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66 Cards in this Set

  • Front
  • Back
Hypothalamus
the master gland
Pituitary gland and Hypothalamus
govern all bodily functions using hormones and negative feedback loops
Anterior Pituitary Hormones (6)
growth hormone, thyroid-stimulating hormone, luteinizing hormone, follicle-stimulating hormone, prolactin, adrenocorticotropic hormone
Posterior Pituitary Hormones (2)
oxytoxin and antidiuretic hormone
Anterior Pituitary Drugs
Somatotropin-mimics GH
Octtreotide-antagonizes GH
Cosyntropin- mimics ACTH
Posterior Pituitary Drugs
Vasopressin, desmopressin-mimics ADH; increases absorption of Na + H2O
Pituitary drugs: indications
replacement therapy
Drug therapy to produce a specific hormone response (in hormone deficiency)
-diagnostic aid (to determine hypo/hyperfuntion)
Somatotropin can increase what?
growth in children
Vasopressin or desmopressin should reduce what?
severe thrist and urinary output
Thyroid Gland: 3 Hormones
Thyroxine (T4)-we have more of this
Triiodothyronine (T3)-more potent
Calcitonin
**ALL NEEDS IODINE TO BE PRODUCED
4 Function of Thyroid Hormones
-regulate lipid and carb metabolism
-for normal G&D
-thermoregulation
-effects on cardiovascular, endocrine, neuromuscular syst.
Hypothyroidism
20% in females over 50
Can be either:
Deficiency in THs-abnormality in the gland itself
Autoimmune- is the most common
Hashimoto thyroiditis
high TSH, low T4
Secondary Hypothyroidism
drug induced: Amiodarone (from high iodine content) and lithium
Transient: postpartum period
gland dysfunction: does not secrete TSH needed to trigger THs
Hypothyroidism S&S
thickened skin, hair loss/brittle hair, constipation, anorexia, goiter, weight gain, depression, cold intolerance, lethargy
Levothyroxine
used for hypothyroidism
-decreases THs
-works the same way as thyroid hormones
-preferred agent because it is predictable and standardized
Levothyroxine: SE
-cardiac dysrhythmia, heat intolerance, hyperthyroid S&S, insomia
Levothyroxine: Implications
increased effect of oral anticoagulants
decreased effects of hypoglycemics
may take several months before therapeutic response
Hyperthyroidism
excess T3 and T4 and shuts off TSH
Hyperthyroidism: caused by
Graves' disease -autoimmune, body receptors mimic TSH increasing T3 and T4
Toxic nodular disease
Multinodular disease
Hyperthyroidism: S&S
goiter, diarrhea, exopthalmos, sleep disorder, flushing, increased appetite,tremor, fatigue, palpitations, nervousness, heat intolerance, warm moist skin, increased sweating
Tx of Hyperthyroidism
radioactive-destroys thyroid gland
surgery
antithyroid drugs- thioamide derivatives
ex: methimazole, propylthiouracil(FIRST LINE DRUG)
Antithyroid Agents: SE
may cause liver and bone marrow toxicity
Type I Diabetes
- lack of insulin production
- 10% of casess
- prone to ketoacidosis
Type II Diabetes: Causes
Beta Cell Dysfunction-- beta cells responsible for insulin production
Insulin Resistance- cells have diminished ability to respond to insulin
liver over produces glucose
impairs after meal (post-prandial) glucose metabolism for the response to insulin deficiency
____ is responsible for 80% of deaths for those with diabetes
CVD
Gestational diabetes
2-4% in pregnancies
dev. glucose intolerance
30% dev type II diabetes within 10-15 yrs.
Hyperglycemia
FBG > 6.1 [<5.6]
GTT (glucose tolerance test)-75 g glucose is prediabetic
Hypoglycemia
blood glucose < 2.8
2 types of antidiabetic agents
human insulin and oral antihyperglycemic agents
Insulin restores client's ability to: (3)
metabolize carbs, fats, proteins
store glucose in liver
convert glycogen to fat stores
Intensive therapy: Insulin: why use Basal-bolus regime?
to prevent onset and progression of microvascular complications
what is a basal-bolus regime?
first use a basal insulin= intermediate or LA insulin given bid/od + fast acting insulin bolus before meals
Human-based insulin: Rapid acting
Peak 60-90 min, 15 onset, shorter duration
ex. lispro (humalog), insulin aspart
Human-based Insulin: Short acting
Peak 2-4 hrs, 30-60 min onset, the ONLY insulin that can be given IV bolus, IV infusion, or IM
-uses sliding scale
ex: regular insulin (Humulin-R, novolinge-toronto)
Human-based Insulin: Intermediate acting
cloudy appearance, slow onset and long duration
ex: Isophane insulin suspension (NPH, Humulin-N), Insulin zinc suspension (Lente, humulin-L)
Human-based Insulin: Mixed
a combo of insulin (diff duration and onsets)
Lispro/aspart: onset and peak
onset 10-15 min, peak at 60-90 min
Human regular: onset and peak
onset 30-60 min, 2-4hrs
Human NPH/Lente: onset and peak
onset 1-3hrs, peak 5-8 hrs
Ultralente: onset and peak
onset 3-4 hrs, peak 8-15 hrs
Glargine: onset and peak
onset 90 min, peak (vary)
Sliding scale insulin dosing is adjusted according to...
sc regular insulin adjusted according to blood glucose test results
- sc regular insulin doses increases as blood glucose level increases
Oral antidiabetic agents: is it used for type I or II?
used for type II diabetes alone or in combo with injection
Oral antidiabetics: 5 Types
sulfonylureas
biguanides
alpha-glucosidase inhibitors
thiazolidinediones (TZDs)
DDP4-Inhibitors
Sulfonylureas ex:
gliclazide, glyburide
Sulfonylureas: mechanism
simulate insulin secreation from beta cells; beta cells must be in working condition
Improve sensitivity to insulin in tissue
prevent liver from braking down insulin
Biguanides ex:
metformin
Biguanides: 3 mechanisms
-decrease production of glucose by liver
-decrease intestinal absorption of glucose
-improves insulin receptor sensitivity in liver, adipose, muscle
**** DOES NOT CAUSE HYPOGLYCEMIA -because it does not increase insulin from pancreas
Biguanides: metformin drug rxn with
iodinated contrast
Alpha-glucosidase Inhibitors ex:
Acarbose (Prandase)
Alpha-glucosidase Inhibitors: considerations
taken with the first bite of each meals
-must be taken with meals to prevent postprandial blood glucose elevations
- causes bloating, abd pain
Acarbose: Mechanism
-reversibly inhibit alphaglucosidase that releases glucose from small intestine
-reduces rate of digestion of complex carbs delaying absorption of glucose
Thiazolidinediones (TZDs) ex:
pioglitazone(actos), rosiglitazones (avandia)
TZDs: mechanism
decrease insulin resistance
"glitazones"
"insulin sensitizing agents"
-increase glucose uptake and use in skeletal muscles
-inhibit glucose and triglyceride production in the liver
DDP4-Inhibitors ex:
Januvia, very new and improve PPG control, increase amt of incretin
Oral hypoglycemics is usually given ___min before meals
30 min
% of ppl with type II that are overweight or obese
80-90%
BMI Overweight
25-29.9
BMI obese class I
>= 30
BMI obese class II
30-34.9
BMI obese class III
>= 40
waist circum. of men and women should be
men < 102cm
women < 88cm
Healthy wt loss
5-10% of initial body wt loss
1-2kg/month
Anorexiants/antiobesity drugs
-drugs to reduce weight which is clinically important
-significant in reducing doses of hyperglycemic agents
ex: Orlistat, Sibutramine
Orlistat: mechanism
blocks absorption of fat from GI by 30%