Flashcards in E2: Endocrine Pt 1: Thyroid & Diabetes Deck (76):
LACK of iodine in diet leads to excessive secretion of ____, resulting in thyroid hypertrophy aka a _______.
_______ hypo/hyperthyroidism = disease of THYROID gland
________ hypo/hyperthyroidism = disease of pituitary or HYPOTHALAMUS gland
WHAT is the precursor to making thyroid hormones T4 and T3??... T4 and T3 are IODINATED derivatives of this...
WITHOUT iodine, build-up of TH precursor, resulting in a ______
Syn and storing Thyroid hormone: Occurs as part of the synthesis of ________, a large glycoprotein....This form is NEVER secreted into the bloodstream
Getting T3 and T4 made! Lysosomes fuse with vesicles resulting in ________ of thyroglobulin and release of iodinated amino acids (T3 and T4).
YAY recycling! ____________ and ___________ undergo deiodination, allowing for recirculation of iodine
Diiodotyrosine and moniodotyrosine
What are the TWO synthetic thyroid preparations made by industry?
1.Sodium Levo-thy-rox-ine (T4=Synthroid/Levoxyl) 2.Sodium Lio-thy-RO-NINE (T3 = Cytomel) where the f did this name come from?
What is the PREFERRED DRUG for most cases of HYPOthyroidism?
Sodium Levo-thy-rox-ine (Synthroid, Levoxyl)
What is the most widely sold brand name for Sodium Levo-thyroxine?
Sodium levothyroxine (T4 = Synthroid)-Use: replacement or supplement therapy in __________
Sodium levothyroxine (T4 = Synthroid)-MECH: Affects DNA transcription and stimulates ________... Promotes ___________....Mobilizes ______ stores ****Increases __________!
protein synthesis... gluconeogenesis.... glycogen.....basal metabolic rate
What are 4 signs of overdose of Sodium Levothyroxine??? (hyperthyroid)
1.tachycardia/palpations 2.Nervousness/sweating 3.increased appetite 4.wight loss (WOMEN abuse this)
What do we use to treat HYPERthyroidism??? Lets start with the Canadian drug, eh? How does it work??
PTU (Put Thyroid Under) i mean PropylThioUracil...Blocks iodination reaction (blocks oxidation of iodine) in thyroid gland; blocks synthesis of T4 and T3
What are three side effects of Propylthiouracil?
Skin rash, nausea, aGRANuloCYtosis
Lets get broad: what are the 4 drugs for HYPERthyroidism?
1.PTU (PropylThioUracil) (Canadian) 2.Iodides 3. THE BIG ONE: METHimAZole (TapaZOLE) 4.Radioactive Iodide 131
What drug am I? Mechanism of action is not clear: probably reduces secretion of thyroid hormone Use: used in conjunction with propylthiouracil to prepare patients for surgery
What drug am I? Use: palliative treatment of hyperthyroidism, return the patient to a normal metabolic state prior to thyroidectomy; control thyrotoxic crisis that may accompany thyroidectomy
Gotta LOVE those Mechanisms!!! What drug AND fill in the BLANK: Blocks iodination reaction (blocks _______ of iodine) in thyroid gland; blocks iodine’s ability to combine with ______ to form T3 and T4
Why is METH-im-AZole SO UNDESIREABLE??? Undesirable drug: ________, inconvenient (requires monitoring; compliance), adverse effects (eg: ________ disorders, fever, rash, vasculitis, arthralgia)
WHEELHOUSE: What are the 2 ORAL side effects of good ole METH-im-AZole?
Oral side effects: taste alteration, salivary gland swelling
SOO cool! Radioactive Iodide Tx: _____ ray emission (15-30 millicuries) destroy thyroid tissue.. How lone does this take?
Beta ray emission (15-30 millicuries) destroy thyroid tissue..takes about 3 months
WHEELHOUSE: Dental Considerations for Hypothyroid Pts....They are usually cold and _____ and are more sensitive to _______ so give them a lower dose..
fatigue...CNS depressants=lower dose of sedatives, opiods
HOLY CRAP: which active condition is an ABSOLUTE CONTRAINDICATION TO EPINEPHRINE????
Unlike the hypothyroid pt, the hyperthyroid pt is _____ sensitive to CNS depressants so they require a ____ dose!
What are the two likely outcomes of giving a Hyperthyroid Pt epinephrine?
What is the most important/first intervention that a dental professional can do with a diabetes patient while they are in the chair?
tell them to test their blood sugar regularly!
Simple mech: Type 1 diabetes...Whats the CAUSE?
Beta cells are not producing insulin correctly...autoimmune destruction of pancreatic beta cells
Simple Mech: Type 2 diabetes
Insulin RECEPTORS become blocked/INSENSATIVE
What is the ONLY effective drug in the Tx of Type 1 Diabetes?
What % of diabetics are Type I?
10% and it significantly decreases life expectancy (10 years!)
Structure of Insulin : 2 chains connected via _________
Insulin stimulates ________ processes in muscle, liver and fat cells....Binds to ________ receptor to initiate signal propagation within the cell
What are the three ways Insulin is classified?
1.Onset 2.Peak 3.Duration of Action
What is the most popular Type 1 diabetes drug? What else can it treat? WHEELHOUSE-What are the oral complications?
Lantus SoloStar...can also treat Type 2! ORAL: NUMBNESS of the MOUTH!!
How many types of Type 1 diabetes drugs are there? What are the 5 categories?
7 total...1.Short Acting 2.Rapid acting 3.intermediate 4.intermediate to long 5. long
Type 2 diabetes usually develops after ____ years of age (now occurring at younger ages)...Significant blood levels of ______ present
INTERESTING! Type 2 DM: _______ is needed to elicit response in RESISTANT cells..
More insulin...its like heroine i guess.
What is the typical result of untreated Type 2 DM?
For Type 2 diabetes: ________ are oftentimes used as supplementation with oral medications, especially if patient is poorly controlled
What are the 3 main goals of drugs for Type 2 DM? What is the risk with these Tx's?
1.Increase insulin secretion in glucose-dependent manner 2.Suppress hepatic GlucoNeoGenesis 3.Improve insulin sensitivity...Risk: hypOglycemia
THE O.G.> SulFonylUreas: Promote insulin release from _________
Pancreatic BETA cells
THE O.G.> SulFonylUreas: Newer drugs (2nd generation) are more _______ but not more effective
THE O.G.> SulFonylUreas: WHAT IS THE BOARD FAVORITE? The one that "everyone should know"
What do all of the O.G.-SulFonylUreas end in?
2nd Gen SulFonylUreas: What is the main one "everyone should know"?
Glip-iz-ide (GlucoTrol)... i like that one! (control glucose!)
2nd Gen SulFonylUreas: these are __ to ____ times more _____ than 1st generation
10 to 100...POTENT!!! WOAH
2nd Gen SulFonylUreas: What do these bad boys end in?
DANGER WILL ROBINSON: SulfonylUreas are linked to Increased _________ mortality
DANGER WILL ROBINSON: SulfonylUreas....allergy = contraindicated in patients who are allergic to ________
DANGER WILL ROBINSON: SulfonylUreas....Caution with use if severe _______ disease
DANGER WILL ROBINSON: SulfonylUreas....Simultaneous administration of _______ and sulfonylureas may enhance the hypoglycemic response to the sulfonylurea...WHAT is the result of this interaction????
ASPIRIN...The aspirin appears to displace the sulfonylurea from plasma proteins causing increased blood levels of the sulfonylurea drug....RESULTS in HYPOGLYCEMIA
DANGER WILL ROBINSON: SulfonylUreas....the interaction with ASPIRIN is ALSO said to be salicylate inhibition of ________ synthesis, a.t.STILL resulting in _______
What is the MOST POPULAR class of Type II DM drug? What is the specific drug name and its brand name?
What are the 4 MAGICAL mechanisms for the BIGuANIDES-metformin (Glucophage)?
1.inhibits absorption of glucose from the gut 2.decreases hepatic glucose production 3.increases insulin sensitivity 4.increase peripheral glucose uptake and utilization
What are just 3 of the 7 freaking advantages/benefits of metformin as your most popular Type II DM drug?
1.More EFFECTIVE at reducing glycemic level 2.Reduces CARDIOVASCULAR mortality 3.Reduces rates of CANCER!
What is a BIG risk for Metformin users that have RENAL impairment?
Which Type II DM drug is it REALLY recommended to AVOID EtOH?
What are the 4 organs Metformin can have a big impact on?
1.kidney 2.liver 3.heart 4. G.I.
What are the 2 Alpha-GlucoSidase Inhibitors for the Tx of Type II DM?
Type II DM-Alpha-GlucoSidase Inhibitors: Inhibits the enzyme (alpha- glucosidase) responsible for degrading __________ in gut...What is the result?
complex carbohydrates...no monosaccharides avail to absorb!
Type II DM-Alpha-GlucoSidase Inhibitors: Did you know?? There is ______ in blood glucose concentrations after a meal when taking these drugs
DELAY...just a delay councilor, just a delay
Which Type II DM drug “resets” insulin receptors = reduces insulin resistance
Thiazolidinediones--Activity depends on the presence of ______ for activity
Thiazolidinediones--Decreases _____ glucose output....Increases insulin-stimulated glucose uptake in ________....Decreases _______ in adipocytes
What are the two Thiazolidinediones?
1.PioGlitAZone 2. RosiGlitAZone
Which Type II DM drug is associated with MORE THAN 30 FREAKING LIVER FAILURE DEATHS!??!? (classic BOARDS question)
Thiazolidinediones ask have an Increased risk of ________ so it is *contraindicated in these pt's
What do the Thiazolidinediones end in?
"-zone" GET IN THE ZONE!
What Type II DM drugs Mimic hormones produced by the body to stimulate the release of insulin?
What are the two types of incretins?
1.GLP-1 receptor agonists (GlucagonLike Peptide-1) 2.DPP-4 Inhibitiors (DiPeptidyl Peptidase-4)
What do all of the incretin DPP-4 inhibitors end in?
DANGER WILL ROBINSON: INCRETINS---New concerns that these drugs cause inflammation and possible pre-cancerous changes of _______
pancreas...NO FREAKING BUENO
What is the GOLD STANDARD for measuring diabetes? Whats a Normal value? What is the goal for diabetics?
the GLYCATED HEMOGLOBIN (HbA1c) Test...less than 6% is normal...goal for diabetics is under 7% (you are diagnosed at 6.5%)