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OCHT Term II > PHARM - Cardiac, Respiratory, Endocrine > Flashcards

PHARM - Cardiac, Respiratory, Endocrine Flashcards

1
Q

Types of heart drugs (6)

A
  1. Beta blockers
  2. ACE inhibitors/ARB inhibitors
  3. Nitrates/vasodilators
  4. Calcium channel blockers
  5. Anti-arrhythmics
  6. Anti-coagulants/anti-platelets
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2
Q

Common heart conditions (12)

A
  • cardiomyopathy
  • cholesterol
  • AAA
  • Atrial fibrillation
  • Arrhythmias
  • cardiac arrest
  • STEMI
  • angina
  • HTN
  • endocarditis
  • pericarditis
  • non-ischemic chest pain - can be related to any of the above conditions (primarily endocarditis and pericarditis; and breathing disorders like pneumonia)
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3
Q

Anti-arrhythmic drugs

A
  • Class 2 Beta blockers that block impulses that cause irregular heart beats
  • interferes with hormonal influences such as adrenaline on the heart cells
  • helps reduce BP and rate
  • Suppresses abnormal rhythms of the heart (beating too quickly or slowly)
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4
Q

Conditions warranting use of anti-arrhythmics

A
  • Atrial fibrillation
  • Atrial flutter
  • SVT
  • Irregulary bradycardia
  • uncontrolled tachycardia
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5
Q

Drug names: anti-arrhythmics

A
  • amiodarone
  • procainamide
  • metoprolol - does not fall into anti-arrhythmics family but is a BETA BLOCKER with anti-arrhythmic qualities
  • Verapamil
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6
Q

Adverse reactions and side effects of anti-arrhythmics

A
  • arrhythmia worsens
  • slower heart rates can sometimes be dangerous (may put your heart into asystole before SA node starts firing again to put heart back into NSR)
  • chest pains
  • diplopia
  • edema to lower extremities - backflow and improper circulation
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7
Q

Beta-blockers

A
  • known to block Beta -1 adrenergic ?blocking agents (did she mean receptors)
  • help reduce BP
  • work by blocking effects of hormone epinephrine and norepinephrine
  • heart beats more slowly and with less force thereby reducing BP
  • some affect HR while others affect HR and blood vessels (depends on your comorbidities and hx)
  • Use of BB can also result in bronchoconstriction in patients with asthma
    • this is because although it works on beta-1 receptors it may also work on some other beta cell (such as beta-2 leading to bronchoconstriction and potentially asthma attacks)
  • varied in effects (mild to significant BBs)
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8
Q

Family name for Beta-blockers

A

-lol or -olol

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9
Q

Effect of beta-blockers (i.e. chronotropic, ionotropic, etc.)

A

-ve chronotropic, -ve ionotropic

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10
Q

Beta-blockers usually keep HR in what range

A

50-60 BPM range; never over 80-100 BPM

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11
Q

Describe the physiological changes that occur with use of beta blockers.

A
  • beta blockers bind to beta-1 receptors which do not allow norepinephrine and epineprhine to bind to receptors (affects receptors in the heart and blood vessels)
  • arteries are dilated which lowers blood pressure
  • beta blockers also slow SA node whcih allows the left ventricle to fill completely, lowering heart workload
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12
Q

Conditions for Beta blockers

A
  • chest pain (from a variety of cardiac conditions)
  • HTN
  • Post STEMI
  • Cardiomyopathy
  • Arrhythmias such as a-fib
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13
Q

The LOLs

A
  • Acebutolol
  • Atenolol
  • Bisoprolol
  • Metoprolol
  • Propanolol
  • Nadolol
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14
Q

Adverse Reactions and Side Effects of Beta-blockers

A
  • dizziness, weakness
  • drowsiness or fatigue
  • cold hands or feet - can result in gangrene, with increased risk in those with some sort of peripheral vascular disease)
  • dry mouth, skin and eyes
  • headache
  • upset stomach
  • diarrhea or constipation (depending on diet)
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15
Q

You come on scene to a patient whom is feeling faint. His medications include: atenolol, bisoprolol, and lasix. He most likely has a hx of?

a) MI
b) HTN
c) CA (cancer)
d) enlarged prostate

A

can be a) or b)

+ this patient is on lasix which is a diuretic for reducing high BP or getting water out of the heart after surgeries/heart attack

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16
Q

ACE Inhibitors

A
  • aka Angiotensin Converting Enzyme Inhibitors
  • stop the body’s ability to convert angiotensin I to angiotensin II (working at the lungs)
  • works by binding with smooth musles of arteries, allowing arteries to relax and dilate, increasing the amount of blood your heart pumps - raises blood flow and return
  • helps to lower heart’s work load and lowers blood pressure
  • also treats heart failure - because it works on our kidneys
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17
Q

Angiotensin Converting Enzyme (ACE)

A
  • central component of the renin angiotensin system which controls BP by regulating volume of fluids in the body
  • Angiotensinogen released from liver, renin that is released from kidney acts on angiotensinogen to convert it to angiotensin I
  • converts Angiotensin I to active vasoconstrictor angiotensin 2 at the lungs
  • primarily works on the kidneys to increase sodium and water retention, and everyone has ACE!
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18
Q

Common adverse effect of ACE inhibitors

This adverse effect would cause which population to not be a candidate for ACE inhibitors?

A

dry tickly cough

this is an adverse effect rather than a side effect because if the coughing can’t be stopped then this can lead to COPD exacerbations which are equivalent to significant asthma attacks - therefore those with COPD or emphysema would not be a candidate for ACE inhibitors

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19
Q

Family name for ACE inhibitors

A

-pril

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20
Q

Conditions for ACE inhibitors

A
  • heart failure
  • HTN
  • prevention of kidney damage from DM
  • prevention of continuous damage after MI
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21
Q

The PRIL’s

A
  • Captopril
  • Enalapril
  • Fosinopril
  • Lisinopril
  • Quinapril
  • Ramipril
  • these can be marketed (aka have brand names)
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22
Q

Adverse Reactions and Side Effects of Prils

A
  • dry cough
  • hyperkalemia
  • fatigue
  • dizziness
  • headaches
  • loss of taste
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23
Q

Angiotensin Receptor Blocker (ARB)

A
  • Angiotensin 2 receptor blocker helps lower BP
  • works the same as ACE inhibitors but without the “dry tickly cough”
  • blood vessels dilate and BP is reduced
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24
Q

Family name for Angiotensin Receptor Blocker (ARB)

A

Sartan

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25
Q

Mechanism of Action of Angiotensin Receptor Blockers (ARBs)

A

ARBs block action of angiotensin II from binding to angiotensin II Type 1 (AT1) receptor but not type 2 receptors (AT2); allows angiotensin II to bind to AT2 triggering vasodilation

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26
Q

What do both ACE inhibitors and ARBs have in common?

A

They both work on the renin-angiotensin-aldosterone-system (RAAS), lowering BP

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27
Q

Nitrates/vasodilators

A
  • helps dilate arteries to the heart
  • increases oxygen-rich blood flow to the heart
  • helps relieve angina symptoms or chest pain
  • also dilates veins in body so they can hold more blood, thus reducing the workload on your heart
    • however, note that with vasodilation you can flood it to the point where all the workload is taken off of the heart which can cause hypovolemic or cardiogenic shock
  • can be used for chronic or emergency problems (meds like nitro works almost instantaneously so can be used in emergencies)
  • pill, sublingual, tablet
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28
Q

Difference between nitrates and vasodilators

A

Nitrates - are meds derived from nitroglycerin

Vasodilators are not derived from nitroglycerin

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29
Q

Conditions for Nitrates/vasodilators

A
  • HF - when used ith other cardiac medications (such as ACE inhibitors, ARBs, and BBs)
  • angina pains
  • HTN
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30
Q

Nitrate medications

A
  • also called anti-anginal medications
  • Common meds:
    • Nitroglycerin
    • Diltiazem
    • Felodipine
    • Nifedipine and Verapamil
  • note: verapamil - has qualities of vasodilation AND anti-arrhythmics (ONLY used in emergency settings)
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31
Q

Adverse reactions and side effects of nitrates

A
  • headache - due to vasodilation in brain as well
  • dizziness, lightheadedness (dropping of BP)
  • nausea
  • flushing - because systemic vasodilation
  • burning or tingling under the tongue for SL (SL can also cause flushed face)
  • circular patches on skin (ex. nitro patches may localize the dilation)
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32
Q

Calcium Channel Blockers (CCB)

A
  • prevent calcium from entering the cells of the heart and blood vessel walls (CCB binds to calcium channel to block it)
  • CCB reduces electrical conduction within the heart and decreased force of contraction of muscle cells
  • dilates arteries, reuslts in lower BP
  • slows HR (to allow left ventricle to fill completely, and lowers heart workload)
  • helps control irregular heart beat
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33
Q

Family name for Calcium Channel Blockers (CCBs)

A

dipine

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34
Q

Effect of calcium channel blockers (i.e. ionotropic, chronotropic, etc.)

A

-ve dromotropic, -ve ionotropic, -ve chronotropic

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35
Q

Conditions for CCBs

A
  • treating HTN
  • tx for rapid heart rhythms as it decreases excitability for heart muscles (SVT, uncontrolled a-fib, atrial flutter)
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36
Q

Medication names for CCBs

A
  • Amlodipine
  • Felodipine
  • Isradipine
  • Nicardipine
  • Nifedipine
  • Verapamil
  • Diltiazem - vasodilator but also has characteristics of CCBs
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37
Q

Adverse Reactions and side effects of CCBs

A
  • headache
  • constipation
  • rash
  • nausea
  • flushing - sign of BP getting too low at certain sites
  • edema - pooling caused by decreased BP
  • drowsiness
  • low BP - may lead to hypovolemic shock

overdosing on CCB medications can be lethal, causing hypotension, shock, and body system collapse

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38
Q

Anti-coagulants and Anti-platelets

A
  • “blood thinners”
  • used for heart diseases (ex. a- fib) and patients with MI and pacemakers
  • anti-coagulants: slow down body’s processes of making clots
  • anti-platelets: prevent blood cells from clumping together to form a clot
  • without these drugs, clots can block circulation and lead to heart attacks/CVAs
  • both work to prevent clots but work in different ways
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39
Q

A patient on ketoralac/toradol cannot be on what other medication (i.e contraindication)?

A
  • cannot be on an anti-platelet - taken in combination, they both have anti-platelet properties which would increase risk/severity of bleeding
  • can be on anti-coagulant though
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40
Q

Patients who have fallen and hit their head, who are also on blood thinners can be at risk for what?

A

hematomas

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41
Q

Why would patients with pacemakers be placed on a blood thinner?

A

because anytime something foreign enters the body, the body will try and reject it so the body will try to create blood clots to encapsulate the pacemaker (which would cause it to fail)

Taking a blood thinner will prevent this problem

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42
Q

Conditions for Blood Thinners

A
  • heart disease
  • poor blood circulation
  • recent surgeries requiring drainage (such as major abdo or breast surgery where drains are great entry ways for infection and clotting leading to blockages so patients will be placed on blood thinners until drains are removed)
  • abnormal heart beats (a-fib)
  • congenital heart defects
  • clotting conditions - Hx of MI, CVA, angina, DVT, PE
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43
Q

Anti-coagulants - what are they, common medications, and who they are prescribed to

A
  • drugs that keep your body from clotting easily by interfering with the blood clotting process
  • used to prevent ischemic strokes and TIAs
  • # 1 anticoagulant: warfarin (Coumadin, Jantoven, Marfarin)
    • ​Short term therapy - injection
    • Long term therapy - pill
  • used to prevent clots from forming or to prevent existing clots from getting bigger
  • Often prescribed to: people with artificial heart valves, those with irregular heart beats, or those who have had hx of heart attack/stroke
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44
Q

Anti-platelets - what are they, medication names, and who they are prescribed to

A
  • prevent blood clots; work by making it more difficult for platelets in your blood to stick together (the first step in clot formation)
  • clopidogrel (Plavix) and aspirin (although ASA has anti-platelet properties but not considered a true anti-platelet)
  • Sometimes prescribed to: those with hx of ischemic strokes or heart attacks
  • Are taken on a regular basis for an extended period for prevention of heart attack and stroke
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45
Q

Medication names for anti-coagulants

A

heparin

warfarin

rivaroxaban

apixaban

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46
Q

Medication names for anti-platelets

A

clopidogrel

aggrenox

ASA properties

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47
Q

Adverse Reactions and Side Effects of Blood Thinners

A

Symptoms are usually on initial onset of taking the drug, then subside/go away all together

  • increased bruising (such as hematomas)
  • red or pink urine
  • stools that are coffee grounds
  • inreased menstrual bleeding
  • purple toes - circulation issue (stagnant blood that gets deoxygenated, as well as improper perfusion
  • pain with temp changes
  • blood thinners take away temp regulation properties (so ppl often feel cold as blood cannot rise up and stay)
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48
Q

Dyslipidemia/Cholesterol Lowering Medications

A
  • works by blocking a subtance your body needs to make cholesterol
  • lowers bad cholesterol (LDL) & has properies to safely prevent heart disease in certain aults (40-75 y.o.)
  • may also help body reabsorb cholesterol that has built up in plaques on your artery walls, preventing further blockage in your blood vessels and thus heart attacks
  • related to cardiac meds because of dx of DLD = risk of HTN and MI as well
  • besides medications, stents can also be used to widen arteries (up to 5 stents - CABG)
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49
Q

Family drug name for DLD medications

A

statin

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50
Q

Medication names for DLD

A
  • Lipitor (atorvastatin)
  • Altoprev (lovastatin)
  • Livalo (pitavastatin)
  • Pravachol (pravastatin)
  • Crestor (rosuvastatin)
  • Zocor (simvastatin)
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51
Q

Cardiac medications that paramedics can give patients

A

NTG (nitroglycerin)

ASA (aspirin)

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52
Q

Paramedic use of nitroglycerin (NTG)

A
  • QUICK-ACTING (within minutes)
  • used as a vasodilator
  • used to treat angina symptoms - chest pains or pressures (extremely high pressures like pulmonary edema)
  • helps restore blood flow into the heart
  • reduces how hard the heart has to work to circulate oxygenated blood
  • if the pains go away (it was angina); if it doesn’t go away (then not angina)
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53
Q

Paramedic use of ASA

A
  • treat pain, fever, or inflammation
  • chest pains or MI
  • used as anti-clotting agent
  • used to prevent secondary heart attacks or CVAs
  • for MIs, must be chewed (passive diffusion - works in a couple minutes)
  • Dose: 2 x 80mg ASA (if they’ve already self-administered prior to EMS arrival and are still having pain, paramedics can dose them again)
  • Therapeutic dose: 380 - 420 mg of ASA
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54
Q

Which will always be beneficial in saving lives, ASA or nitroglycerin?

A

ASA - will always be beneficial

vs

nitro may sometimes turn someone into asystole

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55
Q

Cardiomyopathy

A

disease of heart muscles - three types:

hypertrophic

dilated

restrictive

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56
Q

Hypertrophic cardiomyopathy

A
  • one side of the heart is excessively large (usually LV) - more muscular/thickened
  • diastolic dysfunction
  • risk of sudden death in young athletes
  • thickened left ventricular wall
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57
Q

Dilated cardiomyopathy

A
  • enlargement of all cardiac chambers
  • systolic dysfunction
  • MOST COMMON TYPE
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58
Q

Restrictive Cardiomyopathy

A
  • rigid ventricular walls
  • diastolic dysfunction
  • LEAST COMMON TYPE
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59
Q

True or false. HTN is always caused by some other underlying condition.

A

True. It’s a finding/secondary disease to some other cause

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60
Q

Treatment for cardiomyopathy.

A

remember that you cannot determine what kind of cardiomyopathy the patient has (until an autopsy is done) so treatment applies to all types

  • anti-arrhythmics: keeps heart beating with a normal rhythm/prevent arrhythmias
  • ACE inhibitors, ARBs, BBs, or CCBs: lower BP
  • anticoagulants: to prevent formation of blood clots
    • often used to those who have dilated cardiomyopathy to PREVENT blood clots
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61
Q

Treatment for atrial fibrillation.

A
  • beta blockers, anti-arrhythmics, blood thinners
  • anyone with a-fib should also already be on a blood thinner (to reduce stroke risk) and beta blocker (to control irregular heart rhythm)
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62
Q

True or False. Right ventricular infarctions are treated with nitro.

A

FALSE. giving patient with RVI nitro will dilate heart and bottom it out, leading to asystole (i.e. induce hypotension and cardiac arrest)

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63
Q

Treatment of STEMIs

A
  • nitro and ASA (exception is RVI)
  • STENTS (bypass ER and straight to HIU)
  • ALWAYS put defib pads on in case of VSA
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64
Q

In STEMIs, muscle damage risk is highest when?

A

in the first few hours

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65
Q

Normal BP

A

SBP <120

DBP < 80

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66
Q

Elevated BP

A

SBP: 120 - 129

DBP: <80

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67
Q

Hypertension (Stage 1)

A

SBP: 130-139

OR

DBP: 80-89

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68
Q

Hypertension (Stage 2)

A

SBP: 140 or higher

OR

DBP: 90 or higher

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69
Q

Hypertensive Crisis

A

SBP > 180

and/or

DBP >120

consult doc immediately

70
Q

True or False. High BP can lead to stroke as the pressure can cause bursting that will mostly likely occur in the brain.

A

True

71
Q

Treatment or HBP

A
  • ACE inhibitors
  • ARBs
  • Diuretics
  • Beta blockers
  • Calcium channel blockers
  • Renin inhibitors
72
Q

Categories of medications affecting respiratory system

A
  1. ​Reliver inhalers (MDIs): metered dose inhalers
  2. Corticosteroids (aerosol or powdered inhalant)
  3. Long-acting muscarinic antagonist - going against wet symptoms (dries cough up
  4. Short-acting muscarinic antagonist
  5. Combination puffers - multiple meds combined into one puffer
73
Q

MDIs

A

Metered dose inhalers - meaning that there is a certain amount of doses with every inhaler

74
Q

Is oxygen a drug?

A

yes - therefore it must be documented when given to patients (because oxygen can hurt a patient)

75
Q

Describe the oxygen dissociation curve and how oxygen dissociation may differ in healthy individuals vs those with respiratory conditions such as emphysema/COPD.

A

Oxygen dissociation curve: describes the relationship between partial pressure of oxygen and oxygen saturation of Hb (i.e. how saturated Hb would be with oxygen at given partial pressres of oxygen)

  • in COPD patients, oxygen dissociation curve is shifted to the right meaning decreased Hb affinity for oxygen (so more readily released by Hb as a compensatory response to unload oxygen at the tissue levels since COPD patients are adapted to being SOB)
76
Q

Respiratory conditions requiring medications

A

1) asthma
2) COPD
3) emphysema
4) pneumonia
5) pulmonary edema
6) CHF
7) Croup

77
Q

Acronym for Asthma triggers, and what does it stand fot

A

ASS-FACE

A: allergens (e.g pollen, moulds) - most common cases in childhood which resolve with age and then just turn into allergies

S: Smoke/scented products - cigarettes, perfumes

S: Stress and anxiety - due to hyperventilation

F: Food preservatives and certain medications - allergic reaction closing airways (causing bronchoconstriction)

A: Arthropods (eg. dust mites)

C: Cold air - cold temps causing bronchoconstriction

E: Exercise - increases resp rate

78
Q

Asthma

A
  • recurrent and reversible SOB
  • can also be associated with anaphylaxis
  • occurs when airways of lungs become narrowed due to:
    • bronchial spasms (bronchoconstriction), bronchial mucosa inflammation/edema, production of mucous
  • alveolar ducts/alveoli remain open but airflow to them is obstructed (does not affect alveoli, just bronchi)
  • Sx: difficulty breathing, wheezing
79
Q

Treatment for Asthma

A
  • Bronchodilators
  • Epinephrine: for status asthmaticus (for severe forms of asthma attacks that may lead to respiratory failure)
  • Oxygen
80
Q

How does asthma medication work?

(i.e. method of delivery, quick vs long term treatment)

A
  • usually taken via inhaler or nebulizer (allows meds to go directly into lungs)
  • quick-relief meds used for flare ups (work within minutes) - bronchodilators
    • relaxes airways and loosens mucous from lungss
  • long-term (preventative) medications: used to reduce chronic inflammation that causes the Sx
81
Q

Chronic Obstructive Pulmonary Disease (COPD)

A
  • continuous inflammation of the bronchi and bronchioles
    • two main types: chronic bronchitis and emphysema
  • often occurs due to prolonged exposure to bronchial irritants (cigarettes, polluted areas, workplaces)
  • alveoli are filled with mucous to the point where they no longer have normal inhalation/exhalation capabilities
  • white and yellow phlegm
  • Sx: adventitious sounds on auscultation, progressive SOB, cyanotic
  • aka blue bloaters
  • to be Dx with bronchitis, productive cough for 3 months is needed
82
Q

Prehospital treatment for COPD

A
  • stopping irritant
  • smoking cessation
  • bronchodilators (ventolin)
  • oral steroids
  • inhaled steroids
  • combination inhalers
83
Q

Emphysema

A
  • condition where air spaces enlarge as a result of dstruction of alveolar walls
  • the surface area where gas exchange takes place is reduced; impaired effectiveness of respirations
  • alveoli burst allowing oxygen to get pushed into the sac that holds the alveoli
    • oxygen then gets metabolized with CO2 as byproduct
  • irreversible
  • Sx: SOB all the time; cherry coloured skin (due to metabolized oxygen that is now CO2 buildup) - aka pink puffers
  • no ability to create pressure for inhalation and expiration (so pursed lip breathing helps to build pressure)
  • PHysiologically, the rib cage becomesbarrel chested to take pressure off lungs
84
Q

Prehospital treatment for emphysema

A
  • Bronchodilators - to relax bronchiolar muscles and improve airflow
  • Corticosteroids - to reduce inflammatory reponse
  • Oxygen
85
Q

Croup

A
  • common respiratory problem in young children (always a secondary problem to another cause such as a cold or upper respiratory tract infetion UTRI)
  • causes swelling and narrowing in the voice box, windpipe and airways that lead to the lungs
    • Adults have linear airways vs children (up to 8 y.o.) have cone shaped aiways so when it’s inflamed, the airway is significantly narrowed in children leading to the hallmark barking cough
  • can develop into asthma as you grow up; once a child gets croup, they are more likely to get it again
  • tends to occur in the fall and water
  • Main Sx: haarsh barking cough (like a seal)
86
Q

Prehospital treatment for croup

A
  • moist air (such as humidifier)
  • cold or cool air
  • fluid and anti-pyreitc for fever (bc of URTI)
  • emergency treatment: EPI 1:1000 via nebulizer (misted with oxygen and inhaled for bronchodilation)
87
Q

Common bronchodilators

A

1) Salbutamol - aka ventolin (blue rescue inhaler)

2) Atrovent - bronchodilator

88
Q

Bronchodilators

A
  • large group of sympathomimetics (adrenergic)
  • stimulates beta-2 adrenergic receptors throughout the lungs (bronchial smooth muscles to caused relaxation)
  • used during acute phase of asthmatic attacks
  • quickly reduces airway constriction to help restore normal air flow
89
Q

How do bronchodilators work?

A
  • begins with a specific receptor stimulated and ends with airway dilation
  • activation of beta 2 receptors activate cyclic addenosine monophosphate which relaxes smooth muscle in the airway resulting in bronchodilation and inccreased airflow
  • patients are usually instructed by their physicians to take 3 doses of their medications prior to calling paramedics if their symptoms do not improve
90
Q

Indications for Bronchodilators

A
  • Relief of bronchospasm related to respiratory disorders (treatment of asthma and bronchitis or other pulmonary disease)
  • treatment and prevention of acute attacks
  • used in hypotension and shock
  • used to produce uterine relaxation to prevent premature labour (uterotonic aspects)
  • ex. albuterol, salbutamol, ventolin
91
Q

Bronchodilator - rescue inhaler

What is it used for, potential side effects, and how is it used

A

SALBUTAMOL (Ventolin, or albuterol in US)

  • used to treat/prevent bronchospasm in patients with asthma, bronchitis, and emphysema)
  • DIRECTLY targets beta-2 adrenergic receptors
  • ventolin also works on beta cells in the heart so it may increase HR (so lots of ventolin may have side effects of palpitations and heart racing)
  • can be nebulized
  • blue MDI
92
Q

Bronchodilator - Atrovent

A
  • a short-acting muscarinic antagonist
  • long term use (usually daily use) aka NON EMERGENCY INHALER
  • relaxes muscles in airway and increases airflow to lungs
  • used to prevnt bronchospasms; used for bronchitis, emphysema, or COPD
  • White, green, and yellow MDI
93
Q

Corticosteroids

A
  • anti-inflammatory properties
  • used for chronic asthma, primarily given to those with COPD (to enlarge alveoli and thus lung space)
  • does not relieve symptoms of acute asthmatic attacks
  • come in oral or inhaled forms
    • inhaled forms reduce systemic effects
  • may take several weeks for full effects to be seen
94
Q

Corticosteroid examples

A
  • Flovent: prevents asthma - solid orange puffer
  • Pulmicort: controls and prevents wheezing and SOB caused by asthma (i.e. more long-term use for prevention and cannot relieve acute asthma symptoms during an attack) - bullet inhaler
  • Beclomethasome: controls and prevents wheezing and SOB caused by asthma, similar to Pulmicort
95
Q

Indications for corticosteroid use in respiratory disorders

A
  • treatment of bronchospastic disorders that are not controlled by conventional bronchodilators
  • not considered FIRST LINE drugs for management of acute asthmatic attacks or status asthmaticus
96
Q

Adverse Reaction to using corticosteroids

A
  • pharyngeal irritation
  • coughing
  • dry mouth
  • oral fungal infections (thrush) - that’s why you need to instruct patients to rinse their mouths after use of corticosteroids
  • systemic effects are rare because low doses are used in inhalation therapy
97
Q

A patient is taking an inhaled corticosteroid for asthma, after the patient takes a dose of the inhaler, they should…..

A

rinse their mouth with warm water (to avoid oral fungal infections i.e. thrush)

98
Q

A patient who is not in an asthma attack and has a bronchodilator and corticosteroid. Which should be taken first?

A

It doesn’t matter, can take whichever first

99
Q

How do corticosteroids work?

A
  • they stabilize membranes of cells that release harmful bronchoconstricting substances (i.e. leukocytes/WBCs)
  • increase responsiveness of bronchial smooth muscles to beta-adrenergic stimulation
100
Q

Corticosteroid: Flovent

A
  • aka fluticasone
  • an orange inhaler
  • prevents release of substance in the body that causes inflammation
  • used to prevent asthma attacks (but not completely) - will NOT treat and asthma attack that has already begun
  • may be used together with Flovent diskus with an oral steroid medicine
101
Q

Corticosteroid: Pulmicort

A
  • aka budesonide
  • purple, turbo inhaler
  • used to control and prevent symptoms (wheezing and SOB) caused by asthma
  • the powder is inhaled after twisting the body of the inhaler to grind it up into powder
  • works directly in the lungs to make breathing easier by reducing swelling
102
Q

Long-acting Muscarinic Antagonist Inhalers

A
  • Spiriva (light green)
    • generic name: Tiotropium
  • used to control and prevent Sx (such as wheezing, SOB)
  • Helps control and prevent an asthma attack or COPD exacerbation from happening, long acting and will probably last 24/h before needing another dose
  • life long - NOT FOR ACUTE EPISODES
103
Q

Short-acting Muscarinic Antagonist

A
  • Atrovent: bronchodilator
  • used in treating Sx of asthma, colds, allergies, COPD due to pulmonary disease
  • yellow and green
  • PREVENTER not a rescue inhaler
104
Q

Combination inhalers

A
  • inhalers that are a combination of bronchodilators and corticosteroids
  • not a rescue inhaler
  • used to stop or treat Sx of asthma or COPD (emphysema, chronic bronchitis)
  • lowers swelling in breathing passages and lungs
  • bronchodilators open up air passes to make breathing easier
105
Q

Combination Inhaler examples

A
  • Combivent
  • Advair
  • Symbicort
106
Q

Combivent

A
  • MDI containing combination of albuterol (Ventolin) and ipratropium (Atrovent)
  • both bronchodilators to relax muscles in airways & increase air flow to lungs
  • used as an inhaled medication to prevent bronchospasm in COPD, and often a supplementary medication so prescribed alongside other medications
  • orange and green
107
Q

Advair

A
  • used to prevent asthma, prevent flare ups/exacerbations of COPD associated with bronchitis or emphysema
  • in people with COPD, Advair is LT treatment
  • in person with asthma, it’s ST treatment until Sx are well-controlled with other meds
  • purple inhaler (powder inside), diskus
108
Q

Symbicort

A
  • contains combination of budesonide (Pulmicort) and formoterol
  • Budesonide: steroid that reduces inflammation in body
  • Formoterol: bronchodilator that relaxes muscles in airways to improve breathing
  • used for asthma (ST treatment)
  • used for COPD (LT treatment)
  • can be for anyone, any age
109
Q

What is the #1 most common endocrine-related call (for paramedics)?

A

diabetes

110
Q

Components of the endocrine system

A
  • hypothalamus
  • pituitary gland
  • pineal gland
  • thyroid and parathyroid glands
  • pancreas
  • thymus
  • ovaries (in female)
  • placenta (during pregnancy)
  • testicle (in male)
111
Q

Common endocrine emergencies with need for pharmacological treatment

A
  • hypo/hyperglycemia
  • DKA
  • thyroid and adrenal emergencies
  • menopause (if associate with vaginal bleed, may be vaginal/uterine cancer)
  • Diabetes insipidus vs Diabetes Mellitus
  • Hypothyroidism
  • Hyperthyroidism = Graves Disease
  • Addison’s Disease
  • Cushing’s Disease
112
Q

Diabetes Insipidus

A
  • rare disorder that occurs when a person’s kidneys pass an abnormally large volume of urine
  • urine is insipid (i.e. diluted and colourless) - body cannot properly concentrate urine
  • people with DI have normal blood glucose levels however kidneys cannot balance fluid in the body allowing the glucose to travel to the cells
113
Q

Diabetes Mellitus

A
  • more common form of diabetes
  • a disease manifested by a dysfunctional pancreas (congenital, burdened pancreas by high cholesterol, obesity, surgery, etc.)
    • pancrease doesn’t produce enough insulin to control the amount of glucose/sugar in blood
  • two forms: Type 1 (IDDM) and Type 2 (NIDDM)
114
Q

Normal range for blood sugar

Range of blood sugar for pre-diabetic

At what BGL does a patient need to be at to be cognitively aware?

A

Normal range: 4-7 mmol/L

Pre-diabetic: 8-10 mmol/L

To be cognitively aware: at least 4.0 mmol/L

115
Q

Unless an adult has a pancreatic disorder, what type of diabetes can they NOT develop?

A

Type I diabetes (because this is juvenile diabetes so you gotta be a smol bean)

116
Q

Type I diabetes

A

Insulin-dependent Diabetes Mellitus (IDDM)

  • pancreas does not produce insulin (∴ insulin dependent)
    • immune cells destroy the beta cells in the pancreas
  • without insulin the cells of the body are not able to take sugar into the cells to be used for energy (which is the main fuel of the cell)
  • the type of insulin taken depends on need for fast vs gradual onset, dose, longevity, efficacy etc.
117
Q

In a typical healthy adult, how does glucose get taken up in the cell?

A

1) when there is an excess amount of glucose in the body (such as after a meal), it causes the pancrease to give off insulin
2) insuling can will carry the glucose into the cells of the body (glucose cannot get into cells independently) - carrier-mediated facilitated transport
3) fatal if you don’t have insulin because NO GLUCOSE can be delivered to the brain

118
Q

Type II Diabetes

A

Non-insulin dependent diabetes mellitus (NIDDM)

  • patients are capable of producing insulin (i.e. normal pancreas) however that insulin is not used properly by the body (and producing less insulin)
  • so less glucose is taken up into the cells
  • eventually insulin resistance will happen because pancreas can’t keep up with high loads of glucose, and eventually will stop working
  • these individuals may also need insulin but NOT be type I - you’d be able to tell because they are also on other oral diabetic meds as well
119
Q

Insulin in the body is produced by

A

beta cells in pancreas

120
Q

If obesity is the problem leading to Type II diabetes, is this treatable?

A

YES! lifestyle changes, etc.

121
Q

Other names for insulin

A

humulin

novolin

122
Q

Insulin

A
  • classified as a hormone
  • binds to a receptor on the cell membrane to facilitate transport of glucose into cells & lowers blood sugar
  • type of insulin required will be determined by lifestyle
  • usually found in the fridge
123
Q

Oral diabetic medications

A
  • oral hypoglycemic agents OR oral anti-hyperglycemic agents
  • there are different classes of ani-diabetic drugs and their selection depends on nature of diabetes, age, and situation of person, and other factors
124
Q

Hypoglycemia

A
  • insufficient intake of sugar or excessive dosing/action of medication
  • most common reaction experienced by diabetic
  • bodies’ response is to release glucagon which mobilizes glucose stored in the liver and muscle in the form of glycogen (which breaks down into glucose) - i.e. glycogenolysis
125
Q

S/Sx of hypoglycemia

A
  • <4 mmol/L
  • lightheadedness, sick, dizziness
  • *note: if a diabetic person drops <4, they are still functionally quite well ((vs. a nondiabetic person who may be unconscious at the same BGL)
126
Q

Treatment for hypoglycemia

A
  • mild Sx: eat (hangry)
  • mod to severe: <4 or someone who presents as unconscious
    • IV access - dextrose (D10) which takes seconds to work (vs. glucagon takes ~5min); increases blood glucose concentrations
    • glucagon
    • oral glucose
127
Q

IV Dextrose

A
  • natural sugar, not a hormone
  • increases blood glucose
  • anti-hypoglycemic agent
  • immediate onset and action (within 30 seconds) since if follows zero order kinetics
  • short acting meaning they have to eat afer to keep their blood surgar high after initial dextrose administration
128
Q

Glucagon

A
  • hormone
  • IM administration (if IV not accessible)
  • makes its way to the pancreas to stimulate glycogenolysis
  • mobilizes glucose stored in the liver and muscle in the form of glycogen
  • converts liver glycogen into glucose
  • patients may not show immediate improvement secreted by the pancreas in response to low blood sugar
129
Q

Oral glucose

A
  • Treatment of choice (or use of glucose tablets)
  • simple sugars for a patient to eat (apple/orange juice, PB)
  • patients would need a patent airway and increased GCS
  • if not immediate improvements are noted, you need to follow with glucagon adminsitration
  • advise patient to eat food/take tablets/paste after IV dextrose (because after the initial tx, it’ll wear off and patient would crash again)
130
Q

What are the 3 things that our brains need to live?

A

blood

oxygen

glucose

131
Q

Hyperglycemia

What is it and what are the symptoms

A
  • abnormally high blood sugar (fasted blood sugar)
  • hallmark sign of diabetes or pre-diabetes
  • BGL can range from 8 to 18-20 mmol/L
  • Sx: increased thirst and frequent urination
132
Q

Treatment for hyperglycemia

A

metformin

glyburide

^ both oral hypoglycemic agents

133
Q

Metformin

A
  • class of medication: biguanide
  • primary function is to reduce glucose production by the liver
  • also promotes glucose uptake by skeletal muscles to reduce circulating glucose levels
  • lowers blood sugar
  • useful in delaying continued problems in obsese individuals (used for type II diabetes)
134
Q

Glyburide

A
  • classified as secretagogues (sulfonylureas)
  • aka glicazide
  • triggers beta cells to release insulin (to increase glucose uptake and lower blood sugar levels)
  • lower risk of GI problems than with Metformin
  • for type II diabetes
135
Q

Diabetic Ketoacidosis (DKA)

A
  • >20 mmol/L blood sugar
  • occurs most commonly in patients with IDDM
  • KEY problem is a lack of insulin
  • no sugar to use energy so body breaks down fat with produces acid and chemicals known as ketone bodies (breakdown of fat into glucose)
  • sweet candy breath, +ve ketone bodies in urine (via ketone strip)
136
Q

What is the four main S/Sx that would indicate someone is in the DKA emergency?

A

1) has IDDM
2) has abdo pain
3) N/V
4) blood sugar is 16+

137
Q

TX of DKA

A
  • correction of dehydration
  • IV fluids
  • insulin
  • Complications: heart complication and acidosis - need to be corrected
138
Q

Diuretics

A
  • promote diuresis - increased production of urine
  • aka water pills/pee pills
  • designed to increase water and sodium expelled from the body as urine, reduces amount of fluid in the body
  • designed to help with HTN (but diuretics are typically not the #1 choice for HTN, usually put on other meds)
    • lowers BP as it controls urine production in the kidneys
139
Q

What kind of patients would take diuretics

A

HTN

edema - gravitational pooling (such as those sitting in wheelchairs)

kidneys not functioning well

CHF

140
Q

What are the 3 main types of diuretics?

A

1) thiazide diuretics
2) loop diuretics
3) potassium-sparing diuretics

141
Q

Thiazides

A
  • most commonly prescribed diuretic
  • often used to treat HTN
  • decreases fluids in the body but also causes blood vessles to relax
  • examples:
    • chlorothiazide
    • hydrochlorothiazide (HCTZ)
    • indapamide
142
Q

Loop diuretics

A
  • often used to treat HF
  • most common: furosemide (tiny yellow pill)
143
Q

Potassium-sparing diuretics

A
  • reduces fluid without losing potassium (where other diuretics may cause pt to lose K+ and end up with arrhythmias)
  • Rx’d for patients with already low potassium
  • doesn’t work as well at reducing BP as others
  • risk: liver failure (cirrhosis) - low potassium
  • common meds:
    • amiloride
    • spironolactone
    • triamterene
144
Q

Thyroid Disorder

A
  • varying range of severities (from goiters that need no tx to life threatening cancer)
  • most common thyroid problems involve abnormal production of thyroid hormones
  • anti-psychotics can also chemically destroy your thyroid
145
Q

too much thyroid hormone

A

hyperthyroidism

146
Q

insufficient thyroid hormone production

A

hypothyroidism

147
Q

Hyperthyroidism

A
  • aka Graves disease
  • common cause of hyperthyroidism
  • over production of thyroid hormone
  • causes enlargement of thyroid
  • other Sx:
    • exophthalmos (bulging eyes)
    • heat intolerance
    • anxiety
148
Q

Causes of hyperthyroidism

A

1) Toxic adenomas: nodules develop ini thyroid gland and begin to secrete thyroid hormones, upsetting body’s chemical balance; some goiters may contain several of these nodules

2) Subacute thyroiditis: inflammation of thyroid gland causes gland to “leak” excess hormones, reuslting in temporary hyperthyroidism that generally lasts a few weeks but may persist for months

3) Pituitary gland malfunctions or canerous growths in thyroid gland: rare

149
Q

Hypothyroidism: What is it and S/Sx

A
  • condition with insufficient thyroid hormone production
  • Sx: puffy face, enarlged thyroid, weight gain, lethargy, restlessness, diarrhea, restless leg syndrome, sleep disturbances, can’t uptake nutrients
  • If untreated for long periods of time, this condition can bring on a myxedema coma, a rare but potentially fatal condition that requires immediate hormone treatment
150
Q

Causes of hypothyroidism

A

1) exposure to excess amounts of iodide: cold and sinus meds, heart med amiodarone, certain contrast dyes given prior to Xrays may expose you to too much iodide

2) Lithium

3) removal of thyroid gland: surgically removed (thyroidectomy) or chemically destroyed (such as by drug methimazole [tapazole] which is usually used to treat hyperthyroidism)

151
Q

Medication used for underactive or destroyed thyroid (basically for hypothyroidism)

A

Synthroid

152
Q

Synthroid

A
  • aka levothyroxine
  • synthetic hormone which replaces hormone normally produced by the thyroid gland to regulate body’s energy and metabolism
  • given when thyroid does not produce on its own
153
Q

What are the two common endocrine disorders and what is the difference between the two?

A

Addisons Disease

Cushings Disease

They are the exact opposite of each other (symptoms, cause, etc.)

154
Q

Addisons Disease

A
  • condition caused by inadequate production of steroid hormones and/or secretion by adrenal cortex (cortisol and aldosterone) which typically play an important role in regulating many functions of the body
  • considered primary insufficiency - because adrenal cortex is damaged resulting in low production of steroid hormones (little to no cortisol)
  • can be life threatening
155
Q

Sx of Addisons Disease

A
  • extreme fatigue
  • weight loss
  • hyperpigmentation
  • decrease in BP - fainting
  • salt cravings: to replace lost electrolytes (Na+)
  • N/V/D and abdo pain
156
Q

Adrenal crisis

A
  • severe adrenal insufficiency caused by insufficient levels of the hormone cortisol (can result from Addisons diesase)
  • Fever
  • Syncope
  • Convulsions
  • Hypoglycemia
  • Hyponatremia
  • V/D
  • Patient may also present with abdo pain, hypotension, headache, fever, abdnormal ECG, and loss of appetite
157
Q

Treatment of Adrenal crisis

A
  • hydrocortisone injection (can reset crisis within 1 hour of injection)
  • treat and transport with IV fluids and check capillary blood sugar (CBS) monitoring, and provide glucose if needed (glucagon will likely NOT have an effect)
  • CTAS 1
158
Q

Cushing’s Disorder

A
  • disorder that occurs when body has high levels of cortisol hormone
  • Causes:
    • pituitary gland is releasing too much ACTH
    • tumor or excess growth of pituitary gland
  • Sx: weight gain, obesity
    • buffalo hump (fat pad b/w shoulder blades) or forehead
    • fatty deposits on abdomen
    • round moon shaped face
    • dark purple stretch marks
    • breast tissue on males, bruises easily
    • pendulus or apron belly
    • thin arms and legs
159
Q

Cortisol

A

body’s main stress hormone (built in alarm system) that works with certain parts of your brain to control mood, motivation, and fear

160
Q

Main concern with obesity?

A

high cholesterol

161
Q

Causes of obesity

A

Common specific causes:

  • eating poor diet
  • sedentary (inactive) lifestyle
  • pregnancy (weight gained during pregnancy can be difficult to lose an eventually lead to obesity)

Other causes:

  • not sleeping enough, which can lead to hormone changes that make you feel hungrier and crave certain high calorie foods
  • genetics - affecting how body processes food into energy and how fat is stored
  • growing older: less muscle mass and slower metabolic rate, making it easier to gain weight
162
Q

Is obesity hereditary?

A

No. Being a larger person may be hereditary but not obesity

163
Q

Hyperlipidemia/High cholesterol - Causes and S/Sx

A
  • results from sedentary lifestyle, obesity, genetics, environmental lifestyle
  • Symptoms:
    • chest pain/angina (due to plaque buildup and ischemic sx)
    • heart attack
    • stroke
    • pain while walking caused by blocked arteries that are unable to send blood to the legs
164
Q

What family of medication do you take for high cholesterol?

A

Statins

165
Q

Statin med examples (7)

A
  • Lipitor (atorvastatin)
  • Lescol (fluvastatin)
  • Mevacor (lovastatin)
  • Altocor (also lovastatin)
  • Pravachol (pravastatin)
  • Livalo (pitavastatin)
  • Zocor (simvastatin)
166
Q

What do statins do and who will they be prescribed to?

A
  • prescribed to people who continue to be at high risk of heart disease (need to be taken for life)
  • blocks enyme in liver that helps to make cholesterol, leading to a reduction in your blood cholesterol level
  • reduces risk of heart attacks and strokes as it lowers cholesterol levels and reduces chance of fatty deposits of LDL building up in blood vessels that lead to ishemic events
167
Q

Oral Contraception (BCP)

A
  • two types: combination pill (has estrogen and progestin) or a mini pill (only estrogen)
  • Estrace
  • Estrogen
  • Femara
  • Alesse, Aviane, Diane, Yaz, Yasmine
168
Q

What sort of compliations may BCPs have with other medications/drugs?

A
  • OTC herbal supplements: ex. St. Johns Wort may affect effectiveness of BCP
  • Cigarette smoking and BCPs - can cause pulmonary embolus
  • SSRIs and antibiotics: may reduce efficacy of pill and pregnancy may result
169
Q

Hormone Replacement Meds (HR)

A
  • can be used for cross sex hormone therapy, menopausal hormone replacement therapy
  • administed by injections, patches, or gels
  • differing types:
    • estrogen vs testosterone replacement
    • feminizing hormone therapy vs masculinizing hormone therapy
170
Q

Feminizing Hormones

A
  • have significant impact on physical appearance
  • estrogen and progesterone makes hips widen and breasts grow in size as they produce female sex characteristics
  • the opposite can be said for taking masculiniing hormones (testosterone, spironolactone)
171
Q

Risks of feminizing hormones

A
  • bloot clots
  • elevated levels of triglycerides
  • stroke
  • hyperkalemia
  • T2 diabetes
  • HTN
  • weight gain
  • infertility
  • men who are cisgender have less risk for breast cancer
  • CV disease

OCHT Term II (31 decks)

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