Module 6 Flashcards
(85 cards)
1
Q
Honey-fountain
A
What diabetes is named after. Talking about the gross amount of dilute urine these patients produce. With a sweet smell.
2
Q
Prevalence of T1DM vs T2DM
A
T1DM - 5% of all DM people
T2DM - 90-95% of DM people
3
Q
Pathophysiology of T1DM
A
Autoimmune destruction of beta-cells in the pancreas. These are the cells that are responsible for the production of insulin in the body. This beta-cell destruction results in absolute deficiency of insulin leading to the need for exogenous insulin replacement needs.
T1DM typically develops during early childhood but can develop later in life.
4
Q
Pathophysiology of T2DM
A
Typically develop later in life and progress. At first it starts as just a insulin resistance but overtime the beta cells in the pancreas slow their production of insulin leading to a decreased production on top of the insulin resistance.
5
Q
What accounts for the increased insulin resistance seen in T2DM?
A
- Reduced binding of insulin to its receptors
- Reduced receptor numbers
- Reduced receptor responsiveness
6
Q
There is a genetic predisposition to development of T2DM among family members.
A
7
Q
What are the 3 major factors that increase the risk for gestational diabetes?
A
- There are increased cortisol levels during pregnancy - promote hyperglycemia
- The placenta antagonizes insulin which leads to decreased effectiveness.
- Glucose can freely pass through the placenta and effect the fetus development.
8
Q
Gestational DM
A
Defined as diabetes that appears in the pregnant patient but goes away after birth.
9
Q
What does the hemoglobin A1c show?
A
The hemoglobin A1c - is an average of glucose levels over the last 2-3 months. Useful in determining how bad diabetes can be long-term.
10
Q
Prediabetes
A
Impaired glucose:
- FBG - between 100-125 (8 hours without food)
- Impaired glucose tolerance - 140-199 (2 hours after)
11
Q
This type of DM relies on insulin injections for survival
A
T1DM - they make no insulin themselves which means they rely on exogenous replacement to control their glucose levels
12
Q
Criteria for DM dx
1. Fasting glucose
2. Random plasma glucose
3. OGTT (oral glucose tolerance test)
4. A1c
A
- Above 126 fasting (no food for 8 hours)
- RPG - above 200 glucose plus symptoms of DM
- Above 200 glucose 2 hours after admin
- A1c above 6.5
13
Q
What are the preferred HTN treatment for patients with DM? What about nephropathy? What about dyslipidemia?
A
HTN - ACEI and ARBs
Nephropathy - ACEI and ARBs
Dyslipidemia - statins
14
Q
How does physical activity decrease glucose levels?
A
Muscles require glucose to function, even when insulin levels are low physical activity can lower glucose levels by using the available stores for energy.
15
Q
If a patient is found to have a increased glucose level at an office visit, what other tests should be performed?
A
- Screening for dyslipidemia - high LDL, VLDL, triglycerides. Low HDL.
- Screening for HTN
- Nephropathy
- Retinopathy
- Neuropathy
16
Q
What is the current standard of initiating treatment in patients with new type 2 DM?
A
Starting the patient on lifestyle factors - exercise, diet changes, fasting, thing like that in combination with an oral antidiabetic medication. Typically metforamin.
17
Q
What is the step approach to prescribing DM medications?
A
Step 1 - lifestyle changes plus metformin
Step 2 - addition of a second oral anti-hyperglycemic. Basal insulin should be considered if these first two medications aren’t doing the job.
Step 3 - A third medication is prescribed while considering the risks the patient has. Typically injectable insulin is on board at this point.
18
Q
What are the adult DM targets with treatment?
A
- A1c less than 7%
- Premeal plasma glucose 80-130
- Peak post-meal - 180
19
Q
Where is insulin synthesized in the body?
A
The beta cells of the pancreas within the islets of langerhans.
20
Q
What stimulates insulin release in the body?
A
- Elevation of glucose levels - primary
- Amino acid release, fatty acids, and ketone bodies
21
Q
Beta stimulation VS alpha stimulation of the pancreas
A
Beta - promotes insulin secretion
Alpha - decreases insulin secretion
22
Q
How does insulin resistance result in hyperglycemia? 3 actions
A
- Increased glycogenolysis - this is the process of breaking down glycogen into free glucose.
- Increased gluconeogenesis - creation of glucose
- Reduced use of glucose
23
Q
Human insulin vs human insulin analogs
A
Human insulin - are identical to the insulin that is naturally created in the body
Human insulin analog - modified forms of human insulin that are slightly altered to adjust their length of action.
24
Q
Short duration : rapid acting insulin
1. Brand
2. Onset
3. Peak
4. Duration
5. When typically taken?
A
- Insulin lispro - Humalog
- Onset of action - 15-30 minutes
- Peak - 0.5 to 2.5 hours
- Duration - 3-6 hours
- Typically taken right before a meal to compensate for the glucose intake. Postprandial.
25
Short duration: short acting insulin
1. Brand
2. Onset
3. Peak
4. Duration
5. When taken?
1. Regular insulin - Humalog R
2. Onset - 30 to 60 minutes
3. Peak - 1-5 hours
4. Duration - 6 - 10 hours
5. Regular insulin is less expensive. It can be used postprandial like the rapid acting forms. It can be used to control basal insulin levels. It can also be used to mix together with intermediate acting types. Comes in U100 and U500.
26
U500 concentration
When is this type contraindicated?
This is unique to regular insulin. This is an extremely strong concentration that requires additional education. They have specialized insulin syringes for administration to avoid hypoglycemia.
Never use U500 IV
27
Intermediate duration insulin
1. Brand
2. Onset
3. Peak
4. Duration
5. When used?
6. What is unique about this one?
1. Neutral protamine Hagedorn insulin (NPH) - Humulin N
2. Onset - 60-120 minutes
3. Peak - 6-14 hours
4. Duration - 16 - 24 hours
5. NPH is used to control basal insulin levels. It is given 2-3 times a day to control basal levels. Longer onset of action means it cannot be used to control postprandial glucose levels.
6. NPH is created by mixing regular insulin with a protein called protamine. Protamine delays the action of the insulin leading to its delayed onset of action. Because protamine is a foreign protein, it can result in allergic reactions.
28
Long duration insulin
1. Brand
2. Onset
3. Peak
4. Duration
5. When used?
6. How does it work?
1. U-100 Insulin glargine (Lantus)
2. Onset - 70 minutes
3. Peak - None
4. Duration - 18 - 24 hours
5. Used to treat basal insulin levels in T1DM and T2DM. Used as a once daily admin or twice daily admin to control basal.
6. A prolonged effect is achieved by adding four amino acids to the solution which leads to the prolonged action. Releases small amounts of the insulin overtime.
29
Ultralong duration insulin
1. Brand
2. Onset
3. Peak
4. Duration
5. When used?
1. Insulin glargine U-300 (Toujeo)
2. Onset - 360 minutes
3. Peak - None
4. Duration - more than 24 hours
5. This medication is used as an option for people who are unable to see just a one-a-day administration with the long acting insulin (lantus).
30
What insulins can be mixed together? How should this insulins be mixed?
Rapid acting (lispro) or Regular insulin (humlin R) can be mixed with NPH. The short-acting insulin should be drawn first to avoid contaminating the vial with the NPH.
31
What is the preferred medication to treat gestational DM?
Injectable insulin
32
What are some situations or conditions that result in increased glucose levels?
Surgery, infection, stress, obesity, adolescent growth spurt, pregnancy after the first trimester.
Pregnancy during the first trimester lowers glucose levels. Exercise does as well.
33
Who is ultimately in charge of diabetic treatment success?
The patient
34
What is hypoglycemia? What can precipitate hypoglycemia? What are the signs and symptoms hypoglycemic? What should be done to avoid these complications or correct them?
Blood glucose less than 70.
Extreme exercise, insulin or other antihyperglycemic medications, vomiting, diarrhea, starvation, excessive alcohol consumption.
CNS changes - headache, confusion, drowsiness, decreased alertness, can progress to coma.
Sympathetic response - palpitations, tachycardia, sweating, nervousness.
Frequent blood sugar monitoring, especially in patients with tight glycemic control. Always carrying a snack that is an oral carbohydrate that can combat the low glucose levels. Patients should also have ID showing that they are diabetic.
35
What is hypoglycemia unawareness?
Patients that are frequently exposed to lower levels of blood glucose have adjustments made where the normal signs and symptoms do not show until at lower levels, when they are too low to deal with
36
What are the potential complications of insulin use?
- Hypoglycemia
- Hypokalemia
- Lipohypertrophy
37
Hypokalemia and insulin use
Usefulness
Insulin causes potassium to be pumped into cells in exchange for sodium. This exchange process can result in decreased potassium levels in the serum which can precipitate cardiac dysrhythmias if allowed to drift too low.
This effect can be useful in lowering dangerously high levels of potassium quickly by giving IV insulin.
38
What is Lipohypertrophy?
A build up of subcutaneous fat if insulin injections are repeatedly injected into the same area without rotation.
39
What medications are known to increase glucose levels?
1. Thiazide diuretics
2. Sympathomimetics - epinephrine, norepinephrine, and other similar medications
3. Glucocorticoids
4. Antipsychotics
40
How do beta blockers effect glucose levels?
B-Blockers can delay hypoglycemia signs and symptoms by suppressing the sympathetic S/S that are seen with hypoglycemia - tachycardia, sweating, nervousness, and palpitations. They also can block the bodies counterregulatory system to respond to hypoglycemia.
40
What oral antidiabetic medication is started when diabetes is initially dx?
Metformin (Glucophage)
41
What are the two oral antidiabetic MOA that most of the drugs cause? What is a safety difference between these two MOAs?
1. Sulfonylureas and glinides work to stimulate increased insulin from the beta-cells of the pancreas. Increased insulin secretion leads to decreased glucose levels. These medications can result in hypoglycemia if taken when glucose levels are normal or low.
2. Biguanide, alpha-glucosidase inhibitors, and SGLT-2 inhibitors all modulate the rise in glucose levels after a meal. This does not cause a forced drop in glucose and therefore is not associated with hypoglycemia.
42
Biguanides
1. Prototype drug
2. Brand
3. MOA
* Pharmokinetic
4. Uses
5. Adverse effects
6. Interactions
7. Dose
8. Patient education
9. BBW
1. Metformin (Glucophage)
2. Glucophage
3. Metformin lowers blood glucose levels in three ways.
- Inhibits glucose production in the liver
- Slightly reduces glucose absorption in the gut
- Sensitizes insulin receptors in target tissues (fat and skeletal muscle) leading to increased glucose uptake
* Metformin is not metabolized in the body. It is excreted by the urine unchanged. This leads to a potentially bad adverse effect if the patient is renal compromised.
4. Used as a first line treatment alongside healthy lifestyle changes to control blood glucose levels.
- PCOS - is a combined endocrine/metabolic disorder that results in insulin resistance and and excessive androgen production. Metformin increases insulin sensitivity and decreases insulin levels which in turn reduce androgen levels.
- Prevention of T2DM in prediabetic patients. Significantly more effective in younger patients when compared to older populations. Not as effective as lifestyle changes though.
- Gestational diabetes - proven to be as effective as insulin injections when used with pregnancy.
5. Adverse effects:
- Metformin is not metabolized in the body, being excreted unchanged in the urine. This leads to the potential accumulation of metformin in patients whose renal function is bad. Build up of lactic acid is a potentially fatal condition.
- GI upset - anorexia, nausea, and diarrhea can occur.
- Weight loss - a potential side effect
- Decreased absorption of Vitamin B12 and Folic acid
6. Interactions:
- alcohol - limits the ability of the body to breakdown lactic acid, this can exacerbate the potential of metformin also causing this.
- Cimetidine - a h-2 histamine blocker - can increase the risk for lactic acidosis
- Contrast dye - contrast dye that contains iodine can result in renal impairment which can result in buildup of metformin resulting in toxicity leading to lactic acidosis. Metformin should be discontinued a day or two before the imaging and resumed around two days after.
7. Dose:
- 500-850mg daily or 500mg twice daily. Take with meals to decrease Gi upset.
9. BBW:
- Metformin can result in lactic acidosis in patients with impaired renal function
43
What type of antidiabetic medication is preferred for treatment in patients who may skip meals?
Metformin or another agents (alpha-glucosidase inhibitors or SGLT-2 inhibitors) that do not stimulate increased insulin production. This avoids the risk for hypoglycemia.
44
What is PCOS? What are the signs and symptoms? What does it have to do with insulin and glucose? What medication is prescribed to treat the condition?
Polycystic ovarian syndrome - a condition of metabolic and endocrine dysfunction that results in:
- Increased androgen levels
- Increased insulin resistance
This two process result in the signs and symptoms of:
- Hirsutism - excessive thick, dark, coarse hair growing in a male type pattern.
- Deepening of voice
- irregular periods
- acne
- anovulation
- Infertility
PCOS is a condition that suffers from increased insulin sensitivity. This can lead to high glucose levels. Metformin can increase sensitivity, decrease glucose levels and lower androgen levels.
45
What is androgen?
Androgens is a group of hormones that stimulate male characteristics. They are found in both males and females but are much more concentrated in males. Deepened voice, increased muscle mass, and coarse hair on face are promoted by high levels of androgen hormones.
Testosterone
Dihydrotestosterone
Others
46
When is metformin contraindicated?
- Renal impairment
- Upcoming radiographic imaging (iodine)
- Hepatic impairment
- Alcoholism
- Shock
All these conditions can result in decreased metformin clearance or increased lactic acid buildup.
47
What are the signs and symptoms of lactic acidosis? How is this treated?
- Hyperventilation
- Malaise
- Lethargy
- Somnolence
- Myalgia
Treatment of this condition is corrected via HD
48
Sulfonylureas
1. Prototype drug
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Interactions
7. Dose
1. Glyburide (diabeta)
2. Diabeta
3. The MOA of sulfonylureas results in stimulation of the beta-cells in the pancreas to increase insulin production. This can result in hypoglycemia if taken when glucose levels are not high enough. ATp - potassium - calcium - release of insulin
4. Used:
- Used for treatment and management of hyperglycemia
5. Adverse effects:
- Hypoglycemia - this is increased in patients that have difficulties metabolizing and excreting the drugs. Renal and hepatic insufficiency can result in worse or more often hypoglycemic episodes.
- Weight gain - insulin promotes use of calories that ingested. Prior to taking the medication, much of the sugar would just be eliminated via urine.
6. Interactions:
- Alcohol - alcohol intake can result in a "disulfiram reaction - flushing, nausea, palpitations. Alcohol can also increase the risk for hypoglycemia
- NSAIDS, sulfa antibiotics, and alcohol all can intensify hypoglycemia.
- Beta - blockers - suppress insulin release
7. Dose:
0.75 to 3mg daily - hold if NPO or hypoglycemic
49
Why are sulfonylureas not prescribed to T1DM?
It is necessary that the beta cells in the pancreas are able to make insulin. Otherwise, the MOA would be ineffective.
50
Thiazolidinediones (TZDs)
1. Prototype
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Interactions
7. Dose
8. BBW
1. Pioglitazone (Actos)
2. Actos
3. Reduces insulin resistance by increasing insulin utilization. Decreases glucose production by the liver. Activates PPAR gamma - a gene that helps regulate lipid and carbohydrate metabolism. Activation of this gene increases skeletal muscle and adipose tissue uptake of glucose.
4. Used to treat T2Dm alongside lifestyle changes and metformin. The presence of insulin is needed for the medication to work, so there is no benefit of T1DM patients taking it.
5. Common - URTI, headache, sinusitis, and myalgia.
Serious - Can cause ovulation in anovulatory pre-menopausal women. Contraceptive means. Possibly increases the risk for bladder cancer. Increase risk for fractures in women. Possibly hepatotoxic. Can increase LDL but also can increase HDL and lower triglycerides.
- Ovulation
- Bladder cancer
- Fractures
- Hepatotoxic
- Increase LDL and HDL, lower Triglycerides
*******BBW - contraindicated in patients with HF. The medication causes a mild increase in fluid retention that is handled by patients without HF but can be detrimental in patients with the disease. Specially NYHA III or IV.
51
What is the BBW associated with Thiazolidinediones (TZDs) prototype? What should the patient be educated on>?
The BBW is the contraindication of prescribing this medication to patients with heart failure, specially NYHA class 3 and 4. This is because the medication can cause mild fluid retention that these patients cannot tolerate.
Education should include the signs and symptoms of fluid volume overload - SOB, weight gain, edema, exertional dyspnea.
52
Signs and symptoms of bladder cancer? What medications can this be seen with?
S&S - blood in the urine, worsening urinary urgency, bladder pain, painful urination)
Thiazolidinedione - Pioglitazone (Actos)
53
What is the preferred medication to start in step two of the diabetic care step approach?
1. Lifestyle changes & metformin
2. Glucagon-like peptide-1 receptor agonist (GLP-1) receptor agonist - Liraglutide (Victoza)
54
What are incretin hormones?
Gut-derived peptides that help regulate blood sugar after eating.
GLP-1 and GIP are the two hormones.
They have the following actions:
- Slow gastric emptying, preventing post-meal spikes
- Stimulate insulin secretion
- Suppress glucagon release
- Promote fullness
55
Dipeptidyl Peptidase-4 Inhibitors (Gliptins)
1. Prototype
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Dose
1. Sitagliptin (Januvia)
2. Januvia
3. Increase the actions of incretin hormones (GLP-1 and GIP). These two hormones work to:
- Stimulate glucose dependent release of insulin
- Slow gastric emptying, preventing glucose spikes
- Suppress postprandial release of glucagon
The DPP-4 enzyme that is inhibited as the name suggests normally stops these incretin hormones from doing their thing.
4. Used to treat T2DM with a typically A1C decrease of around 0.5%.
5. Common - URTI, headache, inflammation of throat and nasal passages.
Serious - pancreatitis, severe hypersensitivity reactions - anaphylaxis, SJS, angioedema
6. 25 - 100mg
56
Januvia
Sitagliptin - a Dipeptidyl Peptidase 4 Inhibitor
57
Sodium-Glucose Cotransport 2 Inhibitors
1. Prototype drug
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Interactions
7. Dose
1. Canagliflozin (Invokana)
2. Invokana
3. Sodium-Glucose cotransport 2 is a transporter of glucose in the kidney accounting for 90% of the glucose reabsorbed. Inhibition of this transporter and its reabsorption leads to increased glucose excretion. Can cause weight loss in some patients.
4. Used for treatment of T2DM. Used off label for treatment of T1DM.
5. Adverse effects have to do with increased glucose in the urinary system - infection - UTI, fungal infections, and increased urination. This is particularly an issue for females.
Serious adverse effects - urosepsis, risk for amputation, euglycemic DKA, pyelonephritis.
6. Concurrent use of the medication with other diuretic-like medications can result in dehydration.
7. 100-300mg daily
58
What does sodium-glucose cotransport 2 do? Where is it found?
This is a transport of glucose in the kidneys. Accounts for 90% of glucose reabsorption in the kidney. If this transporter's action is blocked, then this leads to increased secretion of glucose in the urine.
59
Glucagon-like peptide-1 receptor agonist
1. Prototype medication
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Interactions
7. Dose
1. Liraglutide (Victoza)
2. Victoza
3. These medications are often referred to as incretin mimetics. The incretin hormones GLP-1 and GIP are gut-hormones that are released after meals and work to 1. Slow gastric emptying 2. stimulate glucose-dependent release of insulin 3. Inhibit postprandial glucagon 4. Suppress hunger.
They activate GLP-1 receptors, just like the endogenous hormones, resulting in the usual effects of these hormones.
1. Slowed gastric emptying
2. Stimulate glucose-dependent release of insulin
3. Inhibit postprandial glucagon
4. Suppress hunger
These medications can result in weight loss
4. Used in treatment of T2DM
5. Adverse effects:
- Hypoglycemia when used in combination with sulfonurea
- N/V and diarrhea are the most common adverse effects
- Pancreatitis
- Renal impairment - exacerbated by conditions or medicines that can result in dehydration
- Possibly linked to thyroid cancer
- Teratogenic
- Hypersensitivity
7. Dose - can be given twice daily or once weekly
60
What are the signs and symptoms of pancreatitis? What medications can this occur with?
Pancreatitis - severe abdominal pain that can radiate to the back. N/V. Pain worsens after eating. Fever.
Medications:
- GLP-1 RA (Liraglutide - Victoza)
- DPP-4 Inhibitors (Sitaglipitin - Januvia)
61
T3 and T4 names
T3 - triiodothyronine (liothyronine)
T4 - Tetraiodothyronine (Levothyroxine)
62
T3 VS T4 release amounts
T3 is released in smaller amounts to the body.
T4 is released in larger amounts but most of it undergoes conversion into T3. 80% of plasma T3 comes from converted T4.
63
What are the primary functions of thyroid hormones? 3 of them.
1. Stimulation of energy use - increases energy use by raising the basal metabolic rate. This increases oxygen consumption and heat production.
2. Stimulation of the heart - increases heart rate and force of contraction which increases CO. Can make the body more prone to arrhythmias.
3. Promotion of growth and development - important roles in brain and other nervous system development as well as skeletal muscle.
64
Which of the thyroid hormones is thought to have the greatest effect?
T3 is thought to have the greatest effect, if not the entire effect brought about by thyroid stimulation.
T4 has a longer half-life and is thought to serve as a source of T3 after conversion.
65
What organs are involved in the release of thyroid hormones?
1. Hypothalamus - the hypothalamus releases thyrotropin-releasing hormone (TRH) in response to low circulating T3 and T4 levels.
2. TRH stimulates the anterior pituitary gland to secrete thyrotropin (thyroid stimulating hormone (TSH)).
3. TSH stimulates the thyroid to produce its hormones. As plasma levels of T3 and T4 increase, the negative feedback loop reduces the TRH production until low levels are detected again.
66
How does iodine affect thyroid function? In what populations or situations is iodine diminished?
Iodine is used by the thyroid to make T3 and T4. Reduced iodine in the body can result in decreased T3 and T4 production which leads to increased TSH production which can lead to increased size of the thyroid gland (goiter).
67
How is hypothyroidism typically dx?
1. Looking at TSH levels - if there is diminished amounts of thyroid hormone, then this will reflect in increased TSH presence.
2. Check the levels of T3 and T4.
68
How to determine between primary and secondary hypothyroidism?
Primary - high TSH levels - low T3 and T4 lead to high TSH levels as the body tries to correct the imbalance.
Secondary - TSH is low or normal despite T3 and T4 also being low. Anterior pituitary gland issue.
69
How is hyperthyroidism dx?
TSH levels
Free T3 and T4 levels
S&S
70
Mild vs moderate signs and symptom of hypothyroidism?
Mild - signs and symptoms can be unrecognizable or unable to attribute to anything
Moderate to severe:
- Face - pale, puffy, expressionless
- Skin - cold and dry
- Hair - brittle and hair loss can occur
- Heart rate and temperature are lowered
- Lethargy, fatigue, and cold intolerance
- If excessive TSH is released due to low levels of T3 and T4 then thyroid enlargement can occur
71
Chronic autoimmune thyroiditis
Hashimoto disease
72
What are the causes of hypothyroidism
1. Hashimoto disease
2. Thyroid malfunction
3. Insufficient iodine consumption
73
Hypothyroidism and pregnancy
1. How can it affect the baby?
2. When are these effects decreased?
3. What adjustments need to be made to thyroid related medications during pregnancy?
4. Recommendations when patients is found to be pregnant?
1. Hypothyroidism during pregnancy is especially dangerous to the fetus during the first trimester. Neuropsychological deficits can occur due to hypothyroidism in the fetus during this time.
2. Effects of MATERNAL hypothyroidism on the fetus diminish after the first trimester because at this point the fetus's own thyroid function is up and running.
3. Pregnant women who suffer from hypothyroidism and are taking levothyroxine should have their dose increased as much as 50%. This need needs to be addressed between weeks 4-8 most often.
4. Pregnant women, even if not previously dx with hypothyroidism should be screened for it to avoid adverse effects of the fetus.
74
Congenital hypothyroidism
Can be permanent or transient. Signs and symptoms include - large tongue that protrudes, potbelly, small statue. Impaired nervous system, teeth, and muscle development.
75
What are the two major forms of hyperthyroidism?
1. Graves disease
2. Plummer disease - toxic nodular goiter
76
Graves disease
1. Who is affected most often?
2. Characteristics
3. Causes
4. Treatment
One of the two common forms of hyperthyroidism. The most common form.
1. Characteristics - women aged 20 to 40 are most commonly affected.
2. Characteristics - exophthalmos, rapid heartbeat, excess heat production, weight loss if adequate calories aren't eaten, arrhythmias, nervousness, insomnia, weakened skeletal muscles and atrophy, increased hunger, intolerance to heat.
3. TSIs thyroid stimulating immunoglobins
4. Treatment:
- Surgical - removal of thyroid tissue
- Radioactive iodine use to destroy tissue
- Suppression of thyroid hormone stimulation
77
Exophthalmos
Protrusion of one or both eyes from their sockets. Seen in graves disease but not in toxic nodular goiter.
78
Thyrotoxicosis
- Rapid heartbeat or palpitations
- Weight loss despite normal or increased appetite
- Heat intolerance and sweating
- Tremors, anxiety, or irritability
- Menstrual irregularities
- Fatigue and muscle weakness
Seen with hyperthyroidism or increased T3 and T4 circulation.
79
Toxic Nodular Goiter
Caused by a thyroid adenoma. Results in over production of thyroid hormones. Has the same signs and symptoms seen with graves disease minus the exophthalmos.
80
Thyrotoxic crisis
1. AKA
2. When does it occur?
3. Characteristics
4. Treatment
1. Thyroid storm
2. It occurs alongside severe thyrotoxicosis, when patients undergo major surgery, major illness (sepsis).
3. Characteristics - hyperthermia (105 or even higher), severe tachycardia, restlessness, agitation, and tremor. Coma, HF, and death can ensue.
4. High doses of potassium iodide or strong iodine solution are given to suppress thyroid hormone release. Methimazole is given to suppress thyroid hormone synthesis. BBlocker to reduce HR. Sedation, cooling, IV fluids.
81
Medication for hypothyroidism
1. Prototype
2. Brand
3. MOA
4. Uses
5. Half-life
6. Adverse effects
7. Interactions
8. Patient education
1. Levothyroxine (T4)
2. Synthroid
3. A synthetic form of the naturally occurring T4 hormone. Does the same thing. Administered to replace the lack. Most of it will be converted to T3.
4. Uses - hypothyroidism - lack of T3 and T4.
5. Half-life - synthroid has a long half-life of 7 days leading its ideal long-term therapy use. Takes a month to become therapeutic though.
6. Adverse effects - no real adverse effects when taken therapeutically. If overdose - will result in thyrotoxicosis.
7. Interactions:
- Decreased absorption of synthroid occurs with PPIs, Carafate, Calcium supplements, iron supplements
- Synthroid use increases effectiveness of warfarin by degrading the vitamin K clotting factors
- Synthroid increases the effectiveness of catecholamines
8. Education:
- Take 30 to 60 minutes before breakfast. Food decreases absorption
- Stick with the same brand, brands are not interchangeable.
82
When to take synthroid?
30-60 minutes before breakfast because food decreases absorption
83
Thionamides
1. Prototype
2. Brand
3. MOA
4. Uses
5. Adverse effects
6. Interactions
7. When is the other drug in this class preferred?
1. Methimazole (Tapeazole)
2. Tapeazole
3. First line treatment for hyperthyroidism. Works by preventing the enzyme peroxidase from doing its work. This prevents oxidation of iodide into the active form iodine. Prevents iodinated tyrosines from coupling.
4. Uses
- Treatment of hyperthyroidism (Graves disease) long-term
- Adjunct to radiation therapy until therapy effects are evident (decreased thyroid hormones)
- Suppress thyroid hormone synthesis before subtotal thyroidectomy
- Treatment for thyrotoxic crisis
5. Adverse effects
- Teratogenic in first trimester
- Pass through the placenta and breast milk
- Agranulocytosis
- Hypothyroidism when given at high enough doses
7. PTU is preferred when the patient is pregnant
-
84
Agranulocytosis
What medication can cause this?
Extremely low counts of granulocytes (WBC that play a role in immune system)
- Sudden fever, chills, or sore throat
- Fatigue, muscle weakness, or rapid heart rate
- Mouth ulcers or bleeding gums
- Infections that progress rapidly, like pneumonia or sepsis
Agranilocytosis is associated with Methimazole (Tapezole) use.
