Unit 12 Flashcards
hormone mechanisms can be amplified and spread throughout the cell by
second messengers
diverse structure of hormones
amines and amino acids
peptides
proteins
steroids
fatty acid
different hormones have different
half lives
what are the different ways a hormone can be destroyed
enzymes, by the cell, by the liver
2 types of hormone receptor interactions
surface (second messenger) and intracellular interactions
examples of surface hormone receptor interactions
cAMP, glucagon, insulin, epinephrine, pth, TSH, ACTH, FSH, LH, ADH
up regulation
cells make more receptors
down regulation
cells make fewer receptors
response of a hormone depends on the receptor number and
affinity
your patient has low levels of circulating thyroid hormone. how will the cells of the thyroid gland respond
up regulation
aniterior pituitary
gland
posterior pituitary
neural
hypothalamus detects the state of the bodys
temp
blood osmolarity
blood nutrients
blood hormones
inflammatory mediatiors
emotions
pain
T/F: the pituitary gland controls the release of thyroid hormone
T
the pituitary gland tells other organs/glands to produce and secrete or inhibit the appropriate hormones. Where does the pituitary glad receive the cue to act from
hypothalamus
hypofunction
underproduction
causes of hypofunction
decline with aging
atrophy
congenital defects
disruption in blood flow
infection
inflammation
autoimmune responses
neoplastic growth
receptor defects
hyperfunction
excessive hormone production
causes of hyperfunction
excessive stimulation and hyperplasia of the endocrine gland
hormone producing tumor of the gland (PARENOPLASTIC)
primary disorders
originate in the target gland
secondary disorders
target gland is normal but its function is altered by defective levels of stimulating hormones or releasing factors from the pituitary system
tertiary disorders
result from hypothalamic dysfunction
both pituitary and target organ are under stimulated
T4 is inactive until converted into __ in tissues
T3
both thyroid hormones exert a
negative feedback
thyroid hormone increases metabolism and ________ synthesis
protein
if there is thyroid deficit in infancy this may cause
mental retardation
thyroid has strong interactions with
SNS and ANS
if you suspect you might have a thyroid issue what is the first test that would be done
blood sample
HYPOthyroid BMR is
decreased
HYPOthyroid will have ___________ sensitivity to catecholamines
decreased
HYPOthyroid will have ______________ features
myxedematous
HYPOthyroid will make people feel
sluggish
HYPOthyroid ____________ CO
decrease
HYPOthyroid _______cardia
brady
HYPOthyroid will have ________ with their bowel movements
constipation
HYPOthyroid will have ______ventilation
hypo
HYPOthyroid will be _____ intolerant
cold
HYPOthyroid will have weight
gain
HYPOthyroid will have coarse ____ skin and hair
dry
HYPOthyroid will have ________ muscle tone
decreased
HYPERthyroid will have BMR
increased
HYPERthyroid will have ________ sensitivity to catecholamines
increased
HYPERthyroid will appear with exophthalmus which is what
bulging eyes that look like a pug
HYPERthyroid will make the patient feel
restlessness, irritability, anxiety
HYPERthyroid will have _________ CO
increased
HYPERthyroid will have _______cardia
tachy
HYPERthyroid will have what kind of bowel movements
diarrhea
HYPERthyroid will have what kind of breathing
dyspena
HYPERthyroid will be _______ intolerant
heat
HYPERthyroid will have weight ________
loss
HYPERthyroid will have thin and ______ hair and skin
silky
HYPERthyroid will also have the patient
tremor and twitching
if there is a lack of iodine the T3 and T4 will
not be made
the lack of iodine will cause no negative feedback there for
TRH and TSH will continue to be made
when there is a lack of iodine the patient may present with a
goiter
you need what to make T3 and T4
iodine
hypothyroidism can be
congenital or acquired
an example of acquired hypothyroidism besides the thyroidectomy is
Hashimoto thyroiditis
Hashimoto thyroiditis is
autoimmune
2 types of hyperthyroidism
graves and thyroid tumors
graves is
hyperthyroidism
a person with graves disease may physically present how?
with wasting, goiter, opthalmopathy (esothalamus)
graves disease is most common in
women
graves is an
autoimmune disorder
graves disease will have an abnormal stimulation of thyroid gland by
thyroid stimulating antibodies
in graves disease exophthalmos results when
antibodies interact with antigens found in fibroblasts in orbital tissue behind the eyeball
thyroid storm is a life threating form of
thyrotoxicosis
thyroid storm can be causes by
stress, infection, DKA, trauma
thyroid storm is manifested by
very high fever, tachycardia, CHF, angina and exaggeration CNS symptoms
can you treat thyroid storms with out urgency
NO must treat with urgency, life threatening
T/F: goiters are always associated with increased production of thyroid hormone
F, can occur with hypo, hyper and euthyroid
euthyroid is
when the thyroid is functioning normally
adrenal medulla secretes
epi and norepi
the adrenal cortex is responsible for
life essential hormones
cortex secretes
glucocorticoids, mineralocoricoids, adrenal sex hormones
mineralocoricoid example
aldosterone
mineralocoricoid function in balance of what 3 things
sodium, potassium, water
adrenal sex hormones example
androgens
glucocorticoids example
cortisol
glucocorticoids are essential for survival in
stress
glucocorticoids regulates metabolic functions of body and controlling
inflammatory resposne
actions of cortisol
plasma proteins increased, immune/inflammatory systems suppressed, muscle breakdown, free fatty acids increased, SNS response increased, blood glucose increased
cortisol release can be impacted when
there is a disease, stress or use of pretinzones
glucocorticoids diurnal variation peak in
early morning
glucose metabolism stimulates __________ and __________ glucose use which causes ________ in glucose
gluconeogenesis, decreased, increase
many people do not like to take glucocorticoids because of
psychological effect
long term therapy with pharmacolgoic preparations of the adrenal cortical hormone may casue
adrenal insufficiency on withdrawl
when on glucocorticoids for extended periods of time the adrenals
atrophy
if you have been talking glucocorticoids for extended periods of time and stop abruptly will you or will you not have any adrenal function
you will not, recovery might take 12 months
a primary diease of adrenal insufficiency is
Addisons disease
Addisons disease is caused by
destruction of gland
Addisons disease is
rare autoimmune
Addisons disease does not manifest until ___% is destroyed
90
adrenal insufficiency secondary results from a disorder of
HPA system
glucocorticoid hormone excess
cushings syndrome
cushings syndrome can be caused by
parenoplastic tumor, long term therapy
cushings syndrome apperances
buffalo hump, moon face, protruding abdomen, purple striae, muscle wasting, osteoporosis, 20% become DM, hypokalemia, hypertension, inhibited immune response
HPA system is the
target of steriods
Addisons disease will present with
bronzy tan hyperpigmentation, hypoglycemia, loss of weight, hypotension, adrenal atrophy, urinary losses, retention of potassium
types of cushings syndrome
Cushing diease, ectopic cushings syndrome, iatrogenic Cushing syndrome
Diabetes Mellitus is a disorder of ______, ______, and _____ metabolism resulting from a lack of insulin availability or a reduction in the biological effects of insulin
carb, protein, fat
what is the new tool to diagnose DM earlier
A1C
normal A1C is
4-6%
type 2 diabetes mainly affects
white people non hispanic
why would someone have a higher risk for type 2 diabetes
overweight/obesity, 45 and older, first gen relative with type 2 diabetes, physically active less than 3 times a week, had gestational diabetes, gave birth to a big baby, or certain race
alpha cells released
glucagon
beta cells release
insulin and amylin
glucagon
causes cells to release stored food into the blood
insulin
allows cells to take up glucose from the blood
ways to test for DM
fasting plasma glucose test
random glucose test
oral glucose tolerance test
capillary whole blood glucose monitoring
hemoglobin A1C
increased blood glucose causes
insulin secretion
insulin stimulates uptake, use, and storage of
glucose
glucose to glycogen
glycogenesis
glucose to fat
lipogenesis
insulin inhibits
glycogen breakdown
fat breakdown
protein breakdown
glycogen breakdown
glycogenolysis
fat breakdown
lipolysis
protein breakdown into glucose
gluconeogenesis
if someone lacks insulin what happens to their blood glucose levels
increase
if someone lacks insulin what happens to their blood pH
decreases, become acidosis
liver regulates blood glucose through 3 processes
glycogenesis, glycogenolysis, gluconeogenesis
synthesis of glucose from non carb souces
gluconeogenesis
glucose levels rise
removed form blood and converted to glycogen
glucose levels fall
liver glycogen stores broken down and release into circulation
liver only uses a small amount of fatty acids for its own energy needs; converts the retainer into
ketones and is released into the blood
ketones
organic acids that cause ketoacidosis when they are present in excessive ammounts
when someone has severe metabolic acidosis you will have an increase in __ ____ into the cell which causes __ to leave the cell
H ion, K+
K+ is the main ____________ ion
INTRACELLULAR
ketoacidosis causes an increase in K+ how do you fix this
fix the acidosis and the K+ will fix it self
insulin lowers glucose by
facilitating movement of glucose into body tissues
actions of insulin include
promotes glucose uptake by target cells, glucose breakdown, inhibits gluconeogenesis, increases protein synthesis
decreased blood glucose leads to
glucagon secretion
glucagon stimulates release of glucose into
blood
glycogen into glucose
glycogenolysis
fat into fatty acids for energy
lipolysis
amino acids into glucose
gluconeogenesis
glucagon maintains blood glucose by increasing the release of
glucose from the liver into the blood
glucocorticoids stimulate ______________ 6-10 fold increase
gluconeogenesis
type 1A
autoimmune destruction of pancreatic beta cells
type 1B
idiopathic diabetes
type 2
beta cell dysfunction and insulin resistance, increased hepatic production of glucose
T/F: DM 2 is more common than DM 1
true
in type 1 diabetes with the absence of insulin
free fatty acids are released from fat cells and converted to ketoacids in the liver
what type is more prone to DKA
type 1
all type 1A are
insulin dependent
if there is better A1C there will be
less complications
type 2 metabolic abnormalities leading to
peripheral insulin resistance, deranged beta cell secretion of insulin, increased hepatic glucose production
metabolic syndrome is ______ resistant
insulin
metabolic syndrome includes ________ obesity
central
metabolic syndrome people have ____________ which is increased triglycerides, low HDL
dyslipidemia
metabolic syndrome have hyper ot hypo tension
hyper
metabolic syndrome do or do not have atherloslcerosis
do
metabolic syndrome has acanthuses nigricans which are
dark skin folds
metabolic syndrome have what kind of inflammation
systemic chronic inflammation
is gestational diabetes a small or large percent
small 5-10%
how can we diagnose gestational diabetes
fasting plasma glucose >126 or random >200
up to 60% of women with GDM will develop
type 2 diabetes after delivery
a child that was born from a mom with GDM will
have an increase risk of developing type 2
manifestations of type 1 are slow or rapid
rapid
are manifestations of type 1 specific or nonspecific
very specific
manifestations of type 2 are slow or rapid
slow
manifestations of type 2 specific or nonspecific
nonspecific
three polys that present with DM
polyuria, polydipsia, polyphagia
glucose is a _______, osmotically active molecule
small
high blood glucose levels exceeds amount that can be reabsorbs by _______ (aka renal threshold)
kidney
the glucose exceeds renal threshold this causes
glycosuria and large water losses in urine
intracellular dehydration causes
thirst
cellular depletion of carbs, fats and proteins causes
hunger
type 2 may present with
blurred vision, fatigue, paresthesias, skin infections
polyuria is caused in DM because
glucose levels exceeds renal threshold
polydipsia is caused in DM because
because urinating so much
polyphagia is caused in DM because
glucose is not in the cell where it should be
why can we not give insulin via mouth
it is destroyed in the GI tract
DKA causes include
infection, inadequate use of insulin, pregnancy, stress
DKA is a
metabolic acidosis
DKA will present with deep breathing because of
compensation to the metabolic acidosis
when a patient with DKA is breathing deep and hard what is this called
kussmaul breathing
when blood pH decreases this causes decreased nerve firing which can lead to
confusion and coma
when a patient has large amounts of ketones in their blood some patients are able to tell because of
acetone/fruity smell on breath
if a patient is in DKA why would they be breathing heavy
R ALK
if a patient is in DKA why would they be urinating so much
glucose has exceeded renal threshold
if a patient is in DKA why would they be dehydrated
because they are losing fluid because of increased amounts of urination
you find a man collapsed on the sidewalk and he is wearing a diabetic alert bracelet and has an insulin syringe in his brief case.
What happened?
Does he need insulin?
Why?
Hyper/hypo?
it happened suddenly so it is hypoglycemia. He does not need insulin he needs glucose/glucagon
is DKA a slow or fast onset
slow
DKA will have _________ tenderness
abdominal
in DKA can or cannot patients tell if they are going through DKA
they can with an odor on their breath
how will patients in DKA present BP and respiration wise?
hypotension and kussmaul breathing
does hypoglycemia have slow or rapid onset
rapid
when in hypoglycemia they will have altered _______ function and could lead to _____ and ________
cerebral, coma, seizures
hypoglycemia will first have PNS which will present as
hunger
in hypoglycemia after PNS is active then SNS will become active and present as
anxiety, tachycardia, sweating, skin cool/clammy
in an elderly patient in hypoglycemia they may only present with ____ changes
CNS
does a patient with HHS have a pH change
no
HHS is characterized by hyperglycemia of
> 600
HHS may mimic a
stroke
HHS presents with (besides glucose count)
hyperosmolarity, dehydration, absence of ketoacidosis, depression of DNS
DKA is normally in type
1
HHS is normally in type
2
somogyi effect
insulin induced hypoglycemia caused by a compensatory increase in catecholamines, glucagon, cortisol, and growth hormone which lead to hyperglycemia
dawn phenomenom
hyperglycemia between 5A-9A with out following hypoglycemia
if a patient who has known DM (don’t know what type) and their pH is 7.1
DKA or HHS
DKA
if a patient who has known DM (don’t know what type) and their pH is 7.4
DKA or HHS
HHS
if a patient who has known DM and their pH is 6.9, what type do they have
type 1 (DKA)
if a patient who has known DM and their pH is 7.39 what type do they have
type 2 (HHS)
nerve cells produce _________ ______ to keep their osmolarity balanced with the blood
intracellular osmoles
DM can lead to chronic complications
diabetic neuropathies, nephropathies, retinopathies
nephropathies can lead to
end stage renal diease
retinopathies are the leading cause of acquired
blindness
diabetic foot ulcers
impaired pain sensation contributes, risk of amputation if ulcers are not treated
somatic neuropathies
diminished perception of vibration, pain and temp
autonomic neuropathy
impaired motility of the gastrointestinal tract- gastroparesis
