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Pharmacology > Nurs 605 Module 11 > Flashcards

Nurs 605 Module 11 Flashcards

(66 cards)

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1
Q

Describe the pathophysiology of hypothyroidism

A

low levels of TSH, elevated levels of TSH to try and stimulate excess TSH (remember negative feedback)

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2
Q

What are the clinical manifestations of hypothyroidism?

A 
may be asymptomatic, non specific symptoms
hair loss, brittle nails
fatigue, dry skin
constipation
cold intolerance
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3
Q

What are the causes of hypothyroidism

A 
iodine deficiency (rare)
autoimmune disorder
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4
Q

What serum biomarker level would be abnormal in a person with hypothyroidism

A

increased levels of TSH

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5
Q

What are the pharmaceutical choices for someone with hypothyroidism

A

levothyroxine

liothyronine

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6
Q

What is the mechanism of action of levothroxine

A

synthetic T4 isomer that converts to T3

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7
Q

What are some considerations when dosing levothyroxine?

A

takes about 6 weeks to reach steady state

dose changes can occur every 4-6 weeks

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8
Q

In what patient population would you want to start low levels of levothyroxine in?

A

elderly patients with CAD

start at 12.5mcg

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9
Q

What is the mechanism of action of liothyronine?

A

synthetic T3

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10
Q

What is first line choice of medication for hypothyroidism? Second choice?

A

levothyroxine

liothyronine

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11
Q

Why is liothyronine a second choice drug for hypothyroidism?

A

less tolerated than levothyroxine

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12
Q

are you allowed to use levothyroxine and liothyonine together?

A

no!

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13
Q

What are some considerations for pregnant women that are on thyroid medications?

A

TSH lower due to HcG levels

thyroid drugs are safe in pregnant women

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14
Q

Why is it necessary to increase thyroid medications in pregnant women? How many would you increase by>?

A

TSH levels are lower due to increased HcG levels

need to increase thyroid meds by 2 tabs/week then adjust

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15
Q

Describe the pathophysiology of hyperthyroidism

A

increased production of TSH

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16
Q

What are the causes of hyperthyroidism

A

usually caused by autoimmune disease such as Graves

tumour, cancer, excess iodine levels (rare)

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17
Q

What are the clinical manifestations of hyperthyroidism?

A 
eyelid lag
protruding eyeballs 
goiter
palipitations
heat intolerance
excess sweating
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18
Q

What is a thyroid storm and its clinical manifestations?

A 
life threatening manifestation of excess thyroid hormone
diarrhea
liver failure
hypoxia
tachycardia
changes in LOC
fever
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19
Q

What are the non pharmalogical therapies for hyperthyroidism?

A

cut it out, removal of thyroid

goiter removal

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20
Q

What are some pharmaceutical choices for hyperthyroidism?

A

iodine ablation -radiation of iodine
beta blockers- control HR; prevents conversion of T4 to T3
PTH/methimazole- prevents conversion from T4 to T3

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21
Q

What are some considerations for pregnant women with hyperthyroidism?

A

mostly due to Graves disease

manageable, should treat to upper levels of T4 and T3

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22
Q

What are the phamaceutical choices for pregnant women with hyperthyroidism?

A

PTH is preferred treatment in 1st trimester

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23
Q

What is a potential adverse effect of individuals taking PTH or methmiazole?

A

can develop neutropenia; usually occurs in the first 90 days

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24
Q

What are some considerations for breastfeeding women on antithyroid medications for hyperthyroidism?

A

can have detrimental effects on the mother

babys TSH levels should also be checked in case baby is suspected of hyperthyroidism

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25
What is the main regulator of blood sugar, and when is it stimulated? Where is it produced?
insulin -main regulator stimulated when there is too much glucose in the blood produced in the pancreas, b cells
26
What is stimulated when there is not enough glucose in the blood?
glucagon
27
What substance inhibits glucagon and insulin?
somatostatin
28
What substance inhibits glucagon and insulin?
somatostatin
29
Discuss the differences between Type 1 and Type 2 DM
DMT1- body is unable to make insulin; autoimmune disease where body destroys B cells; causes hyperglycemia DMT2- body able to make insulin but can't bind to sites; ineffective; causes hyperglycemia
30
What are the clinical manifestations of DMT1?
``` polydipsia polyphagia weight loss frequent urination DKA weight loss (thin paitnets) usually quick onset ```
31
What are the clinical manifestations of DMT2
``` slow progress may be asymptomatic fat people polydipsia excssive urination excessive thirst ```
32
What are the risk factors for DM T2?
``` relative with DMT2 ethnicity pre diabetes risk obesity POS ```
33
What are the complications of DMT2?
``` macrovascular-CAD, peripheral vasc disease microvascular-retinopathy, neuropathy DKA increased risk of infection poor wound healing ```
34
Discuss some non-pharmacological therapies for DM management
lose weight stop smoking diet changes eye exams
35
What is the primary pharmacological option for Type 1 diabetes? Discuss the different types
insulin-mainstay bolus and basal types bolus: rapid and short acting basal: intermediate, long acting
36
When should you take rapid, short, intermediate, and long acting insulins?
rapid: right before eating or within 20 mins short: 20-30 mins after eating intermediate: BID long: at HS
37
Name some rapid, short, intermediate and long acting insulins
rapid: lispro, aspart, glulisine short: insulin R intermediate: NPH long: glargine, detemir
38
Discuss how to mix insulins
clear before cloudy (short acting drawn up first) short acting can be mixed with NPH lispro can be mixed with NPH aspart mixed with NPH Glargine/detemir cannot be mixed with other insulins
39
Why can you not ingest insulin and why must insulin be injected?
GI route will break insulin down, no therapeutic response SQ routes only abdomen, arms, thighs
40
Discuss the use of metformin including drug class, MOA, side effects, drug interactions, contraindications and dosing strategies
drug class: buguanide MOA: decreased hepatic glucose production; decreased carb absorption, increased glucose uptake and utilization in skeletal muscle S/E: nausea/vomiting, bloating, flatulence, vitamin b12 deficiency, lactic acidosis drug interactions: increased risk of lactic acidosis with ciemtidine and contrast dyes contraindications: CrCl < 60 dosing strategies: standard vs. high dose affects A1C equally; 500mg BID or 850mg OD
41
Discuss the use of sulfonylureas including common drugs, MOA, side effects, drug interactions, contraindications and dosing considerations
glyburide, glycazide MOA: directly on Beta cells, stimulates insulin production S/E: weight gain, GI upset, photsensitivity, hypoglycemia drug interactions: warfarin, CYP2C9 inhibitors, NSAIDs, antiobotics, ETOH, MAOIs contraindications: hepatic/renal impairement dosing stragetigee: start small., increase as needed glyburide 1.25mg-5mg daily, glycazide 80mg OD
42
Discuss the use of replaglinide including, MOA, side effects, drug interactions, contraindications and dosing considerations
MOA: increases insulin secretion S/E: hypoglycemia, weight gain contraindications: hepatic/renal impairment, >75 years dosing strategies: 1-2mg PO BID - QID WITH MEALs; skip dose if meal is skipped
43
Discuss the use of acarbose including, MOA, side effects, drug interactions, contraindications and dosing considerations
class: alpha glucoside inhibitor MOA: inhibits breakdown of carbs and prevents absoprtion in GI tract S/E; hypoglycemia, GI upset (flatulence, n/v) contraindications: hepatic/renal imparement; CrCL <25, IBS, liver cirrhosis, intesital diseases (any condition that intereres with digestion) Dosing considerations: 50mg PO OD, then BID, then TID take with main meal; skip dose if meal is skipped
44
Discuss the use of TZDS/glitazones including, MOA, side effects, drug interactions, contraindications and dosing considerations
restricted use in Canada (Rosig) due to adverse effects; can only use if all other treatment failed S/E: heart failure, fluid retention, increased risk of bladder CA, resp infection, fractures contrindiations: heart failure, past or present bladder Ca, hepatic/renal impairement dosing considerations: pio 15-30mg OD Rosig 4mg daily caution use in CrCl <30
45
Discuss the use of gliptins/DPP-4 inhibitors including, MOA, side effects, drug interactions, contraindications and dosing considerations
MOA: decrease blood glucose, stimulates insulin seccretion S/E: pancreatitis, cardiovascular, heart failure Contraindications: heart failure, pancreatitis, pancreatic CA, renal/hepatic impairement ``` dosing: approved for monotherpay and add on therapy decreases insulin effectivness when combined weight neutral (does not cause weight gain or loss) ```
46
Discuss the use of glifozin, SGL2 inhibitors including, MOA, side effects, drug interactions, contraindications and dosing considerations
S/E: volume depletion; renal impairement, UTI, ketoacidosis contraindication: renal/hepatic impairement; bladder CA (past or present) dosing: older adult- be aware of volume depletion
47
Discuss the use of exanatide; GLPA1 agonists including, MOA, side effects, drug interactions, contraindications and dosing considerations
sub q injections weight decrease S/E: pancreatitis; GI upset; increased HR drug interactions: if using with insulin-decrease insulin dose; avoid drugs that increase HR; oral contraceptives dosing: no renal impairment; IBS; hypersensitivity; cardiac arrythmias; no thyroid concerns
48
Discuss the evidence surrounding intensive glucose lowering
intestive strategies usually mean polypharmacy and increased risk of hypoglycemic events little evidence to support decrease in premature death, CV events, stroke, neuropathy or blindness risks of intensive monitoring means more pill burden, more financial costs, and more risk of hypoglycemic events (ARI 3.5%!)
49
Which blood glucose lowering medication is considered first line for DMT2?
metformin across the board | cost effective, relative safety profile, wide tolerability
50
What other types of blood glucose lowering medication can be combined with metformin?
sulfonyurea NPH insulin PLUS SU DPP4 PLUS SU
51
What are the risks of combination therapy in DM?
two plus drugs can increase risk of adverse risks of hypoglycemia body weight - long term effect of combination therapies are unknown increase in body weight may occur in SU, meglintines, TZDs, basal insulin
52
What is hypoglycemia and who is at more risk of hypoglycemia?
episodes of low levels of plasma blood glucose that can expose the patient to harm Type 1 DM is more at risk of hypoglycemia than Type 2 2-3x hypoglycemia is more freqeunt in Type 1
53
What are the concerning risks of hypoglycemia? long term risks?
negative impact on patients life, daily acitvities may be difficult can lead to confusion, coma, seizures, death long term: neurological symptoms, inability to identify hypoglycemia int he future
54
Explain the FDA’s and Health Canada’s regulatory process for the approval of glucose lowering medications and be able to explain the implications of that process in terms of patient safety and clinically important patient focused outcomes
FDA- approves drugs withouth an 80% increase of CV risk compared to placebo approvals also based on abibility to lower A1C, not related to morbidity and mortality related to DM may not be actually patient focused, as w need to focus on the patient, not the numbers
55
Determine appropriate frequency for Self Monitoring of Blood Glucose (SMBG) based on specific patient characteristics
T1DM/T2- no optimal frequency for those using insulin; frequency should be individualzzed non insulin drugs-reasonably controlled? routine testing not needed no evidence to support that routine testing wll improve qaulity of life or decrease morbitdity/mortality
56
What is hypoglycemia unawareness?
repetitive hypoglycemia means increased unawareness Type 1 DM up to 25% of them has it can lead to HAAF
57
What is hypoglycemic associated autonomic failure?
failure of autonomic systems due to hypoglycemia | can be adaptive (improved ability to deal with hypoglycemia) and maladaptive (negative consequences)
58
At what blood level does does hypoglycemia lead to loss of consciouness and changes in neurological status?
<2.8
59
What are the risks of hypoglycemia?
``` excess of insulin poor timing of therapy delayed food intake alochol renal failure increased glucose use such as with exercise ```
60
A patient is hypoglycemic, how much would carbohydrate would you provide them
15g, severe 20g
61
A patient is on arcarbose and is hypoglycemic; what pharmacological therapy would you provide to reverse this?
dextrose as acarbose blocks sugar/carbs
62
What is DKA? Who does DKA affect?
diabetic ketoacidosis circulating ketones in the blood affects mostly DM T1 patients dependent on pH, bicarb and mental status; not blood sugar levels
63
What is Hyperosmolar hyperglycemic state?
excess blood sugars, still has insulin in the system so no ketone bodies mostly affects DMT2
64
What are the signs of symtpoms of DKA and HHS? WHat are teh differences?
nausea, vomiting, dehydration, hypothermia, polyuria, polydipsia differences: DKA- Type 1; leaner individuals; kussmaul resps HHS: slower onset; overweight/obese individuals
65
What are the risk factors for DKA and HHS?
infections decreaed insulin newly dosed diabetes
66
What are the goals of therapy for DKA and HHS?
rehydration correct hyperglycemia correct metabolic acidosis fix electroylte imbalances

Pharmacology (13 decks)

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