pubic hair
Precocious puberty
Diagnosis
Xray (show advanced bone age)
GnRH given to evaluate stimulation of hormone
LH, FSH, testosterone, estradiol
Precocious puberty
Tx
GnRH analog/antagonist:
-SQ injection daily
-growth rate slows and sexual characteristics stabilize or regress
(Talk to them like their age not their growth)
Thyroid hormone regulates what
2 types of hormones
Regulates the basal metabolic rate (BMR)
Thyroid hormones (T3,T4)
Calcitonin
Hypothyroidism
Congenital
Acquired
Congenital:
-congenital hypoplastic thyroid gland
-failure of thyroid gland to migrate
-asymptomatic for 1st month
Acquired:
-partial or complete thyroidectomy for cancer or thyrotoxicosis following irradiation for Hodgkin disease or other malignant disease
RARELY occurs from dietary iodine insufficiency in the US
Congenital hypothyroidism:
S/s
EVERYTHING IS SLOW
(Hallmark): protruding tongue
Hypotonia (low tone in muscles/loosey goosey)
Lethargy, poor feeding
Constipation, abdominal distention
Coarse, dry hair/skin
Congenital hypothyroidism
Diagnosis
Tx
WONT KNOW BEFORE THE BABIES DISCHARGED
Diagnosis:
-newborn screen (thyroxine)
-T3,T4 (decreased)
-TSH (increased) (trying to stimulate T3/T4)
Tx:
Levothyroxine (synthroid)
-dose ⬆️ with age
Diabetes mellitus (DM)
Peak incidence when
Types
Peaks incidence is in early adolescence (10-15 y/o)
Type 1 vs 2
Type 1 DM
What is it characterized by
Destruction of beta cells, leading to an absolute insulin deficiency
Typically onset in childhood or adolescence
Type 1 DM
Cause believed to be
Autoimmune disease, arising when a person with a genetic predispostion is exposed to a event such as viral infection
Pathophysiology of insulin dependent diabetes
(type 1)
What body does
Lack of what causes what
Whats the concentration in bloodstream
Body destroyes cells in pancreas that produce insulin
A lack of insulin leads to a state of starvation (for cell)
Glucose cant get into cell leading to increased concentration in blood stream
Pathophysiology of insulin dependent diabetes
(type 1)
Absence of glucose body will do what leading to what
Body chooses an alternate source of energy: fat/protein
Fats break down into fatty acids which are converted to ketones
Ketones lower the blood ph and causes ketoacidosis
Pathophysiology of insulin dependent diabetes
(type 1)
Respiratory system does what
If diabetes isnt treated not treated with what can lead to what
Resp system attempts to compensate for the acidosis (ketones) by blowing off CO2 with (kussmaul resp)
If diabetes isnt treated with insulin, fluid/electrolyte correction can lead to:
-DKA, Coma, Death
Clinical manifestations of the child with diabetes
Blood sugars youll see
Wt loss (breaking down protein/fats)
3 P’s (polyuria, polyphagia, polydipsia)
Fatigue, lethary, irritability
Sores slow to heal
Glucose in the urine
Fasting blood sugar: >126
or
random blood sugar >200
Hemoglobin A1C for children
Less than 8
Insulin therapy 5
-Monitor sugar
-Rotate sites
-SQ tissue injection
-Do not pre-mix any insulin unless advised
(We use pens)
-Timing of injections (want food infront of them, it acts fast)
Insulin injection teaching for children
Need food with injection (acts quick)
Can give own injections w/ supervision
Want to teach have to deal with it rest of their life
Standard injection therapy : insulin
Long acting vs bolus
Lang acting insulin (lantus) administered daily
Bolus of rapid acting insulin with each meal and snack based on CHO grams eaten and blood glucose
Basal-bolus therapy (pump): insulin
Continuous subcutaneous insulin infusion(basal)
-bolus given for carbs, spikes in BG
Diabetic diet
Meals
Counting carbs
Free items
Do not skip meals
Avoid high fat/sugar (CHO) foods
Count grams of carbs (15g CHO= 1 unit insulin)
Free items:
-5 or fewer g of CHO
-limited to 3 free items/day
Free item for diabetics examples
Sugar free jello
Popsicles
Dill pickles
Blueberry
Strawberries
IDDM: sick day management
What is happening
More frequent what
What to do
More swings in BG when sick
More frequent monitoring of blood glucose and ketones (q3h)
Continue take insulin
Push sugar free fluids
IDDM: sick day management
When to call provider
(Signs of DKA):
Blood glucose >240
Positive ketones in urine
Confusion, irritability
Vomiting, unable to tolerate liquids
Rapid breathing, fruity breath (kussmauls resp)
Balancing act with diabetes
Insulin/meds
Food
Activities (sports, need snakcs/extra insulin/sugar free drinks)
Hypoglycemia
Definition
S/s
Less than 70mg/dl
S/s:
Irritability
Shaky
Pallor
Sweating
Hunger
HA
Dizziness
Vision disturbances
Hypoglycemia causes
Too much insulin
Not enough food
Too much exercise
Illness, stress
Hypoglycemia tx
If blood sugar <70 or symptomatic (conscious)
Recheck when
-15 grams of simple CHO
-1/2 cup of OJ or glucose tab/gel
-Follow with more complex carbs (peanut butter and crackers)
Recheck BG in 15 mins
Hypoglycemia tx
If unconscious or unable to swallow
Administer IM glucagon
Notify provider
May give D50 IV if needed
Hyperglycemia s/s
Lethargy, confusion
Abdominal pain
N/V
Thirst (3 P’s)
Rapid breathing, fruity breath
DKA/shock
Hyperglycemia tx
Water/iv fluids
Insulin drip
Activity(?)
DKA
Characterized by
Hyperglycemia >330
Glycosuria
Acidosis:
-pH 7.3
-HCO3 15
DKA causes
Insufficient insulin
Acute stress
Poor management of acute illness
DKA how it works
Glucose unavailable for cell = >
body breaks down alternatives for energy = >
ketones released = >
eliminated thru urine (ketourian) or lungs (acetone breath)=>
Acidosis/coma/death
Long term complications of diabetes
Micro vs macrovascular disease
Microvascular disease:
-nephropathy
-retinopathy
-neuropathy
Macro:
-peripheral vascular
-atherosclerosis
Type 2 diabetes
Incidences?
Presentation?
Associated with?
Increased incidences in childhood d/t obesity
Often no s/s
Associated with:
-Obesity
-Sedentary lifestyle
-Family history
Type 2 DM
Arises how
D/t
Onset?
Insulin?
Education
Arises bc of insulin resistance (not depletion)
Poor diet/exercise
Onset: usually after 45y/o
May or may not need insulin
Important to explain it can be managed and come off meds/insulin vs type 1 is forever
Type 2 DM
S/s: early? Others
Early stage often has no symptoms
Feeling tired
Dry/itchy skin
Frequent infections
Blurred vision
Slow healing cuts/sores
3Ps (polyuria, polydipsia, polyphagia)
Frequent yeast infection (eating all sugars)
Numbness or tingling in hands/feet
