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Pharmacology > Nurs 605 Module 11 > Flashcards

Nurs 605 Module 11 Flashcards

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
Q

What is the main regulator of blood sugar, and when is it stimulated? Where is it produced?

A

insulin -main regulator
stimulated when there is too much glucose in the blood
produced in the pancreas, b cells

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26
Q

What is stimulated when there is not enough glucose in the blood?

A

glucagon

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27
Q

What substance inhibits glucagon and insulin?

A

somatostatin

28
Q

What substance inhibits glucagon and insulin?

A

somatostatin

29
Q

Discuss the differences between Type 1 and Type 2 DM

A

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
Q

What are the clinical manifestations of DMT1?

A 
polydipsia
polyphagia
weight loss
frequent urination
DKA 
weight loss (thin paitnets)
usually quick onset
31
Q

What are the clinical manifestations of DMT2

A 
slow progress
may be asymptomatic
fat people 
polydipsia
excssive urination
excessive thirst
32
Q

What are the risk factors for DM T2?

A 
relative with DMT2
ethnicity
pre diabetes risk
obesity
POS
33
Q

What are the complications of DMT2?

A 
macrovascular-CAD, peripheral vasc disease
microvascular-retinopathy, neuropathy
DKA
increased risk of infection
poor wound healing
34
Q

Discuss some non-pharmacological therapies for DM management

A

lose weight
stop smoking
diet changes
eye exams

35
Q

What is the primary pharmacological option for Type 1 diabetes?
Discuss the different types

A

insulin-mainstay

bolus and basal types

bolus: rapid and short acting
basal: intermediate, long acting

36
Q

When should you take rapid, short, intermediate, and long acting insulins?

A

rapid: right before eating or within 20 mins
short: 20-30 mins after eating
intermediate: BID
long: at HS

37
Q

Name some rapid, short, intermediate and long acting insulins

A

rapid: lispro, aspart, glulisine
short: insulin R
intermediate: NPH
long: glargine, detemir

38
Q

Discuss how to mix insulins

A

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
Q

Why can you not ingest insulin and why must insulin be injected?

A

GI route will break insulin down, no therapeutic response
SQ routes only
abdomen, arms, thighs

40
Q

Discuss the use of metformin including drug class, MOA, side effects, drug interactions, contraindications and dosing strategies

A

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
Q

Discuss the use of sulfonylureas including common drugs, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of replaglinide including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of acarbose including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of TZDS/glitazones including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of gliptins/DPP-4 inhibitors including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of glifozin, SGL2 inhibitors including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the use of exanatide; GLPA1 agonists including, MOA, side effects, drug interactions, contraindications and dosing considerations

A

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
Q

Discuss the evidence surrounding intensive glucose lowering

A

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
Q

Which blood glucose lowering medication is considered first line for DMT2?

A

metformin across the board

cost effective, relative safety profile, wide tolerability

50
Q

What other types of blood glucose lowering medication can be combined with metformin?

A

sulfonyurea
NPH insulin PLUS SU
DPP4 PLUS SU

51
Q

What are the risks of combination therapy in DM?

A

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
Q

What is hypoglycemia and who is at more risk of hypoglycemia?

A

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
Q

What are the concerning risks of hypoglycemia? long term risks?

A

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
Q

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

A

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
Q

Determine appropriate frequency for Self Monitoring of Blood Glucose (SMBG) based on specific patient characteristics

A

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
Q

What is hypoglycemia unawareness?

A

repetitive hypoglycemia means increased unawareness
Type 1 DM up to 25% of them has it
can lead to HAAF

57
Q

What is hypoglycemic associated autonomic failure?

A

failure of autonomic systems due to hypoglycemia

can be adaptive (improved ability to deal with hypoglycemia) and maladaptive (negative consequences)

58
Q

At what blood level does does hypoglycemia lead to loss of consciouness and changes in neurological status?

A

<2.8

59
Q

What are the risks of hypoglycemia?

A 
excess of insulin 
poor timing of therapy
delayed food intake 
alochol
renal failure 
increased glucose use such as with exercise
60
Q

A patient is hypoglycemic, how much would carbohydrate would you provide them

A

15g, severe 20g

61
Q

A patient is on arcarbose and is hypoglycemic; what pharmacological therapy would you provide to reverse this?

A

dextrose as acarbose blocks sugar/carbs

62
Q

What is DKA? Who does DKA affect?

A

diabetic ketoacidosis
circulating ketones in the blood
affects mostly DM T1 patients
dependent on pH, bicarb and mental status; not blood sugar levels

63
Q

What is Hyperosmolar hyperglycemic state?

A

excess blood sugars, still has insulin in the system so no ketone bodies
mostly affects DMT2

64
Q

What are the signs of symtpoms of DKA and HHS? WHat are teh differences?

A

nausea, vomiting, dehydration, hypothermia, polyuria, polydipsia

differences: DKA- Type 1; leaner individuals; kussmaul resps
HHS: slower onset; overweight/obese individuals

65
Q

What are the risk factors for DKA and HHS?

A

infections
decreaed insulin
newly dosed diabetes

66
Q

What are the goals of therapy for DKA and HHS?

A

rehydration
correct hyperglycemia
correct metabolic acidosis
fix electroylte imbalances

Pharmacology (13 decks)

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