Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are 5 drugs that impact the endocrine system?

A

Bisphosphonates

Hypothalamic and pituitary hormones

Exocrine pancreatic enzymes

Antidiabetic agents

Thyroid and antithyroid agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pancreatic Enzyme Uses

A

Cystic fibrosis and pancreatitis

Some bariatric procedures require supplements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Pancreatic Enzyme Pharmacodynamics

A

Inactivated by ph values less than 4; do not crush or chew. Sprinkle on food if powdered form. Take immediately before or with meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pancreatic Enzyme Pharmacokinetics

A

Absorption: none, acts locally in GI tract.

Excretion: feces

Pancrelipase made from pork; pancreatin made from pork, beef, or vegatable sources.

Precautions: antacids decrease effectiveness, decreases absorption of oral iron.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pancreatic Enzymes: ADR and Drug Selection

A

Skin irritation, rashes, stomatitis, nausea
High doses: hyperuricosuria, hyperuricemia

Watch products because they are NOT bioequivalent. Most old formulas are no longer FDA approved.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pancreatic Enzyme Monitoring

A

Pancreatitis: contraindicated during acute exacerbations of chronic illness.

Hypersensitivities: may need products from vegetable sources.

Growth, charts, albumin, cholesterol, glucose, CBC, iron levels, serum uric acid.

Steatorrhea: rates and intensity help monitoring dosing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pancreatic Enzyme Facts

A

Each drug is specified in lipase, protease, and amylase units. Drugs are prescribed in units of lipase.

Many older formulations are not available in FDA approved source, so finding the right dosing is more complex; this is improving over time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pancreatic Enzymes Education

A

Do not chew, crush or drink with water.
Avoid leaving in mouth.
Enteric-coated formulations should not be mixed with alkaline foods prior to ingestion.
If powder spills, wash off skin immediately.
With infants/toddlers; water for aspiration, inhalation.
Lifestyle management: follow dietary guidelines.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Insulin Pharmacodynamics

A

Binds at insulin receptor sites on cell membrane allowing glucose to enter cells.

Acts on liver to increase storage of glucose as glycogen.

Promotes protein synthesis on muscle cells.

Reduces circulation of free fatty acids and promotes storage of triglycerides in adipose tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Types of Insulin (4)

A

Rapid acting
Short acting
Intermediate acting
Long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rapid-acting

A

Lispro (humalog), aspart (novolog) or glulisine (apidra), onset about 5 minutes, peaks in 1 hour, duration about 4-5 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Short-acting

A

Regular (humulin) insulin sometimes used around mealtime. Taken about 30-45 minutes before eating.
Peaks in 3-4 hours
Duration 4-10 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Intermediate acting

A

Normal pressure hydrocephalus mixed with protamine, delaying absorption; insulin looks cloudy and must be mixed before it is injected.
Onset one-half to 1 hour
Peak 4 to 10 hours
Duration 12 to 24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Long-acting

A

Glargine (lantus), detemir (levemir), degludec (tresiba) insulins.
Onset 2-4 hours
Duration 24 hours with little or no peak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Insulin Pharmacokinetics

A

Absorption determined by type of insulin, injection site and volume injected.
Abdominal site absorbs 50% more than other sites
Metabolism: induces CYP1A2
Excretion: urine
Watch for standardized U 100/ml, needs U100 needles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Insulin ADR

A

Hypoglycemia, diabetic ketoacidosis
Watch alcohol use; increases hypoglycemia
Beta blockers mask hypoglycemia symptoms
Pregnant women can use rapid- or short-acting insulin; does not cross placenta.
-Insulin aspart, insulin glargine, and insulin glulisine
Hypothyroidism: delays insulin breakdown; therefore may require less insulin units.
Hyperthyroidism: increases renal clearance, requiring more insulin than baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Insulin Monitoring

A

Glycohemoglobin, renal function, CBC

A1C test twice a year in patients who are meeting treatment goals and have stable glycemic controls

A1C test quarterly in patients whose treatement has changed/not meeting goals

Point-of-care testing A1C allows for timely decisions on treatments changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Insulin Patient Education

A

Goal A1C less than 7% for most nonpregnant adults

Individualized goals for older adults with long-time diagnoses
Administration, understanding types of insulin
Glucose monitoring frequency and recording
Emergency plan for glucose readings and “flu”
Lifestyle management, diet, exercise
Injection site selection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Oral Diabetic Agents Mechanism

A

Type 2 DM more than just insulin resistance

  • Insufficient production of endogenous insulin. Sulfonylureas: cause an increase in insulin production.
  • Tissue insensitivity to insulin. Thiazolidinediones: improve insulin sensitivity. Biguanides: do the same.
  • Impaired response of beta cells. Meglitinides: increase secretion of insulin.
  • Excessive production of glucose by the liver. Metformin: improves hepatic response to elevated BG, decreases glucose production and decreases GI absoprtion. Alpha-flucosidase inhibitors: inhibit absorption of carbohydrate in GI tract
  • Impaired glucagon-like peptide-1 (GLP-1) activity: rapid intestinal glucose dumping. Use of dipeptidyl peptidase 4 (DPP-4) medications to slow inactivation.
  • Continuous weight gain. DPP-4 may stop it or be weight neutral.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Sulfonylureas

A

Glipizide (glucotrol)
Glyburide (diabeta)
Glimepiride (amaryl)

All stimulate insulin release from beta cells.
All potentiate effects of ADH.
Hypoglycemia is a major side effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sulfonylureas Precautions, C.I., ADR and Drug Interactions

A

Cross-sensitivity with sulfonamides or thiazide diuretics
Avoid in pregnant women
Older adults more sensitive to hypoglycemia events
Pediatric: use in children 10-18, but it is unlabeled.

ADRs: hypoglycemia, GI, dermatological rashes, SIADH, hemolytic anemia, leukopenia, thrombocytopenia, weight gain.

D.I.: may increase or decrease hypoglycemic effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Sulfonylureas: Clinical Dosing for DM and DI

A

Clinical use and dosing for DM

  • Use second-generation agents most of the time
  • Individualized dose progression is based on response
  • Start with lowest dose and ncrease every 4-7 days.

Neurogenic diabetes insipidus
-Chlorpropamide is used off-label.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Sulfonylureas: Rational drug selection/dosing

A

Age: chlorpropamide and glyburide used in older adults (use short-acting glipizide)
Cost: many generics available
Concurrent renal disease: glipizide or tolbutamide, or glyburide
Concurrent insulin: only glimepiride FDA labeled for co-administration, but most second-generation agents used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sulfonylureas

A

Monitoring: Hga1c: baseline, then every 3 months while adjusting, then every 6 months.
CBC at onset, then annual unless more if symptoms

Patient education

  • Administration
  • ADRs
  • Lifestyle management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Biguanides

A

Metformin (glucophage, glucophage XR)
-Decreases glucose production in liver, decreases GI glucose absorption, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.
-Dose not stimuate insulin release for beta cells
-Inhibits platelet aggregation and reduces blood viscosity
Patients may lose weight: not labeled use, mostly weight neutral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Biguanides: Pharmacokinetics

A

Absorption: 50-60% after oral dosing; food decreases and delays absorption
Metabolism: no hepatic metabolism
Excreted by kidneys
Alcohol potentiates drug’s effect on lactate metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Biguanides: Precautions, C.I., ADRs

A

Renal or hepatic disease is contraindicated.
Withhold drug 48 hours before and after procedures involving iodine-based contrast mediums.
Watch patients with Vitamin b12 anemia/deficiency.
Not recommended for children younger than 10 years of age.
ADRs: Metabolic acidosis risk! (lactic acid)
Rare, except in dehydration episodes.
Renal disease; watch patients at risk for metabolic acidosis.
Liver disease: risk for lactic acidosis is increased.
GI ADRs usually resolve in 2 weeks after starting dose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Biguanides: Rational drug selection/dosing and Monitoring

A

Immediate release vs. extended release
Type 2 DM: start with 500mg twice/day and titrate up.
If patients do not respond to 4 weeks of high dosing, consider adding oral sulfonylurea or other medication .

Monitoring: assess renal function, ketones, hba1c before starting dosing; check every 6 months.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Biguanides: Patient Education

A

Administration
ADRs: report diarrhea lasting more than 2 days, dehydration
Lifestyle management
Usually not the source of any hypoglycemia
Alert imaging staff about drug presence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Alpha-glucosidase Inhibitors

A

Acarbose (precose)
Miglitol (glyset)

Inhibit the absorption of carbohydrate from GI tract, lowering the BG levels after meals
These are not monotherapy drugs.
Hypoglycemia treated with milk, lactose not sucrose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Alpha-glucosidase Inhibitors: Pharmacokinetics

A

Absorption: less than 2% of acarbose absorbed as active drug
Metabolized by intestinal bacteria and digestive enzymes (lots of gas production!)
Excreted by the kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Alpha-glucosidase Inhibitors: Precations, C.I., ADRs

A

Should not be used in patients with IBD or those at risk for bowel obstruction or renal impairment.
Should not be used during pregnancy.
Not to be used in pediatric population

ADRs: GI symptoms: flatulence, diarrhea, abdominal pain. Do not cause hypoglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Alpha-glucosidase Inhibitors: Drug interactions and Clinical Dosing

A

Acarbose; digoxin.
Miglitol: propanolol, ranitidine

Clinical use and dosing

  • Initial dose is 25mg 3 times per day
  • Increase dose in 4-8 week intervals.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Alpha-glucosidase Inhibitors: Patient Education

A

Administration: should be taken with first bite of meal
Lifestyle: Type 2 DM care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Thiazolidinediones

A

Pioglitazone (actos)
Rosiglitazone (avandia)

Pharmacodynamics:

  • Improve target cell response to insulin by activating receptor cell proteins that improve insulin action.
  • Increase utilization of insulin by liver and muscle cells and reduce liver glucose production.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Thiazolidinediones: Pharmacokinetics

A

Absorption: rapid after oral dosing.
Metabolism: liver via CYP2C8 and 3A4 to both active and inactive metabolites; substrate inhibits CYP2C8, CYP2D6 induces weakly CYP3A4
Greater than 99% protein bound
Excretion: in urine (15% to 30%) and feces as metabolites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Thiazolidinediones: Precautions, CI, ADR

A

Chronic Liver Disease- heavy liver processing
Fluid retention: exacerbates HF
FDA loosening restrictions, but still dangerous drug.
Not approved for children younger than 18.

ADRs: CV- edema, URI, headache, fatigue
Watch for signs of CHF, use with caution with patients with elevated liver enzymes.
Increased r/o bladder CA with pioglitazone use.

Drug interactions: birth control requiring higher dosing of oral contraceptives.
Watch for drugs metabolized by CYP3A4: coricidin, corticosteroids, ketoconazole

Monitoring: liver enzymes at start of therapy, hga1c

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Thiazolidines: Rational drug selection and Patient education

A

Careful selection of patient population
Monotherapy or combination with sulfonylureas, insulin
Initial dosing: 15-30mg/day; maximum dosing: 45mg/day
Strong recommendation for endocrine co-management
Patient education: once-daily dosing
-Administration, ADRs, lifestyle management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Meglitinides

A

Nateglinide (starlix)
Repaglinide (prandin)

Pharmacodynamics

  • Meglitinides increase insulin release from beta cells by closing potassium channels, which leads to the opening of calcium channels, and it is the influx of calcium that release the insulin.
  • Time in plasma is short, less than 2 hours, so these agents only lower postprandial blood glucose levels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Meglitinides: Precautions, CI, ADRs, Drug interactions

A

Liver impairment
Not approved in pediatric population

Hypoglycemia in vulnerable populations

CYP3A4 and CYP2C9 inducers increase meglitinide metabolism.
Antifungals (ketoconazole) and antimicrobials (erythromycin) inhibit metabolism, increasing risk for hypoglycemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Meglitinides

A

Rational drug selection: repaglinide (prandin)
For patients with postprandial hyperglycemia
Patients with hba1c less than 8: start with 0.5 mg before each meal.
Patients with hba1c greater than 8: start with 1 mg before each meal.
Increase slowly: may double every 2 weeks for maximum 16mg/24 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Meglitinides

A

Monitoring: get baseline hba1c and recehck in 3 months

Patient education

  • Administration: no more than 30 minutes before a meal; hold if not eating
  • ADRs
  • Lifestyle Management
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

DPP-4 Inhibitors

-Pharmacodynamics

A

Gliptins
Sitagliptin (Januvia) and saxagliptin (onglyza)
-Inhibits DPP-4
-breaks down GLP-1 and gastric inhibitory polypeptide, which are released in response to a meal
-Leads to increase in the secretion of insulin and suppresses the release of glucagon by the pancreas
-Promotes pre- and postprandial glucose levels
-Promotes mild weight loss in obese patients with diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

DPP-4 Inhibitors: Precautions, C.I., ADRs, Drug interactions, Clinical use and dosing

A

Renal dysfucntion
Pregnancy (check with obstetrician for necessity)
Not approved in children
ADRs: GI, headache

Drug interactions: ACE-Inhibitors: increased r/o angioedema

Clinical use and dosing: Monotherapy or in combination with other anti-diabetic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

DPP-4 Inhibitors: Rational drug selection and Monitoring, Patient Education

A

Age: well-tolerated by older adults
Weight/obesity: patients may lose weight
Cost: more expensive than older drug families

Monitoring: Renal function at baseline and annually
Hba1c every 3 months

Patient education

  • Administration: taken once daily in the morning
  • ADRs: well-tolerated
  • Lifestyle: changes still needed

Monitor for potential thyroid medullary cancer conerns, especially in those with previous nodules

46
Q

GLP-1 Agonists

A

Exenatide (byetta) and others

Pharmacodynamics

  • Injectable drugs
  • Promote insulin release from pancreatic betal cells in the presence of elevated glucose
  • Mimic natural incretins: slow glucose absorption from gut, promote satiety, slow postprandial spikes.
47
Q

GLP-1 Agonists Precautions, C.I., Drug Interactions

A

Precautions & C.I.- Acute pancreatitis noted in post-marketing surveillance
Severe GI disease (colitis, crohn’s)
Pregnancy (cehck with specialists)

D.I.- Increased INR if administered with warfarin
Digoxin

48
Q

GLP-1 Agonists Clinical use, Monitoring, Patient Education

A

Clinical use only for type 2 DM
Add on therapy is typical
Combine with metformin, sulfonylurea, others

Monitoring
-Glycemic control and GI distress
-Potential site reactions
ADRs- GI upset/nausea (major cause of noncompliance)

Patient Education
Administration of subcutaneous injection for rapid release
-60 minutes before meals
-Dosed 6 hours apart
-If dose is missed, wait for next scheduled time
-Lifestyle

Extended-release forms; weekly injections. works as well or better than rapid release on hba1c and weight.

GI issues more transient- rapid and extended release have different impacts on postprandial vs fasting glucose levels.

49
Q

SGLT-2 Inhibitors

A

The “flozin” meds- canaglilozin, dapagliflozin
Reduces blood glucose by blocking absorption of glucose in kidneys
Also reduces BP and can lead to mild weight loss
First choice to add if hga1c is not at goal with metformin d/t significant reducation of CV risk and progression of renal functional loss.
Can cause genital yest infections which can trigger the rare fournier’s gangrene
Sometimes linked with increased K+, bladder cancer and increased lipid levels

50
Q

Glucagon

A

Considered an insulin antidote; used in patients with diabetes who experience hypoglycemia or insulin overdose.

Stimulates hepatic gluconeogenesis and glycogenolysis, raising BG levels.
BG concentration rises within 10 minutes of injection, and maximal concentrations are attained at approximately a half hour after injection.
Hepatic stores of glycogen are necessary for glucagon to produce an anti-hypoglycemic effect.
Well absorbed after parenteral administration.
Extensively metabolized by the liver and kidneys.

51
Q

Glucagon Pharmacokinetics, Precautions, C.I.s. ADRs, D.I.

A

Well absorbed after parenteral administration
Extensively metabolized by the liver and kidneys

Precautions/C.I.s: May be used with pregnant women and children. Administered cautiously to patients suspected of having pheochromocytoma or insulinoma

ADRs: Nausea, vomiting, allergic reactions

Drug interactions: increased anticoagulant effects of oral anticoagulants

52
Q

Glucagon Clinical Use and Dosing. Monitoring, Patient Education

A

Reversal of hypoglycemia; prevention of low sugars for colonoscopy after 3-day preparations

In primary care setting: IM dosing

  • Less than 20kg weight: 0.5 mg or 20-30mcg/kg/dose, repeat every 20 minutes
  • Less than 20 kg weight: adult dosing 1mg/IM, may repeat in 20 minutes

Monitoring BG levels immediately prior to and after injection

Patient Education: Educate family on how to test BG and how to administer IM glucagon.

Glucagon depletes glycogen stores; patient should be given supplemental carbohydrates as soon as he or she awakens and is able to swallow, especially children or adolescents.
ADRs
Lifestyle

53
Q

Thyroid Hormone Synthesis

A

Synthesis is dependent on the hypothalamic-pituitary-thyroid axis.

Thyrotropin-releasing hormone is released by the hypothalamus.

Thyroxine (t4) stimulates synthesis of TSH.

T4 and T3 are synthesized from iodine and tyrosine molecules.

54
Q

Thyroid Function Tests

A

TSH- used to screen for hypothyroidism and hyperthyroidism

Free T4 and free T3 can confirm diagnosis.

Thyroid scan can be used to evaluate for goiter.

Routine screening is not recommeneded.

Screen women before pregnancy and in first trimester.

55
Q

Hyperthyroidism

A

Excessive levels of thyroid hormone

  • May be life-threatening
  • Caused by Grave’s disease, anterior pituitary disorders, plummer’s disease, amiodarone therapy

Clinical effects from hypermetabolic state
-Heat intolerance, tachycardia

Treatment: antithyroid drugs
-PTU and methimazole

56
Q

Antithyroid Agents

A

PTU, methimazole (Tapazole)
Pharmacodynamics
-Block snythesis of thyroxine and triiodothyronine
-Neither drug treats the underlying pathology in hyperthryoidism
-High relapse rates; studies how less if treated for 18-24 months

Goal of treatment: correcting hypermetabolic state

57
Q

Hyperthyroidism: Rational Drug Selection

A

Antithyroid drugs
Radioactive Iodine
Surgery
Iodides

58
Q

Hyperthyroidsm: Drug Therapy

A

Antithyroid drugs used for remission are:

  • Beta blockers may be used to reduce symptoms while waiting for antithyroid drugs to work.
  • Iodidies (potassium iodide of lugol’s solution) may be used as adjuvant treatement.

Antithyroid drugs are used for at least a year in treating Grave’s disease.

Older patients may respond best to radioactive iodine.

Pregnant patients treated with ptu because it is safer.

59
Q

Antithyroid Agents Precautions and Contraindications

A

Pregnancy risk factor D readily crosses placenta
-Recommendation NOT to get pregnant while on these drugs.
PTU not recommended in children

ADRs: agranulocystosis, drowsiness, headache, alopecia, skin rashes, renal/hepatic failure

Drug interaction: lithium, warfarin

60
Q

Preoperative Drugs to Avoid Thyroid Storm While Awaiting Thyroid Surgery

A

Antithyroid drugs
Beta Blockers
Potasium iodide

61
Q

Hyperthyroidism: Drug Therapy Monitoring, Outcome Evaluation, Patient Education

A

Monitoring

  • Clinical Status
  • Thyroid function tests (TSH and free T4)
  • Assessment of visual acuity

Outcome Evaluation

  • Based on TSH and free T4 levels
  • Referral to endocrinology necessary

Patient Education

  • Overall treatment plan
  • Length of treatment (1 year for Grave’s disease)
  • Medication administration
  • Precautions if treated with iodine-131
62
Q

Hypothyroidism

A

Primary hypothyroidism

  • Congenital hypothyroidism
  • Hashimoto’s thyroiditis: an immune-mediated disorder where TSH receptors are damaged
  • Subacute thyroiditis: is inflammation of thyroid

Secondary hypothyroidism

  • Pituitary or hypothalamic failure
  • Cushing’s syndrome
  • Overtreatment with antithyroid drugs
63
Q

Goals of Treatment for Hypothyroidism

A

Correction of hypometabolic state and return to euthyroid state

Rational drug selection: synthetic thyroid hormone. Generic vs. brand name controversy.

64
Q

Thyroid Hormones

A

T4, T3 and liotrix (a 4:1 mixture of T4 and T3)
Pharmacodynamics
- These hormones produce the same effects in the body as do endogenous thyroid hormones.
-They also produce a negative feedback loop to reduce further secretion of tsh and thyroid hormones.
-T4 is the drug of choice for thyroid replacement and suppression therapy because of its longer half-life.

65
Q

Hypothyroidism: Pregnancy and Children

A

Pregnancy

  • Untreated increases maternal health risks, still births, low birth weight and possible abnormal fetal brain development.
  • T4 is pregnancy category a.

Infants and children with hypothryoidism need treatement for normal cognitive and physical development.

66
Q

Hypothyroidism and Concomitant Diseases

A

Recent acute MI
CAD
Osteoporosis: women require careful monitoring
Infertility and menstrual irregularity: may improve with thyroid hormone replacement
Depression: hypothyroid evaluation should be part of depression workup

67
Q

Hypothyroidism Monitoring

A

TSH and free T4 levels should be evaluated every 4-8 weeks until euthyroid state reached.
Druing pregnancy at 8 weeks and 6 months gestation.

Clinical symptoms frequently do not parallel actual value.
Evaluate for anemia.
Monitor BP and lipids.

68
Q

Hypothyroidism Outcome Evaluation

A

Reduction of clinical symptoms and normal TSH/free T4
Endocrine consult considered for:
-Pediatric
-Pregnant
-Cardiac
-Complex patients or those not reponsding to therapy

69
Q

Hypothyroidism Patient Education

A

Overall treatment plan and disease process
Role of iodine intake
Pregnancy
Need for regular follow-up and lab tests, especially dual energy x-ray absorptiometry
Drug administration
-Taken in the AM on empty stomach
-Many drug interactions

70
Q

Hormone Regulation

  • Bone Formation
  • Growth Formation
  • Metabolic Rate Control
  • BP and Fluid Balance Control
A

Bone Formation:
-PTH: calcium, phosphorous

Growth Formation:

  • Estrogens, androgens, testosterone
  • GHRH->GH (somatropin)

Metabolic rate control
-TSH, TH

BP and fluid balance control
-Cortisol, aldosterone, ADH

71
Q

Human Growth Hormone

A

Somatropin (genotropin)

  • Recombinant DNA technology is true human factor.
  • Stimulates the growth and metabolism of nearly every cell in the body
  • Uses: short stature with or without normal GH levels

Contraindicted: patients with closed epiphyses
Dosing is highly individualized on the basis of child’s growth rate and anticipated trajectory of genetic height

72
Q

Human Growth Hormone Pharmacodynamics

A

Initially there is an insulin-life effect
Stimulates growth of linear bones, skeletal muscles and organs.
Stimulates erythropoietin

73
Q

Human Growth Hormone Pharmacokinetics and ADRs

A

IM and SC drugs well absorbed
Metabolism: hepatic, renal 90%
Excretion: renal

ADRs

  • Antibody development
  • Hyperglycemia, edema
  • Hypothryoidism
  • Arthralgia, headache, dizziness, flu-like symptoms
74
Q

Human Growth Hormone Patient Education. Monitoring and Rational Drug Selection

A

Pediatric administration: total weekly dose (0.16 to 0.24mg/kg) divided into 6-7 doses.
ADRs
Lifestyle Management and need to rpevent abuse

Monitoring

  • Hepatic/renal function before and during treatment
  • TSH, glucose, glycohemoglobin, based on symptoms and prior illnesses

Rational drug selection: Not initiated by NP in primary care practice; work with endocrinologist.

75
Q

Thyroid Hormone Pharmacokinetics

A

Absorption: oral- erratic 40-80%; decreased by age, food, health of GI tract, greater than 99% is protein bound.

Metabolism: liver T4 is converted to T3 in the body; T4 produces both hormones.

Excreted: bile/feces

76
Q

Thryoid Hormone Precautions, C.I., and ADRs

A

Contraindicated after acute MI or thyrotoxicosis

Pregnancy risk factor A, and safe with children.

  • Replacement is advised for all pregnant women.
  • Increased metabolic rate during pregnancy may require higher dosing from baseline.
  • Thyroid hormones are minimally excreted in breast milk.
  • Children with hypothyroidism need treatment

ADRs
-Symptoms of hyperthyroidism
CV: angina, BP increase, flushing, palpitations
CNS: anxiety, HA, insomnia
-Long term thyroid replacement associated with decreased bone density in hip/spine in postmenopausal women

77
Q

Thyroid Hormones: Drug Interactions

A

Bile-acid sequestrants, iron salts, antacids decrease absorption: estrogen may decrease response.

Drugs may decrease action of warfarin, digoxin and beta blockers

78
Q

Treatment of Hypothyroidism

A

Indicated in patients with TSH levels greater than 10uiu/ml or in patients with TSH levels between 5-10 in conjunction with goiter or positive antithyroid peroxidase antibodies (or both).

Replacement is typically lifelong.
Consult with pediatric endocrinologist before treating a pediatric patient.

79
Q

T4 Dosing

A

For patients with no known CV disease

  • Initial dose can be started at 50mcg/day for 2-4 weeks and may be increased in inrements of 25mcg/day.
  • Average full replacement 100-125mcg/day.

For patients 50+ years with CV disease or with long-standing hypothyroidism
-Initial dosage of T4 is 12.5 to 25 mg/day.
-An increase of 12.5 to 25 mcg increments at approximately 1- month intervals avoids rapid increases in cardiac workload and symptoms of ischemic heart disease.
If exacerbation’s of angina pectoris occurs, the previous dosage regimen should be administered and titrated up in smaller increments.

80
Q

T4 Rational Drug Selection

A

Drug of choice for thyroid replacement and suppression therapy.
In older adults with no cardiac disease, consider consulting with endocringologist regarding useing t3 or t4 or liotrix.

81
Q

Monitoring T4

A

TSH level should be mesausred in 6-8 weeks, and the T4 dose should be adjusted, as necessary.
The target tsh level should be between 0.3 and 3.0uiu/ml.
Once stable, annual exam is appropriate.
Monitor for osteoporosis in high-risk populations.
Many drugs affect tsh levels.

82
Q

T4 Patient Education

A

Take medication each day in the morning, before breakfast because absorption is increased.
Learn how to measure HR
Lifestyle management

83
Q

Propylthiouracil and Methimazole (Antithyroid agents)

A

PTU, tapazole
Both block synthesis of T4 and T3
Neither drug treats the underlying pathology in hyperthyroidism.
High relapse rates exist but are less likely if treated for 18-24 months

84
Q

Antithyroid Agent Pharmacokinetics

A

Absorption: rapidly absorbed after oral dosing; peaking within 1 hour 85-95% bioavailability.
PTU is 75-80% protein bound, methimazole is NOT protein bound.
Both metabolized in the liver; both have short half-life; excreted in urine. 35% of PTU, 80% of methimazole

85
Q

Antithyroid Agent Precautions, C.I., ADRs

A

Pregnancy major concern; readily crosses the placenta. Recommend that patient not get pregnant while on these drugs.
High concentration in breast milk.
Not recommended in children.
ADRs; agranulocytosis, drowsiness, HA, alopecia, skin rashes, renal/hepatic failure
Drug reaction: Lithium, warfarin

86
Q

Antithyroid Agent Rational Drug Selction/Monitoring

A

Thyroid studies, CBC, liver/renal panels before starting drug
Recheck in 1-2 months after starting drug

87
Q

Antithyroid Agent Patient Education

A

Administration: very important to NOT miss doses; if missed, do NOT make it up.
Teach about hypothyroid symptoms; prolonged sub clinical hyperthyroidism is associated with bone loss, a-fib, and impaired left ventricular diastolic filling.
Dietary sources of iodine should be reduced because they interfere with action of drugs.
Watch use of OTC cold medications.

88
Q

Posthyperthyroid Treatement

A

Patients need to expect that they will become hypothyroid.
This may not occur for several months.
Patients must take thyroid supplements for life.

89
Q

Diabetes Mellitus

A

Chronic, progressive metabolic disorder resulting from abnormalities in glucose, protein, and fat metabolism

Categorized into four clinical classes

Type 1 diabetes, which results from beta-cell destruction, leading to absolute insulin deficiency

Type 2 diabetes, which results from a progressive insulin secretory defect or insulin resistance

Diabetes resulting from other causes (e.G., Genetic defects in beta-cell function or insulin action; diseases of the exocrine pancreas, such as cystic fibrosis; and drug- or chemical-induced)

Gestational diabetes mellitus (GDM), which is diagnosed during pregnancy

90
Q

Type 1 Diabetes Mellitus

A

Pathophysiology
Autoimmune destruction of the pancreatic beta cells
Genetically linked susceptibility
Long preclinical period
Absolute deficiency of insulin production by beta cells

Treatment
Insulin

91
Q

Type 2 Diabetes Mellitus

A

90% of cases are type 2 DM

Pathophysiology
Genetics
Insulin resistance
Obesity

Insulin may be low, normal, or high.

Patients develop hyperlipidemia and hypertension.

We now understand the role of glucose absorption from the gut associated with alteration of dipeptidyl peptidase 4 (dpp-4) and glucagon-like peptides (glps).

92
Q

Complications of Diabetes Mellitus

A 
Macro and Microvascular diseases of:
Eyes
Kidneys
Heart
Peripheral Vascular System
Periodontal disease
Lipid metabolism 
Platelet function
Neuropathy
-Autonomic
-Peripheral
93
Q

Screening for Type 2 DM

A

Patients 45 years of age or more with body mass index (BMI) greater than or equal to 25 kg/m2 should be tested. Those with values within normal limits should be tested every 3 years.

Patients younger than 45 years of age with bmi greater than or equal to 25 kg/m2 who have additional risk factors should have more frequent testing.

Additional risk factors are physical inactivity; having a first-degree relative with diabetes; member of high-risk ethnic group (african american, hispanic, native american, asian american, pacific islander).

Delivery of a baby weighing more than 9 lb or previous diagnosis of GDM

hypertension (blood pressure - BP - greater than 140/90 mm hg)

high-density lipoprotein (HDL) cholesterol less than or equal to 35 mg/dl and/or triglyceride level greater than or equal to 250 mg/dl

polycystic ovary syndrome (PCOS)

impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) on previous testing

other clinical conditions associated with insulin resistance (PCOS or acanthosis nigricans)

history of cardiovascular disease.

94
Q

Insulin

A

Pharmacodynamics
Promotes protein synthesis by increasing amino acid transport into cells
Stimulates glucose entry into cells as energy source
Increases storage of glucose as glycogen (glycogenesis) in muscle and liver cells
Inhibits glucose production in liver and muscle cells (glycogenolysis)
Enhances fat storage (lipogenosis) and prevents mobilization of fat for energy (lipolysis and ketogenesis)
Inhibits glucose formation from noncarbohydrate sources, such as amino acids (gluconeogenesis)

95
Q

Tight Insulin Dosing Plan

A

Dosing: 50% bolus, 50% basal needs
Depends on blood gas (BG) levels, diet, exercise, weight
Based on type of DM, type of insulin, calories, exercise
Average insulin doses: 0.3 to 0.8 units/kg/24 hours

Example: 60 kg adult type 1 DM (using 0.5 units/ kg/24 hours)
Requires 30 units
Insulin glargine (lantus): 15 units at bedtime
Insulin lispro: 15 units total divided over meals
Before breakfast: 5 units
Before lunch: 5 units
Before dinner: 5 units

96
Q

Selecting Oral Antidiabetic Agents

A

Insufficient production of endogenous insulin

Sulfonylureas cause an increase in insulin production.

Meglitinides, insulin secretagogues, increase secretion of insulin from beta cell.

Dpp-4 inhibitors act on the incretin hormone system to indirectly increase insulin production.

Tissue insensitivity to insulin

Thiazolidinediones (tzds) improve insulin sensitivity.

Impaired response of beta cells
Meglitinides increase secretion of insulin.

97
Q

Selecting Non-Insulin Injectables

A

The goals for treatment remain the same.
Same micro-gauge needles; similar availability of pens.
Not for insulin pumps; not insulin substitutes!
Also come in extended release weekly modes which increase adherence.

98
Q

Goal of DM Treatment

A

Near normalization of blood glucose
Individualized goals for children, pregnant women, and older adults
Prevention of acute complications
Prevention of chronic complications
Appropriate individualized self-management

99
Q

DM Treatment Targets

A

Glycemic control
Hba1c less than 7% (unless > 65 years)
Pre-prandial plasma glucose 70 to 130 mg/dl
2-hour postprandial plasma glucose less than 180 mg/dl
BP less than 130/80 (if tolerated, and not frail older adult)
Lipids
Low-density lipoprotein (LDL) less than 100 mg/dl
Triglycerides less than 150 mg/dl
HDL greater than 50 mg/dl
Random urine albumin/creatinine (cr) less than 30 mcg/mg creatinine

100
Q

DM Rational Drug Selection

A

Treatment protocol is chosen on the basis of:
Type of diabetes
Desired glycemic target
Severity of hyperglycemia
Patient variables
Review most recent american diabetes association guidelines.

101
Q

Setting Glycemic Targets

A

HBA1C is primary target for glycemic control.
Should be less than 7%
Goals should be individualized, especially for older adults.
Special populations require special considerations: children, pregnant women, older adults.
Less intense glycemic goals may be indicated in persons with severe or frequent hypoglycemia.
With change of control to below 6.5% in previously high HBA1C, patients should be evaluated for frequent hypoglycemic episodes and NOT assumed to have actual control.

102
Q

Lifestyle Modifications

A

All patients should be referred to a certified diabetes educator for self-management education.
Individualized plan for all patients
Medical nutrition therapy goals are:
Attain and maintain recommended targets.
Modify nutritional intake as appropriate.
Improve health through healthy food choices and physical activity
For children: ensure adequate growth.
For pregnant women: maintain adequate energy.

103
Q

Self-Management Education

A 
Seven target behaviors
Monitoring
Medications
Meal planning
Activity/exercise
Healthy coping
Problem solving
Preventing complications
104
Q

Type 1 DM Drug Therapy

A 
Insulin 
Multidose injections required
Basal: long- or intermediate-acting
Bolus: rapid- or short-acting
Common insulin dosing regimens (refer to text)
Possible need for glucagon kit
105
Q

Basic Knowledge Before Dosing Insulin

A

Each 15 gm CHO serving raises BG approximately 50 mg/dl.
1-unit bolus of insulin lowers glucose approximately 20 to 60 mg/dl.
Determine cho-to-insulin ratio.
Split basal insulin needs and bolus insulin needs evenly (50% each).
Generally, 50% to 75% of daily insulin is given as an intermediate- or long-acting form of insulin.
Initial dose of insulin is 0.3 to 0.5 units/kg/day in divided doses.
Patient needs to have emergency plan for hypoglycemia.
Patient needs to have “sick day” plan when oral intake is compromised.

106
Q

Diabetic Drug Therapy Impacts

A

Metformin: weight loss, low risk of hypoglycemia.
Sulfonylurea: weight gain and hypoglycemia
Tzds: weight gain, edema, heart failure (HF)
DPP-4: weight neutral, nausea
GLP receptor agonists: weight loss, low risk of hypoglycemia
Sodium–glucose transport protein-2 (SGLT-2) inhibitors: genital yeast infections, potential weight loss
Insulin: weight gain, hypoglycemia

107
Q

DM Drug Therapy in Children

A

Children
Managed by specialty team
Modify glycemic targets for planned activity and growth.
Insulin for type 1 dm
Type 2 DM treatment
Metformin and/or insulin and/or liraglutide if >10 years
Lifestyle changes

108
Q

Drug Therapy in Older Adults

A

Older adults
10% higher glycemic targets
Avoid first-generation sulfonylureas, tzds.

109
Q

DM Patient Variables

A

Obesity
Metformin, DPP-4, SGLT-2 and GLP-1 RA help with weight loss.
Coronary artery disease/hf
Intensive therapy with insulin reduces microvascular damage.
Angiotensin-converting enzyme inhibitor (acei), aspirin, and statin
SGLT-2 and GLP-1 meds have CV risk and heart failure reduction
Hyperlipidemia: statins
Hypertension: ace or angiotensin II receptor blockers until chronic kidney disease (CKD) stage 3
Nephropathy: ace preferred; SGLT-2 and GLP-1 retard progression.
Neuropathy: tricyclic antidepressants, gabapentin/pregabalin (lyrica)

110
Q

DM Frequency of Preventative Care

A 
Annually
Lipids
Comprehensive foot examination
Dilated retinal examination
Microalbumin
Dental examination
Every 3-6 months
Bp
Hba1c
Foot examination if risk
Depression screening
Smoking cessation
Weight management

Pharmacology (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions