F Endocrine Flashcards

1
Q

What does the endocrine system do?

When is system complete

A

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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2
Q

Endocrine structures

Thyroid
Parathyroid
Adrenal
Pancreas

A

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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3
Q

Endocrine structures:

Hypothalamus
Pituitary gland (anterior and posterior)
Ovaries
Testes

A

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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4
Q

Disorders of the pituitary:

Anterior vs posterior

A

Anterior:
-GH deficiency
-precocious puberty

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

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5
Q

Posterior pituitary: FOR ATI NOT EXAM

DI vs SIADH

A

DI:
-increased UOP), Na, thirst
-low specific gravity

SIADH:
-decreased UOP, Na
-high specific gravity
-fluid overloaded,

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6
Q

Hypopituitarism:
GH deficiency

AKA
What is it

A

Dwarfism

Failure of anterior pituitary OR hypothalamic stimulation to produce sufficient GH

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7
Q

Hypopituitarism:
GH deficiency

Causes

A

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

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8
Q

Hypopituitarism:
GH deficiency

Diagnostics

A

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

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9
Q

Hypopituitarism:
GH deficiency

S/s

A

-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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10
Q

Hypopituitarism:
GH deficiency

Tx

A

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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11
Q

Precocious puberty

What is it
More common in who
Other causes

A

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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12
Q

Precocious puberty

S/s

A

Accelerated growth

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

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13
Q

Precocious puberty

Diagnosis

A

Xray (show advanced bone age)

GnRH given to evaluate stimulation of hormone

LH, FSH, testosterone, estradiol

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14
Q

Precocious puberty

Tx

A

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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15
Q

Thyroid hormone regulates what

2 types of hormones

A

Regulates the basal metabolic rate (BMR)

Thyroid hormones (T3,T4)
Calcitonin

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16
Q

Hypothyroidism

Congenital
Acquired

A

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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17
Q

Congenital hypothyroidism:

S/s

A

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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18
Q

Congenital hypothyroidism

Diagnosis

Tx

A

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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19
Q

Diabetes mellitus (DM)

Peak incidence when

Types

A

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

Type 1 vs 2

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20
Q

Type 1 DM

What is it characterized by

A

Destruction of beta cells, leading to an absolute insulin deficiency

Typically onset in childhood or adolescence

21
Q

Type 1 DM

Cause believed to be

A

Autoimmune disease, arising when a person with a genetic predispostion is exposed to a event such as viral infection

22
Q

Pathophysiology of insulin dependent diabetes
(type 1)

What body does
Lack of what causes what
Whats the concentration in bloodstream

A

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

23
Q

Pathophysiology of insulin dependent diabetes
(type 1)

Absence of glucose body will do what leading to what

A

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

24
Q

Pathophysiology of insulin dependent diabetes
(type 1)

Respiratory system does what

If diabetes isnt treated not treated with what can lead to what

A

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

25
Q

Clinical manifestations of the child with diabetes
Blood sugars youll see

A

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

26
Q

Hemoglobin A1C for children

A

Less than 8

27
Q

Insulin therapy 5

A

-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)

28
Q

Insulin injection teaching for children

A

Need food with injection (acts quick)

Can give own injections w/ supervision

Want to teach have to deal with it rest of their life

29
Q

Standard injection therapy : insulin

Long acting vs bolus

A

Lang acting insulin (lantus) administered daily

Bolus of rapid acting insulin with each meal and snack based on CHO grams eaten and blood glucose

30
Q

Basal-bolus therapy (pump): insulin

A

Continuous subcutaneous insulin infusion(basal)
-bolus given for carbs, spikes in BG

31
Q

Diabetic diet

Meals
Counting carbs
Free items

A

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

32
Q

Free item for diabetics examples

A

Sugar free jello
Popsicles
Dill pickles
Blueberry
Strawberries

33
Q

IDDM: sick day management

What is happening
More frequent what
What to do

A

More swings in BG when sick

More frequent monitoring of blood glucose and ketones (q3h)

Continue take insulin
Push sugar free fluids

34
Q

IDDM: sick day management

When to call provider

A

(Signs of DKA):

Blood glucose >240
Positive ketones in urine
Confusion, irritability
Vomiting, unable to tolerate liquids
Rapid breathing, fruity breath (kussmauls resp)

35
Q

Balancing act with diabetes

A

Insulin/meds

Food

Activities (sports, need snakcs/extra insulin/sugar free drinks)

36
Q

Hypoglycemia

Definition
S/s

A

Less than 70mg/dl

S/s:
Irritability
Shaky
Pallor
Sweating
Hunger
HA
Dizziness
Vision disturbances

37
Q

Hypoglycemia causes

A

Too much insulin
Not enough food
Too much exercise
Illness, stress

38
Q

Hypoglycemia tx

If blood sugar <70 or symptomatic (conscious)
Recheck when

A

-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

39
Q

Hypoglycemia tx

If unconscious or unable to swallow

A

Administer IM glucagon
Notify provider
May give D50 IV if needed

40
Q

Hyperglycemia s/s

A

Lethargy, confusion
Abdominal pain
N/V
Thirst (3 P’s)
Rapid breathing, fruity breath
DKA/shock

41
Q

Hyperglycemia tx

A

Water/iv fluids

Insulin drip

Activity(?)

42
Q

DKA
Characterized by

A

Hyperglycemia >330

Glycosuria

Acidosis:
-pH 7.3
-HCO3 15

43
Q

DKA causes

A

Insufficient insulin

Acute stress

Poor management of acute illness

44
Q

DKA how it works

A

Glucose unavailable for cell = >

body breaks down alternatives for energy = >
ketones released = >

eliminated thru urine (ketourian) or lungs (acetone breath)=>

Acidosis/coma/death

45
Q

Long term complications of diabetes

Micro vs macrovascular disease

A

Microvascular disease:
-nephropathy
-retinopathy
-neuropathy

Macro:
-peripheral vascular
-atherosclerosis

46
Q

Type 2 diabetes

Incidences?
Presentation?
Associated with?

A

Increased incidences in childhood d/t obesity

Often no s/s

Associated with:
-Obesity
-Sedentary lifestyle
-Family history

47
Q

Type 2 DM

Arises how
D/t
Onset?
Insulin?
Education

A

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

48
Q

Type 2 DM

S/s: early? Others

A

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