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NUR516 Patho & Pharm 1 > Unit 5 > Flashcards

Unit 5 Flashcards

1
Q

Renovascular hypertension.

Symptoms (6)

A 
<30, >50 yr
Abdominal bruit
Sudden HTN, or worsen HTN
When take ACE,  Cr go up>=30%
Recurrent pulmonary edema, or other vascular disease
Resist to 3 drugs
(Googled it to help with memorize: 
Narrow of artery that carry blood to kidney-> also called renal artery stenosis—> this cause HTN—> called renovascular hypertension)
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2
Q

Hyperaldosteronism

A

Hyperaldosteronism: a disorder that adrenal gland release too much aldosterone into the blood.

High Na, low K

Adrenal adenoma can be the cause. If adrenal adenoma, stablize BP, and book surgery

Resist to 3 drugs too

Google (for memory): adrenal adenoma is benign tumor in adrenal glands.

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3
Q

Pheochromocytoma (5)

A

Rare tumor of adrenal gland.—> trigger SNS, affect HR, BP, metabolism

Labeled BP
Headache
Sweating, panic attack
Adrenal mass

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4
Q

Routine HTN investigation of all patients (7)

A
  1. Urinanalysis
  2. blood work: Na, K, Cr
  3. Fasting glucose
  4. Cholesterol panel
  5. 12 lead electrocardiograph: tachycardia? Beta- blocker is better
  6. Pregnancy test
  7. ECG if CAD, HF, LVH or LV dysfunction.
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5
Q

When to start BP drug, and what do you want BP at

A 
Low risk (no organ damage+ no cardiovascular risk factors):
				 start treatment: SBP>=160; DBP>=100–> 
				goal: SBP<140; DBP,90
High risk of cardiovascular disease:
				start: SBP>=130
				Goal: SBP<120
DM: (same)
			Start: SBP>130; DBP>80
			Goal: SBP<130; DBP<80
All others: (same)
			Start: SBP>140; DBP>90
			Goal: SBP<140; DBP< 90

< 60: 140/90
>60: 150/90

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6
Q

Side effect of beta- blocker (5)

A
  • can’t sleep—> melatonin
  • bradycardia
  • erectile dysfunction
  • bronchospasm
  • vasoconstriction
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7
Q

What needs to watch beta- blocker
Should beta- blocker stop suddenly?
Who should be on BBB
Avoid use BBB on whom

A
  • never stop suddenly, use 14 days to taper it down
  • all post- MI patients should be on BBB
  • avoid use BBB on patients who have:
    • lung disease (asthma, COPD)
    • heart block
    • severe CHF
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8
Q

Generations of beta- blocker

What’s the third generation especially better at

A

1st generation: non selective: propranolol (migraine, tremor, HR) & sorta lol (a- fib to sinus rhythm)

2nd generation: cardioselective: metoprolol, bistro lol, atenolol: treat MI

3rd: additional vasodilation effect: carvedilol
- more effective to reduce BP
- good for CHF patients

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9
Q

Why carvedilol is good for CHF patients

A
  • work at beta 1 receptors:
    • reduce renin release—> reduce RAAS: reduce Na & water retention
    • reduce contractility, HR, conduction—> reduce O2 need
  • block alpha 1- adrenergic: vasodilation
  • extra bonus:
    • help with cardiac remodeling
    • reduce oxidative & inflammatory stress
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10
Q

Alpha 1 blocker

A

Hytrin, prazosin, terazosin
Block post- synaptic alpha receptor: ateriole & vein dilation.
- usually a supplement when patient is resistance to initial therapy
- good to treat BPH

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11
Q

Beta 1 blocker (drug)

Where is beta- 1 receptor, what’s effect, what to watch for, and what’s extra

A

Metoprolol, carvedilol, atenolol, bisprolol, labetalol.

Beta 1 is at heart and kidney: 1. reduce HR. 2. reduce renin. 3. reduce contractility
- cardioselective with limited bronchial & vascular effect as well, so caution use in lung disease patients (but better than beta 2 blocker)

  • some has sympathomimetric activity: reduce HR during workout, but don’t change resting HR: pindolol& acebutolol.
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12
Q

Beta 2 blocker

A

Located almost everywhere: lung, liver, pancreas, arteriolar smooth muscle.
Beta- 2 receptor is bronchodilation + vasodilation, so beta- 2 blocker will cause bronchoconstriction & vasoconstriction

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13
Q

What are drugs treat hypertension

A 
To be a long a
For adults without compelling indicatation for specific agents, these are the recommendation for initial mono therapy for them (1-5)
1. Thiazide/ thiazide- like diuretics
2. BBB (< 60 yr)
3. ACE inhibitor (non black)
4. ARB
5. long acting CCB
————————————-
  1. Alpha blocker.
  2. Central agonist
  3. Direct vasodilator
  4. Renin inhibitor
  5. Adrenergic antagonist
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14
Q

Action of ACE inhibitor

A
  1. Inhibit ACE enzyme, so angiotensin I can’t become II.
  2. Increase prostaglandin synthesis (vasodilator)
  3. Reduce degradation of bradykinin (vasodilator & mild diuretic)
  4. Inhibit smooth muscle hypertrophy
  5. Inhibit nitric oxide (NO) production—> vasodilation
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15
Q

What’s good about ACE inhibitor (4)

A
  1. Don’t effect HR, just BP
  2. Prevent hypertrophy
  3. Glomerular protection
  4. Reduce fasting glucose & H1C
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16
Q

What’s ACE best used for (4)

A
  1. DM patients (because it reduce fasting glucose & H1Ac)
  2. Cardiovascular patients
    • CHF
    • post MI
  3. HTN
  4. Renal disease
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17
Q

Never use ACE inhibitor with what

A

ARB (angiotensin II blocker)

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18
Q

ACE inhibitor new and old

A

New: ramipril & perindopril: (once daily):- more cardio protect & less orthostatic hypotension

Old: captopril: short acting, loads of side effect, not used anymore

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19
Q

ACE inhibitor’s side effects

A
  • dry cough
  • angioedema (in black)
  • increase K & Cr, reduce Na
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20
Q

What do you watch for after patient starts ACE inhibitor and when

A

Watch for K & Cr (might go up), Na (might go low), and cough

Watch these 1 week after drug starts.

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21
Q

What are ACE inhibitor

Drug all has?

A

Pril.

Enalapril, Lisinopril, Captopril, Perindopril, Ramipril

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22
Q

Angiotensin II receptor blocker. What’s its other name. And action of medication

A

ARB

Block angiotensin II to its receptor at tissue

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23
Q

What drugs are ARB

A

“Sartan”, so if patient can’t tolerate “pril”, do Sartan

Losartan, Valsartan, Candesartan, Irbesartan, Telmisartan + Cozar

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24
Q

Who can should use ARB

A

People can’t tolerate ACE inhibitor’s cough or angioedema

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25
Q

Who can’t use ARB

A

Pregnancy (all drugs affect ARB can’t be used for pregnancy)

Caution with renal & liver impaired patients

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26
Q

Action of renin inhibitor

A

Prevent angiotensin becomes angiotensin I—> RAAS negative feedback—? Further reduce renin

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27
Q

Who can’t use renin inhibitor

A

Pregnancy

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28
Q

Types of calcium channel blocker

A

Non DHP(dihydropyridine)

DHP: dihydropyridine

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29
Q

Action of calcium channel blocker

Does it change preload?

A

Prevent Ca across memberance: - muscle relaxation

  • vasodilation
  • reduce heart contraction force
  • don’t reduce preload because they don’t effect vein
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30
Q

What’s inotropy

A

Heart contraction

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31
Q

Non- DHP

What are the drugs and what’s the effect of drugs

A

Verapamil & diltiazem
- reduce AV conduction-reduce HR

  • reduce contractility
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32
Q

What’s effect of non- DHP
What’s the difference between them two
Who is good for non- DHP
Bad for

A

Non- DHP: reduce AV conduction, reduce HR, reduce contractility.
verapamil: negative inotropic & chronotropic (HR)
diltiazem: same with verapamil but less on reducing HR & reducing contractility, but a stronger vasodilator
Bad for CHF (google for memory: possibility of causing bradycardia a& worsen cardiac output)

Good for : rate control, angina, HTN

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33
Q

DHP

Action

A

Potent vasodilator

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34
Q

What are DHP

A

“Dipine”

Amlodipine, nifedipine

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35
Q

What DHP to good for

A

to treat HTN without affecting HR.

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36
Q

Side effect of DHP

A

DHP is Calcium- channel blocker

  • leg edema
  • reflex tachycardia
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37
Q

What Nifedipine is and when it should not be used

A

DHP calcium channel blocker

Should not be used in ER because it causes BP fluctuates & reflex tachycardia

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38
Q

What is spironolactone good for

A

Treat severe CHF

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39
Q

Side effect of loop diuretic

A

When using high dose, it can cause hyperglycemia & hyperlipidemia

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40
Q

Action of beta blocker

Does it affect stroke volume?

A

Block central & peripheral beta receptor—> reduce HR, contraction force & stroke volume (decrease cardiac output + reduce SNS)

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41
Q

Action of central agonist

A

Stimulate alpha 2 adrenergic receptor in brain—> reduce SNS

  • reduce cardiac output
  • reduce peripheral resistance
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42
Q

What’s central agonist: drug
What’s its side effect
What’s it good for

A

Clonidine
Might cause fluid retention
It’s good for withdrawal

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43
Q

What are direct vasodilator

Action of direct vasodilator

A

Hydralazine & minoxidil

Relax arteriolar smooth muscle

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44
Q

What’s direct vasodilator used for

A

Should reserve for severe HTN

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45
Q

What’s good and bad about direct vasodilator, so how to fix this problem

A

Good: CHF for black
Bad: can cause fluid retention & reflex tachycardia, so use with BBB or other drugs to reduce HR

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46
Q

Hydralazine’s special side effect

A

Lupus- like syndrome. Like dermatitis. Dose- related. >300mg/d

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47
Q

Adrenergic antagonist

Action

A

Inhibitor SNS

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48
Q

Why adrenergic antagonist aren’t so popular for HTN

A

Cause depression, and many other side effect associated with reduced SNS.

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49
Q

Who should use loop diuretic

A

CHF
Renal disease. CKD
Hepatitis cirrhosis

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50
Q

Who shouldn’t use loop diuretic

A

Auria
Allergic to sulfonylureas
Hepatic coma
Ethacrynic can’t be used on infants

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51
Q

Side effect of loop diuretic. With increased dose

A

With increased dose, Hyperglycemia & hyperlipidemia might happen

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52
Q

Beta 1 blocker

Beta receptor located at , effect, what’s special

A

Located at kidney & heart.

  • reduce renin
  • reduce heart contractility
  • reduce HR
  • some has sympathmimetric activity: pinto lol & acebutolol: keep resting HR, reduce workout HR.
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53
Q

Calcium channel blocker
Drugs all have what name
Side effect

A

DHP: dipine

Leg edema ( more common in 1st generation) & reflex tachycardia

Nifedipine can also cause BP fluctuates. Never use in ER

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54
Q

Hydralazine
Good for what
Side effect
What’s it’s unique side effect.

A
  • good for treat black people’s CHF
  • cause reflex tachycardia & fluid retention—> use BBB or others to reduce HR
  • lupus -like syndrome, dose related
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55
Q

Hypertension follow- up

A

For HTN with healthy behavior change & stable HTN: 3-6 month

No HTN: yearly
New HTN: every month or 2 month

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56
Q

Cholesterol ‘s function

A
  • maintain cell memberance
  • make steroid hormone
  • make bile acid
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57
Q

Function of triglyceride

A

Store energy

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58
Q

Phospholipid function

A

Cell function & lipid transport.

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59
Q

What are the types of lipid in plasma

Relationship between fat and lipoprotein

A

Fat has 3 forms in plasma:

  1. Cholesterol
  2. Phospholipid
  3. Triglyceride

All three aren’t solutable in plasma so need a transport—> the transport is lipoprotein

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60
Q

What does HDL do?

A

HDL remove all these to liver to metabolize.

  1. LDL in peripheral cells
  2. Triglyceride result form degration of chlomicrons & VLDL
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61
Q

What can cause dyslipidemia

A

95% of people has combination of generic & environmental factors. (Bottom line: elevated lipoprotein)

  1. Genetic: problem with LDL receptor, mutate in apolipoprotein—> increase cholesterol
  2. Environmental:
    Drugs: beta-blocker, contraceptive
    Disease: DM, pregnancy
    lifestyle: smoking, lack of exercise, high fat diet,
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62
Q

Structure of lipoprotein

A

Outside: hydrophilic: apolipoprotein + phospholipid
Inside: hydrophobic: cholesterol + triglyceride

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63
Q

Types of lipoprotein

A
  1. Chylomicrons: diet fat that solulized by bile acid (biggest lipoprotein, usually disappear in 12-14 hr)
  2. VLDL: made of cholesterol & triglyceride
    triglyceride—> lipoprotein lipase & hepatic lipase hydrolysize it —> triglyceride content decrease & lipoprotein becomes smaller & % of cholesterol goes up—>become IDL( short live)—-> go to liver—-> become LDL ( end product of VLDL) bad fat—> 60-75% of total cholesterol are LDL.—> high LDL increase risk of atherosclerosis
  3. HDL: main function is to remove triglyceride that result from degration of chlomicrons & VLDL particles, and IDL to liver to metabolize. Good fat.
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64
Q

Non-pharmacological management for dyslipidemia

A
  1. Smoking cessation: smoking damage endothilial cell & increase platelet aggregation
  2. Control drinking: for women less than 1 drink per day, less than 2 drinks for men
  3. Exercise: average 40 min aerobic workout 3-4 times per week —> reduce LDL increase HDL+ better control DM
  4. Weight loss
  5. Dietary: limit sweet & red meat. DASH, AHA diet. Eat healthy
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65
Q

Dyslipidemia drug categories

A
  1. HMG- CoA reductive inhibitor: statin
  2. niacin
  3. fabric acid derivative
  4. Bile acid resin
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66
Q

Action of HMG- Coa reductase inhibitor

A

Block HMG- Coa to become mevalonate—> reduce cholesterol production in liver, this lead to :

More LDL receptors available—> increase uptake of VLDL & IDL

  1. Reduce triglyceride
  2. Increase HDL
  3. Reduce LDL
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67
Q

Things to watch about HMG- CoA reductive inhibitor

A
  1. Statin takes about 4-6 weeks to start to work, so don’t make adjustment within 4 weeks after drug starts
  2. Atovastatin & rosuvastatin have long half-life, can take anytime during day
  3. Side effect: myopathy, if give high dose or take this with other drugs that also effect statin metabolism, such as erythromycin, cyclosporine, azole- anti fungal
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68
Q

Action of bile acid resin

What’s the problem of this drug

A

This drug binds to bile acid and form insoluble complex, then poop out—> this reduce cholesterol return back to liver—> so more LDL receptor in liver available—-> liver takes more LDL—> reduce LDL

  • this drug increases VLDL & increase triglyceride !
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69
Q

Who can’t take bile acid resin

A

Fasting triglyceride >= 300 mg/dL.

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70
Q

Drug interaction of bile acid resin

A

Bill has low thyroid hormone, has infection, and needs vitamin

  • reduce bioavailability:
    A. Thyroid hormone
    B. Fat- soluble vitamins
    C. Antibiotic
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71
Q

What does Niacin do?

A

VII:

  • decrease VLDL synthesis in liver
  • decrease lipolysis in fat tissue
  • increase lipoprotein lipase activity

Final: reduce triglyceride & LDL & cholesterol level

FYI: niacin is just vitamin B. If give 100 to 300 times of recommended daily vitamin dose—> it can improve cholesterol level

72
Q

What’s wrong with Niacin

A
  • little to do with ASCVD
  • many people can’t use this meds (6)
    liver problem, severe hypotension, hyperglycemia, new- a fib, active peptic ulcer, increase uric acid.
  • anyway, not for new a-fib, DM, gout, liver, patients.
73
Q

Risk factors of angina

A 
Nonmodifiable:
1. First relative/ black
2. Age: men> 40yr; women> 65
3. Gender: 
	<65: more men 
	> 65: more women (menopause)
———————————————————
Modifiable:
  1. Smocking: vasoconstriction+ catecholamine release+ increase lipid in blood—> increase LDL, reduce HDL, increase BP, increase platelet formation—> CHD
  2. HTN: high BP—> injury to artery—> CHD
  3. Dyslipidemia: high LDL, low HDL
  4. DM: not sure why, but the risk is equal to hex of MI
  5. Obesity: not sure why, but usually they also have HTN, dyslipidemia, and DM
  6. Lazy lifestyle: should workout at least 5 times a week
74
Q

Difference between stable angina & unstable angina

A
  1. Stable angina: occurs when physical exertion or emotional stress.
    Symptom disappear when rest or nitroglycerin.
    no change in stimulating factor, degrees or duration of chest pain for past 60 days
  2. Unstable angina: doesn’t go away with rest. Increase frequency, duration and severity of chest pain.
75
Q

What’s anginal equivalent

A

Anginal symptoms that are not common anginal symptoms. Unique to that person

76
Q

What’s common angina symptoms

A

Left chest pain
Radiate to back, neck, jaw, throat, arms
Last 1-15 minutes.

77
Q

MI will cause

A

Myocardial infarction causes complete blockage & irreversible ischemia, cause permanent myocardial tissue damage

78
Q

Uncommon cause of angina, and what associated with it. What’s associated with it

A

Coronary artery vasospasm: not sure why, but neurogenic stimulation causes coronary artery smooth muscle to contract—> narrow of coronary artery—> restrict blood supply

Smoking & hyperlipidemia are associated with it

Fat smoker容易抽

79
Q

ACE inhibitor interact with what meds

A

Lithium-> reduce lithium renal excretion—> lithium toxicity

80
Q

What’s treatment for angina

123line of treatment.

A
  1. First line: Beta- blocker
  2. Second- line: If beta- blocker doesn’t work: add calcium- channel blocker or long- acting nitrate
  3. Third- line: usually if patient don’t response to those 2 drugs, refer to a specialist, but can Ca+ Beta+ long acting nitrate
81
Q

Nitrates vs nitrite

A

Both to treat angina:
Nitrite: “Amyl” is inhalation for angina” . “Butyl & Isobutyl” make you high: cause head rush, skin flushing, & muscle relaxation

Nitrates: nitroglycerin. Relax smooth muscle of blood vessel to cause vasodilation. —> increase blood flow.

82
Q

What’s cardiac glycosides

What’s it good for

A

Most well- known and used is digitalis: increase cardiac contraction force—> better emptying heart chambers.

Positive inotropic effect.

Good for CHF, super ventricular tachycardia.

*** in learning activity

83
Q

Who’s good friend with Nitrates? And why

A

Nitrate can cause reflex tachycardia, so cardioselective beta- blocker is good friends with it because it reduce HR & heart contractility. But if use high dose of cardio selective beta- blocker, it will become non cardio selective ! Dose depends on patient’s eGFR

84
Q

What is verapamil

What’s side effect

A

Nondihydropyridine calcium channel blocker:

Reduce both AV, SA conduction, reduce HR, depress contractility

Verapamil’s side effect: constipation

85
Q

How ACE inhibitor & ARB affect preload, afterload, and EF

A

Reduce preload, afterload, and EF

86
Q

What to watch in ACE inhibitor/ ARB

Who can;’t have these

A

K & renal function.

Pregnancy, renal artery stenosis can’t have these.

87
Q

Nitrates
Action.
What’s the end effect of the drug action

A

Dilate coronary artery, peripheral artery, and veins

Reduce LV filling volume, reduce preload & heart workload & more blood can go to myocardium

88
Q

Type of nitrates

A

Fast acting: must be sublingual!
used for acute angina episode. Release symptoms less than 1-5 minutes,repeat dose if not relief within 1-5 minutes.
e.g. nitroglycerin (Nitrostat, Nitroquick), isosorbide dinitrate.

Long- acting nitrates: isosorbide dinitrate & nitro patch or gel
- isosorbide dinitrate: start with 5mg then slowly increase every 1-2 weeks

 - nitro patch: start with 0.2 (5mg), or 0.4 (10 mg). (10-12 hour nitrate free interval)
- nitro gel: apply 1.5 inch ointment to skin before bed. 8-12 hour nitro free interval.
89
Q

Nitrate side effect

A
  • orthostatic hypotension

- reflex tachycardia

90
Q

Nitrate’s drug interaction. Should we stop nitrate suddenly?

A

Never use with phosphodiesterase- 5 inhibitor—> additive hypotension effect

Never sudden stop nitro!

Phosphodiesterase-5 inhibitors are: nafil

91
Q

Does nitro have chronotropic or inotropic action of heart?

A

No. Just vasodilation.

92
Q

Updated beta 1 blocker:

What’s not a complete beta 1 blocker

A

Metoprolol, atenolol, carvedilol, bistro lol, nebivolol

  • labetalol is not a pure beta 1 blocker it also affect alpha 1!
  • and beta 1 blockers are better in lung disease and PVD patients than beta 2 blocker
93
Q

Beta 2 blocker. What are they

A

Non- cardio selective. Block both 1 & 2 :

Propranolol
Naldo lol
Timonolol.

94
Q

Pindolol and acebutolol

A

They have intrinsic sympthomimetic activity: they are beta- blockers but they also activate a more potent catecholamines—> lead to diminished effect on HR & cardiac output. This is good for bradycardia, and heart block patients.

95
Q

Side effect of beta blocker

A 
Bronchoconstriction
Vasoconstriction 
Erectile dysfunction
AV block
Sleep disturbance 
Bradycardia
96
Q

What happen if you stop beta- blocker suddenly?

A

Hypertensive crisis.
Angina, acute coronary insufficiency, even MI

So never stop this drug suddenly

97
Q

Nondihydropyridine (New)

Effects, what are they

A

Vasodilation, slow conduction (AV & SA), reduce HR, reduce contractility.

Verapamil & Diltiazem

98
Q

Anti-platelet agents

A

Aspirin: block prostaglandin synesthesia —> prevent platelet- aggregating substance thromboxane A2
- good for reduce MI by daily aspirin: 75-162 mg/day. > 162 is no good

Plavix: reduce ADP- induced platelet activation

- good choice if patient can’t tolerate aspirin
- 75mg/daily
- better GI tolerance.
- metabolized by 2C19.
99
Q

All the drugs help with angina

A
  1. Beta-blocker (first line)
  2. Calcium- channel blocker
  3. Nitrates
  4. ACE inhibitor/ ARB
  5. anti- platelet
  6. Ranolazine
100
Q

Ranolazine
Action
Drug interaction
When to use it

A

Antianginal drug.

Block Na channel open during hypoxia events, so reduce Ca overload—> reduce heart contractility—-> reduce O2 demand.

Drug interaction: all kinds of 3A4. Inducer & imhibitor

	inducer: dilation, carbapazepam, isoniazid, rifampin, decadron, St. John’s worst
	inhibitor: ketoconazole, itracozazole, clarithromycin, verapamilk, diltiazem
  • increase digoxin level

When to use it: when other drugs aren’t effective alone. Add this.

101
Q

3 classes are best for chronic angina

A
  • beta- blocker
  • calcium channel blocker
  • long- acting nitrates
102
Q

SNS & alpha & beta receptor & its effect

A

SNS: NE/E binds to

- alpha: vasoconstriction
- beta 1: increase heart force & HR
- beta 2: vasodilation.
103
Q

ACE inhibitor is not good for whom (6)

A
  • pregnancy
  • had angioedema during pregnancy
  • renal stenosis
  • acute renal failure
  • black/ indigenous people
  • very old- renal impairment
104
Q

What acute diseases can cause HF.(5)

A
  1. Acute MI
  2. Sepsis
  3. Arrhythmias
  4. Acute myocardial ischemia
  5. Pulmonary embolism
105
Q

What chronic disease can cause HF (8)

A
  1. Alcohol abuse
  2. Liver/ renal disease
  3. Chemo
  4. Heart problems
    • viral myocarditis
    • bacterial endocarditis
    • primary cardiomyopathy
    • cardiac valve disease
  5. Anemia
  6. Thyrotoxicosis甲状腺毒症
106
Q

Drugs that can cause fluid retention

A
  1. Some calcium channel blocker: diltiazem, verapamil, nifedipine. Reduce contractility
  2. Beta- blocker
  3. Steroid
  4. Hormones
  5. NSAID
  6. Sodium- containing drug: carbenicillin, disodium
  7. Lithium
  8. Antihypertensive: hydralazine, nifedipine
  9. Antiarrhythmic: amiodarone, sotalol, disopyramide, flecainide.
  10. Tricyclic antidepressants.
  11. Cardiac toxin: coccaine, amphetamine, doxorubicin, ethanol.
107
Q

HF pathophysiology

Where does cardiac dysfunction happen

A

Heart problem—> not enough blood to tissue or peripheral—> change in lung & peripheral circulation, then body compensate:

  1. Ventricular hypertrophy
  2. Ventricular dilation
  3. Increase preload & afterload
  4. Activate SNS & RAAS

Cardiac dysfunction happens either in ventricular systole (contraction or ejection), or diastole (relaxation or filling).

108
Q

Type of HF

A

Left HF: initially occurs in lung. S3 sound. All about breathing

Right HF: systemic congestion (7):

  1. Peripheral edema
  2. liver congestion
  3. abdominal discomfort (N/V, bloating, constipation
  4. distended jugular veins
  5. portal hypertension
  6. ascites
  7. splenomegaly
109
Q

Stage of HF

A

Stage is all about disease.

A. No heart disease, but a high risk
B. Has heart disease, but no HF
C. Hx of current HF+ heart disease
D. End- stage disease that needs specialized treatment, such as mechanical support, IV inotropic infusion, cardiac transplantation, or hospice care.

110
Q

Class of HF

A

Class is all about symptoms

Class 1: HF symptoms like normal people
Class 2: HF symptoms but ordinary exertion
Class 3: HF symptoms less ordinary exertion
Class 4: HF symptoms at rest

111
Q

Should we encourage HF patients to workout?

A

No heavy workout, but aerobic activity should be encouraged, such as regular exercise, walking, cycling for class 1-2 disease. (Class all about symptoms)

112
Q

What are the drugs treat HF

A 
First- line:
	ACE inhibitor (or ARB) +/ diuretic (depends on fluid retention )

Second- line: ACE (or ARB) +beta- blocker+ diuretic

3rd line: ARB, beta- blocker, aldosterone agonist (spironolactone), diuretic , and digoxin (aabdd)
4th line:
director vasodilator: hydralazine/isosorbide dinitrate (* isosorbide MOnonitrate is not for HF)
Nitrate

No line: new drug: Corlanor

113
Q

ACE inhibitor effect on preload, afterload, EF, cardiac index

A

ACE inhibitor reduce afterload, reduce preload, and increase EF & increase cardiac index

114
Q

If EF< 35%, what drug should be given to treat HF

A

ACE inhibitor

115
Q

ARB’s negative feedback

A

Reduce angiotensin II binds to its receptor-> negative feedback—> increase renin & reduce aldosterone—> reduce water & Na retention —> reduce preload, but can cause small increase in K

116
Q

Patient take ACE inhibitor says no systematic improvement seen, and it has been weeks

A

This drug take several weeks or month to show systemic improvement, if you don’t see any systemic improvement, this drug might have reduced risk the disease progress

117
Q

What’s angioedema

A

Fatal allergic reaction: sudden difficulty breathing, speaking, swallowing, swelling of lips, face, and neck.

118
Q

When to start Ramipril. And what dose

A

A few days after MI

Target dose 5mg BID, reduce to 2.5ng BID if Cr< 25.

119
Q

Lisinopril

A 
Can start 1 day after acute MI
Target dose 10mg OD
Start with 2.5mg, then use 6 week to get to the target dose
If SBP< 120, 2.5mg
If SBP< 90, should be stopped.

Liz is a bitch. Takes forever to get target dose.

120
Q

Trandolapril

A 
Start a few days after acute MI, for stable patients with LV dysfunction.
* good for DM patients,
* reduce proteinuria 
Target dose is 4 mg OD
Start with 1 mg

Trando is stable Diabetic LV dysfunction patient with low protein.

121
Q

Who should take beta- blocker (HF)

A
  • class 2-4 stable patients due to IV dysfunction (EF< 35-40%)
    • ## never use beta- blocker in unstable patients. It’s not a rescue drug
122
Q 
Tell me about carvedilol for HF (8)
Selective or non selective
What benefitS
What to watch for after taking this drug. 
Start dose.
A
  • Non- selective
  • improve exercise tolerance
  • has antioxidant effectL reduce
  • improve insulin resistance—> good for glucose control
  • reduce progress to micro albuminuria
  • this drug can cause fluid retention 3-5 days after this treatment starts, so patient needs to weight themselves
  • watch for light- headed or dizziness 1 hour after take this med
  • start with 3.125 mg BID, then slowly increase over 2 weeks.
123
Q

Who can’t use beta- blocker

A

Bronchospasm disease
Bradycardia
Advanced heart block (if patient has pacemaker can use this drug)

124
Q

Signs of fluid overload

A
  • distended jugular vein
  • 3rd heart sounds
  • pulmonary rale ( rattling lung sounds)
  • dyspnea
125
Q

If patient has severe HF, what drugs should be start right away

A

ACE inhibitor+ beta-blocker+ diuretic

126
Q

Loop diuretic action & who benefits from it

A

Effect loop of Henle, proximal & distal tubules, so loop diuretic is more potent than thiazide diuretic

People with renal impairment & marked fluid retention

127
Q

Lasix

What determines dose
What if patient don’t respond to current dose
How often should adjust dose
What needs to be done

A

Keep increase dose until weight loss & increase urinary output. Weight loss usually is 0.5 to 1 kg per day

20-40mg/ day

If patient don’t respond to treatment:

1. Make it more aggressive: such as IV
2. Add another diuretic
3. Add short- term drug that increase renal flow: dopamine

Dose should be adjusted everyday

Daily weight is important

128
Q

What do you need to watch when start patient on ACE inhibitor & diuretic

A

Don’t start big dose of ACE inhibitor, because ACE inhibitor takes time to show its max effect. (If start big can lead to later hypotension)

129
Q

Diuretic drug interaction

A
  • if pt takes NSAID, increase diuretic

- watch lithium toxicity

130
Q

RAAS chart

A

Hypotension
Hypovolemia—————> renin release—-> angiotensin I—>
Reduce renal flow

-> angiotensin II—-> aldosterone release—> Na & water retention
							I
							I
							I
			Peripheral vasoconstriction
			Norepinephrine release
131
Q

Action of hydralazine/ isosorbide dinitrate
Who benefit it from it

But what

A

Pull blood from venous side of heart to systemic circulation, away from lungs—> so it reduce preload.

Black people who can’t tolerate ACE inhibitor

But!
Hydralazine, prazosin, minoxidil, isosorbide mononitrate are not to treat HF.

But again!
Hydralazine can reduce afterload—> so increase stroke volume & increase cardiac output.

132
Q

What to watch when pt is on hydralazine/ isosorbide dinitrate

A

BP

133
Q

What’s nitrate’s role in treating HF

A

Nitrate alone can’t treat HF

134
Q

Digoxin should be used for what HF patients

A

Class 2 & 3, reduce hospitalization.

Use with ACE inhibitor, diuretic can reduce hospitalization, but not survival rate.

135
Q

For severe HF patients, what’s the best treatment

Especially good for whom?

A 
A combination of 
ACE inhibitor
Diuretic
Beta- blocker 
Digoxin.

Especially good for LV systolic dysfunction due to HF

136
Q

Is digoxin meant to stabilize HF patients?

A

Digoxin alone is not meant to stablize HF patients

137
Q

Digoxin is good for

A

Patient has HF & a- fib.

138
Q

When to check digoxin toxicity

What are the S&S of digoxin toxicity & what diagnostic tests should you order

A

When the steady state reach 1 wk for patient with normal renal function

2-3 week for patient with impaired renal function

S&S of digoxin toxicity: arrhythmia, confusion, nausea, visual disturbance. * people can die from digoxin toxicity

Test: serum digoxin level, ECG, eletrolyte, BUN & creatinine

139
Q

What drugs can increase digoxin level

A
  1. Quinidine
  2. Amiodarone
  3. Spironolactone
  4. Ceramic
  5. Antibiotic (affect gut flora)
  6. Anticholinergic (decrease GI motility)

So if patient use these, decrease digoxin level
Computer sciences QA AA

140
Q

What’s best HF treatment for class I patients

A

ACE inhibitor (or ARB)

141
Q

What’s the best HF treatment for class II patients

A

ACE inhibitor (or ARB) + beta- blocker

142
Q

What’s the best HF treatment for class III patients

A
  1. Aldosterone antagonist
  2. ARB
  3. Digoxin
  4. Hydralazine
  5. Isosorbide
143
Q

What drugs should patient on with MI & reduced EF

A

Beta- blocker & statin

To prevent HF

144
Q

If patient has reduced EF, what drug should patient be on it and why

A

ACE inhibitor or (ARB) to prevent HF

145
Q 
Amiodarone & HF
What is it for
When to use it
Contradicatation
Dosage:
A

Not for treat HF
It’s for treat life- threatening ventricular arrhythmias.
If patient is using other HF drugs (ACE, diuretic…), don’t need this because it has low effacy, only use this when other drugs don’t make improvement.

Contradicatation: hyperthyroidism & advanced liver disease
Maintain Dose: 200-300mg/d

146
Q

Corlanor
What is it
Action

Used for
Drug interaction: say both

A

A new drug to treat HF
Action: reduce pacemaker activity of sinus node by selecting inhibitor If—> reduce HR and that’s it. No effect on preload, afterload, or contractility.

Used for: stable chronic HF with EF<35% with resting HR> 70

Drug intersection: This drug is metabolized by 3A4
3A4 inhibitor increase this drug.
3A4 inhibitor: Azole antifungal, ketoconazole, itraconazole, clarithromycin, HIV inhibitor, diltiazem, verapamil, grape juice.

3A4 inducer: St.John’s worst, dilatin, barbiturate, rifampicin

147
Q

All stable HF patient with LV systolic dysfunction should get

A

Beta- blocker. Doesn’t matter class 1 or 3, once patient gets to class 4 (unstable)—> use ACE + diuretic

148
Q

What’s excitation- contraction coupling

A

The process from membrane depolarization to contraction

149
Q

Ventricular systole

2a. Isovolumetric contraction

A
  1. EDV reached
  2. Ventricular pressure > atrial pressure—> AV valves close—>1st lap sound
  3. Ventricular pressure almost > aortic pressure
  4. Its the later half of QRS
150
Q

Ventricular systole 2b

Ventricular ejection

A
  1. Ventricle pressure> aortic pressure
  2. Semiluninar valves remains open, AV remains close
  3. EDV almost become ESV
  4. Ventricular pressure & aorta pressure reach its peak
  5. From QRS to the first half of T wave
151
Q

Phase 3
Early distole
3a

A

Isovolumatric relaxation

  1. Aortic pressure> ventricular pressure: semilunar valves close: 2nd “dap” sounds
  2. ESV reached because blood get pumped out
  3. Later half of T wave
  4. Dicrotic notch: some blood comes back to aortic. So aortic pressure go up again.
152
Q

Cardiac cycle phases

A 
Phase 1: ventricle filling
	1a: ventricle filling
	1b: atrial contraction
Phase 2: ventricle systole
	2a: isovolmetric contraction
	2b: ventricle ejection
Phase 3: early diastole
	3a: isovolmetric relxation
	3b: ventricular filling
153
Q

3b cardiac cycle

A

Ventricular filing:

  • atrial is filled & is filling ventricle
  • AV opens
  • semi closed
154
Q

How can heart regulates its own pump

A

Pacemaker cells in AV, SA nodes:

  • Na leak channels
  • fast & slow Ca channels
  • K channels
155
Q

What’s cardiac excitation?
How conduction nodes control contraction.
And this also explains what

A

Cardiac excitation is this whole process
SA node—> AV node—> bunch of his—>Bunch branch—> purkinje fibres—> wave of myocardial cells depolarization (through gap junctions)

This also explains why atriam contract before ventricle

156
Q

Equation of cardiac output

A

Stroke volume x HR

157
Q

Afterload work against

A

Peripheral resistance

Aortic diastolic pressure

158
Q

What affect preload, and increase preload means what

A

Preload is affected by filling force applied to heart.
- Frank- Sterling Law: more stretchy, harder the contraction force

Increased preload increase O2 need

159
Q

Frank- starling law

A

Increased End- diastolic volume (volume right before ventricle ejection) leads to increased stroke volume

  • length of heart is proportional to end of diastolic volume

A failing heart can’t do this

160
Q

What determines contractibility

A
  1. Inside of heart:
    • hetermetric: frank starling
    • hemeometric: afterload, HR, flow rate
  2. Outside of heart:
    • nervous:
      SNS: epinephrine & norepinephrine binds to
      alpha 1 receptor ( in blood vessels): vasoconstriction
      beta 1 receptor: (heart & kidney): increase HR & force
      beta 2 receptor (vessel & limbs): vasodilation
      PNS: achtylcholine binds to muscarnic receptor: reduce HR
      • baroreceptor reflex: ( from textbook): baroreceptor are stretch receptors at aortic arch and carotid artery’s. When BP drops, baroreceptor reflex increase HR& force.
    • hormone: thyroid, insulin, glucagon, adrenomedulla, adrenocortisol
    • chemical: PCO2, PaO2.
161
Q

Whst is MAP?
What affect MAP
What does mean arterial pressure tell us
What’s normal MAP

A

Mean arterial pressure: the average pressure in the arteries throughout the cardiac cycle, depends on elastic properties of arterial walls and mean volume of blood in the arterial system
(How stretchy is the vessel & how much water goes through)

It tells us how well we perfuse our body

Normal MAP: 70-110mm Hg

162
Q

Equations of mean arterial pressure (MAP)

What is TPR all about.

A 
MAP= CO x TPR
MAP= (SBP-DBP)/3+ DBP
  • TPR is total peripheral resistance. TPR is all about diameter of vascular system.
163
Q

What’s pulse pressure

A

Difference between systolic & diastolic pressure

164
Q

BP control (when BP is low)

A

Control of BP includes renal and neural.

165
Q

Bottom line of regulation of MAP

A

Cpb

  • control cardiac output
  • regulate peripheral resistance (TPR)
  • change blood volume
166
Q

Layers of artery

A
  • outer: collagen & reticular fibres: tunic
  • middle layer:smooth muscle & collagen, and elastin
  • inner layer: endothelial layer
167
Q

Equation of flow rate (F)

What does this equation tell us

A

F= pressure difference/ pressure gradient
——————————————————-
R (resistance )

Blood flow is proportional to pressure gradient & resistance

168
Q

What causes vasoconstriction

A

SNS
Vasopressin
High O2, low Co2
ADH

169
Q

What causes vasodilation

A

Reduce SNS
Histamine
Heat
Low O2, high Co2

170
Q

What causes hypertension

A
171
Q

How to diagnose HTN

A
172
Q

HTN consequences

A
173
Q

Drugs that increases BP (9)

A
  • contraceptive
  • steroid
  • NSAID
  • some nasal decongestants
  • nicotine
  • appetite suppressant
  • tricyclic antidepressant
  • Venlafaxine (antidepressant)
  • cyclosporine
174
Q

Causes of primary HTN

A

We don’t know the cause for primary HTN
But primary HTN is highly associated with: DM & obesity

Also: SNS, aging, metabolic syndrome (inflammation, dyslipidemia, insulin resistance, glucose intolerance, lipotoxicity)

175
Q

Cause of secondary HTN (7)

A

Secondary HTN means we know the cause, could be:

  1. CKD
  2. Hypothyrodism
  3. Hyperparathyrodism
  4. Sleep apnea
  5. Pheochromocytoma
  6. Medication that causes BP goes up.
  7. Reno- vascular (renal artery stenosis)
176
Q

Ejection fraction
What is it
What’s normal ejection fraction

A

Ejection fraction is the amount of blood ejected per beat

Normal EF for women is 66%+-8%
For men is 58%+-8%

NUR516 Patho & Pharm 1 (3 decks)

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