patho exam 2 Flashcards
what is the function of thyroid hormones?
increases metabolism
increases protein synthesis
necessary or growth of children
disorders of the thyroid are among the _______ and affect how much of the US population?
they are among the most common endocrinopathies
they affect 4-5% of the population
what is the difference between the structure of T3 and T4?
a single atom of iodine
between T3 and T4, which is more active and which is released at a higher quantity?
T3 is more active
T4 is released in higher quantity
which (T3 or T4) is converted into the other?
T4 is converted into T3 once it reaches the target tissues
what does calcitonin do?
opposite action of parathyroid hormone
does NOT increase levels of calcium and phosphorus in blood
inhibits activity of osteoclasts and stops bone reabsorption
describe the structure of the thyroid gland
tiny saclike structures called follicles - func units
each follicle is formed by simply cuboidal epithelium
where are thyroid hormone made and stored?
they are made in the simple cuboidal cells of the thyroid and stored in the lumen attached to thyroglobulin
what are the 3 forms of thyroid hormones in the bloodstream?
bound to thyroxine-binding globulin
T4 binding prealbumin and albumin
free, unbound form - the active form
what enzyme converts T4 into T3?
5’-iodinase
what is a second form that T4 can be converted into?
reverse T3
a physiologically inactive form
actions of thyroid hormones in relation to GROWTH
growth formation
bone maturation
actions of thyroid hormones in relation to CNS
maturation of the CNS
actions of thyroid hormones in relation to BMR
increased Na-K ATPase
increased O2 consumption
increased heat production
increased BMR
actions of thyroid hormones in relation to METABOLISM
increased glucose absorption
increased glycogenolysis
increased gluconeogenesis
increased lipolysis
increased protein synthesis and degradation
actions of thyroid hormones in relation to CARDIOVASCULAR
increased cardiac output
define glycogenolysis
breakdown of glycogen to glucose
define gluconeogenesis
making of glucose from other products like amino acids or fats
what is goiter?
swelling of neck resulting from enlargement of the thyroid gland
what are the causes of goiter?
graves disease
TSH secreting tumor
iodine deficiency
what is hyperthyroidism?
tissues are exposed to high levels of circulating thyroid hormones
what are the causes of hyperthyroidism?
graves - most common
adenoma of thyroid
excessive production of TSH by pituitary adenoma
how many people does graves disease affect?
0.5-1% of population under 40
what is graves disease and its triggering factors?
state of hyperthyroidism, goiter, opthalmopathy
excessive stimulation of thy gland by IgG antibodies
triggering factors:
often unknown
genetic - history, gender
environmental - stress, smoking
clinical manifestations of Graves disease
goiter
excessive sympathetic system activity
increased respiratory rate
increased DTRs
exophthalmos - bulging eyes
sweating, heat intolerance
increased appetite
weight loss
frozen shoulder
calcific tendinitis of the wrist
what is a thyroid storm?
sudden, worsening of hyperthy
high fever
servere tachycardia
heart failure
irritability
what are the precipitating factors of thyroid storm?
trauma
infection
surgery
stress
diagnosis of graves
history
protrusion of eyes
TSH levels
elevated in serum T3/4
antithyroid antibodies
radioactive iodine uptake
cold spot vs hot spot
treatment of graves
reducing thyroid hormone levels
medication that blocks thyroid hormone reproduction
surgical removal of gland
PT considerations of hyperthyroidism
they are deconditioned
know S&S
be familiar with their treatments
some meds can make them fluctuate between hyper and hypo
monitor vitals during treatment
if thyroidectomy: watch for hypoPT signs
radioactive for 24 hrs after treatment
decreased bone density
PT interventions for hyperthyroidism
ultrasound: 15 min @ 25 W/cm2 @ .89 MHz
acetic acid iontophoresis - not proved to be effective
what is hypothyroidism?
deficient thyroid hormone
creates a generalized depression of body metabolism
describe congenital hypothyroidism
un utero hormones supplied by mother
if untreated after birth, intellectual disability
cretinism
describe acquired hypothyroidism
destruction of thy gland
impaired pit function
impaired hypothal function
iodine deficiency
autoimmunity that blocks TSH or TSH receptors - hashimoto thyroiditis
clinical manifestations of hypothyroidism
weakness and fatigue
weight gain, loss of appetite
cold intolerance
decreased GI motility
mental dullness
large tongue
peripheral edema
myxedema coma
delayed relaxation of DTR
bradycardia
hair loss
clinical manifestations of hypothyroidism when myxedema is involved
carboydrate complexes accumulate and draw water into the tissue
fluffy face
tongue enlarged
voice hoarse
slurred speech
carpal tunnel syndrome
what other syndrome do those with hypothyroidism commonly develop?
fibromyalgia syndrome
diagnosis of hypothyroidism
history
T4 levels decreases
TSH levels increased
treatment of hypothyroidism
life long replacement therapy
levothyroxine - synthetic form of T4
hypothyroidism and exercise
exercise for metabolism
positive effect on BMI
help lower BP
help improve QOL
combine aerobic and resistance training
pt education in hypothyroidism
lifelong
medication increased gradually
moisturize dry skin
compliance with meds
what is the function of the parathyroid gland?
regulate Ca+ in ECF
secrete when CA+ levels fall
acts on bone, kidneys and intestine to increase plasma CA+ back to normal
what are the different forms of calcium in the blood?
total - 10mg/dl
40% bound to plasma proteins
10% bound to anions like phosphate, citrate
50% free, ionized Ca+
protein bound cannot be filtered
relationship between calcium and albumin
albumin has neg charge sites which can bind to ca+ or h+
what is hypercalcemia
increase in plasma Ca+ concentration
causes constipation, polyuria, polydipsia, hyporeflexia
what is hypocalcemia
decreased in plasma Ca+
causes muscle cramps, twitching, tingling, numbness, hyperreflexia
3 hormones of calcium hemostasis
PTH
calcitonin
vitamin D
actions of parathyroid hormone
bone remodeling
bone reabsorption
inhibits phosphate reabsorption
stims Ca+ reabsorption
activates vitamin D
when is calcitonin released?
increased plasma calcium concentration
released by thyroid gland
what is the function of calcitonin?
inhibits osteoclastic bone resorption
decreases plasma calcium concentration
what is the function of vitamin D?
regulates Ca+ and phosphate metabolism
reabsorb calcium from GI tract
promote mineralization of new bone
how is vitamin D synthesized?
D3 is ingested in diet or synthesized from skin
which vitamin D is active?
1,25-(OH)2-cholecalciferol
what is the action of vitamin D?
increases plasma phosphate and ca+
promote mineralization of new bone
if kidney cannot produce active vit D what happens?
it will all be inactive no matter how much is supplemented
what is hyperparathyroidism?
over activity of one or more parathyroid glands
elevated PTH
affects women more
what are the manifestations of hyperparathyroidism?
bone damage
hypercalcemia
hypertension
hypercalciuria
hypergastrinemia
diminished DTRs
kidney damage
glove stocking sensory damage
stones, bones, groans, psychiatric overtones
diagnosis of hyperparathyroidism?
in the blood: increase PTH, hypercalcemia, hypophosphatemia
in urine: increased phosphate, increased ca+
treatment of hyperparathyroidism
surgical removal
drugs to lower serum calcium
education for home safety
what is hypoparathyroidism?
insuff secretion of PTH
causes low serum calcium levels and high serum phosphate levels
what are the acquired causes of hypoparathroidism?
accidental removal
inadequate blood supply leading to infarction
TB
trauma
autoimmune
what are the manifestations of hypoparathyroidism?
hypocalcemia
NM irritability
tetany
spasm
paraesthesia
cardiac arrhythmias
what is Chvostek’s sign?
hypopara
hyperirri facial nerve when tapped
what is trousseau sign?
carpal spasm when BP cuff inflated for over 3 min
clinical manifestations of hypoparathyroidism
CNS - irri, anxiety, agitation, depression, seizures
CVS - arrhy, heart failure
dry scaly pigmented skin
thin hair and brittle nails
skin infections
nausea, vomiting
hypocalcemia: increased DTRs
diag of hypoparathyroidism
low PTH, hypocalcemia, hyperphosphatemia
treatment of hypoparathyroidism
aucte:
life threatening
need IV calcium
treat convulsions
chronic:
pharmacological
foods high in calcium and low in phosphorous
what does the pancreas do?
endocrine gland: releasing hormones
exocrine gland: secreting digestive juices
what are pancreatic islets?
clusters of endocrine cells in pancreas
what are the 4 types of cells in the pancreas?
beta cells - secrete insulin
alpha cells - secrete glucagon
delta cells - secrete somatostatin
remaining secrete pancreatic peptide or other peptides
what is insulin?
synthesized by beta cells
hormone of abundance
ensures that nutrients are stored correctly
A chain - 21 amino acids, B chain - 30 amino acids
what is the order of synthesis of insulin?
proinsulin - A and B chains connected by connecting peptide
golgi apparatus cleaves out connecting peptide
insulin and c peptide are released in equal amounts
what chromosome directs the synthesis of insulin
11
where is glucose produced?
beta cells
GLUT2 transporter moves glucose from blood to cell
as calcium increases in beta cells, insulin goes out
what can c peptide help monitor?
as it is unchanged in urine, it can monitor endogenous beta cell function
basis of test for T1D
how does insulin effect nutrient levels?
decreases blood glucose levels
decreases blood fatty acids and ketone concentrations
decreases blood amino acid concentration
ensures ingested K+ will be taken into cells
what are the different actions of glucose?
increases glucose uptake in cells
increases glycogen formation
decreases glycogenolysis
decreases gluconeogenesis
increases protein synthesis
increases fat deposition
decreases lipolysis
increases K+ uptake into cells
what is glucagon?
it is synthesized and secreted by alpha cells
hormone of starvation
maintains blood glucose concentration in fasting state
what are the major actions of glucagon on the liver?
increases blood glucose concentration
- stimulates glycogenolysis
- inhibits glycogen formation from glucose
- increases gluconeogenesis
increases blood fatty acid and ketoacid concentration
- increases lipolysis
what is somatostatin?
secreted by delta cells of islet and hypothalamus
what is the action of somatostatin?
modulate or limit the response of insulin and glucagon to ingestion of food
inhibits the release of GH, TSH and prolactin
if you skipped breakfast and had really low blood glucose levels, which cells of islet would you expect the be stimulates?
alpha cells
what is diabetes mellitus?
increased blood glucose levels (hyperglycemia)
disruption of metabolism of carbohydrate, proteins, fats
what is the 7th leading cause of death in the US?
diabetes
glucose homeostasis
blood glucose rises, beta cells release insulin, body cells taken up more glucose and liver stores glucose as glycogen, blood glucose levels decline
blood glucose levels fall, alpha cells release glucagon, lever breaks down glycogen and releases glucose, blood glucose level rises
what are the two types of diabetes?
type 1 - insulin dependent diabetes mellitus
type 2 - no insulin dependent diabetes mellitus
in adults, what percentage of diabetes cases are T1D/T2D?
T1D- 5-10%
T2D - 90-95%
when does T1D commonly develop?
most common onset in childhood or adolescence
what is T1D?
autoimmune destruction of beta cells
progress can be slow or rapid
what is prediabetes?
early stages of immune destruction
antibodies against beta cells circulating, but not hyperglycemic yet
can last for years
when do sympotms of T1D manifest? (%)
80-90% of beta cell destruction
manifestations of T1D
sudden
blurred vision
fatigue
skin infection
polyuria
fatigue
weight loss
polyphagia
polydipsia
what is diabetic ketoacidosis?
metabolic derangement seen more in T1D
ketones detected in blood and urine
produce hydrogen ions - metabolic acidosis
protein catabolism
treatment of T1D: exogenous insulin types
rapid acting - onset 15 min, immediately before meal
short acting - 30 min, throughout day
intermediate acting - 2-4 hors, throughout day
long acting - 6-10 hrs, nighttime
other - 2-4 hrs, nighttime
normally one shorter acting and one longer acting
what are the ways someone can take insulin?
syringes
insulin pen
insulin pump
treatment of T1D
exogenous insulin
transplant of pancreatic islets
- at least 2-3 donors needed
diet
exercise
when does T2D onset?
late in life
associated with obesity and PI, genetic susceptibility
who is at high risk for T2D?
age greater or equal to 45 yrs old
hypertension
positive family history
HDL chol <35 mg/dl
triglycerides greater or equal to 250 mg/dl
obesity
sed lifestyle
cigarette smoking
pathophysiology of T2D
insulin is present but not used by tissues
beta cells gradually fail
normally diagnosed while being treated for something else
what is the diagnostic criteria for T2D?
random BG levels equal to or more than 200 mg/dl
fasting BG levels
2 hour glucose tolerance test
HbA1c-glycated Hb
what is the normal level for fasting blood glucose levels?
<100mg/dl
what is the prediabetes level for fasting blood glucose levels?
100-125 mg/dl
what is the diabetes level for fasting blood glucose levels?
greater to equal to 126 mg/dl
what is the normal level for HbA1c levels?
<5.7%
what is the prediabetes level for HbA1c levels?
5.7 - 6.4%
what is the diabetes level for HbA1c levels?
greater than or equal to 6.5%
what is the normal level for oral glucose tolerance test levels?
< 140 mg/dl
what is the prediabetes level for oral glucose tolerance test levels?
140-199 mg/dl
what is the diabetes level for oral glucose tolerance test levels?
greater than or equal to 200 mg/dl
diagnostic criteria for diabetes
FPG greater than or equal to 126 mg/dl
2-hr PG greater than or equal to 200 mg/dl in OGTT
A1C greater than or equal to 6.5%
random plasma plasma glucose greater or equal to 200mg/dl
laboratory tests for T2D
glucose present in urine
ketones present in urine
presence of antibodies against islet cells
manifestations of T2D
insidious
blurred vision
fatigue
skin infections
polyuria
fatigue
polydipsia
complications of long-term diabetes: leading cause of
blindness
chronic kidney disease
lower extremity amputations
all organs are effected
complications of long term diabetes
macrovascular:
atherosclerosis
reduced blood flow
gangrene
limb amputation
microvascular:
low blood flow
ESRD
foot ulcers
susceptible to infections
loss of sensation
weakness and atrophy
loss of control of blood pressure, temp, sweating
UTI
MSK problems associated with long term diabetes
dupuytren’s contracture
flexor tenosynovitis
trigger finger
carpal tunnel syndrome
adhesive capsulitis
tendinopathy with thickening of plantar fascia, achilles
osteoporosis
treatment of T2D
medications:
alpha-glucosidase inhibitors - slows carb digestion
biguanides (metformin) - prevents excess glucose release from liver
meglitinides - more secretion of insulin
sulfonylureas - more secretion of insulin
thiazlidinediones - increases sensitivity to tissues to insulin
diet
excerise
what are the extreme complications of hypoglycemia?
< 70 mg/dl
shakiness
pale skin color
cold clamy skin
dizziness
sweating
clumsy/jerky movements
hunger
seizure
headache
increased HR
coma - below 50 mg/dl
what are the extreme complications of hyperglycemia?
> 300 mg/dl with ketones
ketones with one or more of the following require ER
DKA: rate and depth of respiration increases
marked fatigue
nausea and vomiting
breath that smells fruity
a very dry mouth
what are the extreme BG levels where you do not do therapy?
< 70 mg/dl
>250 with ketones
what are the complications of diabetes treatment?
overdose of insulin
skipped meals
overexertion in exercise
excessive alcohol ingestion
change in meds
when does a person need to be hospitalized for hypoglycemia?
< 50 g/dl
how can a person become hypoglycemic?
overdose on insulin
skipped meals
overexertion in exercise
excessive alcohol ingestion
change in meds
what is the somogyi phenomenon?
increased fasting blood glucose levels during early morning that is triggered by preceding hypoglycemic event
cause:
large insulin doses
skipped meals
heavy exercise
what is the dawn phenomenon?
increased fasting blood glucose in the early morning not triggered by hypoglycemic event
more common
result of circadian variation in hormone secretion
what is gestational diabetes?
during pregnancy
usually temporary
insulin resistance and inability to create more insulin
risk of c section due to large baby
what percent of pregnancies develop gestational diabetes?
15%
diag in 5-6th month
treatment of gestational diabetes
diet
exercise
drugs/insulin
