F Endocrine Flashcards by Brendon Allen

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

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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

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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

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Disorders of the pituitary:

Anterior vs posterior

Anterior:
-GH deficiency
-precocious puberty

Posterior:
DI (diabetes insipidus)
SIADH (syndrome of inappropriate antidiuretic hormone)

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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,

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Hypopituitarism:
GH deficiency

AKA
What is it

Dwarfism

Failure of anterior pituitary OR hypothalamic stimulation to produce sufficient GH

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Hypopituitarism:
GH deficiency

Causes

Causes:
-idiopathic
-tumors of the pituitary
-chemo/radiation
-head/brain trauma
-infection

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Hypopituitarism:
GH deficiency

Diagnostics

IGF-1, IGFBP-3 (serum)
GH stimulation test (serum)
Xray (to determine skeletal maturity)
CT

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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

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Hypopituitarism:
GH deficiency

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

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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

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Precocious puberty

S/s

Accelerated growth

Isolated sexual development signs:
-breast development, menarche (menses)
-facial hair: boys
-pubic hair

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Precocious puberty

Diagnosis

Xray (show advanced bone age)

GnRH given to evaluate stimulation of hormone

LH, FSH, testosterone, estradiol

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Precocious puberty

GnRH analog/antagonist:

-SQ injection daily
-growth rate slows and sexual characteristics stabilize or regress

(Talk to them like their age not their growth)

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Thyroid hormone regulates what

2 types of hormones

Regulates the basal metabolic rate (BMR)

Thyroid hormones (T3,T4)
Calcitonin

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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

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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

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Congenital hypothyroidism

Diagnosis

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

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Diabetes mellitus (DM)

Peak incidence when

Types

Peaks incidence is in early adolescence (10-15 y/o)

Type 1 vs 2

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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