Clinical Medicine Review Q's (same Q's but via subject) Flashcards

Question

What's the first organ to develop?

Answer 1

b. Positive inotropic effect

Answer 2

voltage gated channels | (insures appropriate ion distribution)

Answer 3

the maximum amount ventricles can pump per minute 250bpm

Answer 4

insures the R-R intervals are the same, if its a regular heart rate

Answer 5

insufficient oxygen to vital organs

Answer 6

shock them- because this condition has a tendency to destabilize quickly

Answer 7

if hemodynamically stable, treat with pharmacotherapy! (except if ventricular tachycardia, then shock them even if they're stable- because they become unstable quick)

Answer 8

false, they're only used in normally structured hearts

Answer 9

c. Atropine

Answer 10

appropriate = due to a secondary reason ex/ exercise inappropriate = no cause

Answer 11

Supraventricular Tachycardia (SVT) also known as paroxysmal supraventricular tachycardia (PSVT) occurs suddenly and stops suddenly. While Sinus Tachycardia occurs slowly and fades slowly.

Answer 12

**AVRT**→ anatomical reentry because of extra conducting tissue that ain't the AV node (bundle of Kent is the conductor) **AVNRT**→ functional reentry that occurs in the structurally normal AV node (the impulse is premature and it causes a circuit- activating the atria and ventricles at the same time + at a faster rate then SA)

Answer 13

young patients

Answer 14

Paroxysmal supraventricular tachycardia (PSVT) **no P waves**, narrow QRS complex, **ST depression**, and regular but **high** heart rate (AVNRT is the most common form of PSVT) \*\* technically you can only say its paroxysmal if you see it going from a normal rate to tachycardia... so this is SVT only

Answer 15

myocardial ischemia/ coronary artery disease (but when its a young patient check PSVT because it also causes ST depression)

Answer 16

carotid massage (because its a vegal maneuver that slows down the AV node) + adenosine (if no difference)

Answer 17

IV Beta Blocker IV Diltiazem (ca channel blocker) IV Verapamil (the goal is to interrupt the circuit at the AV node; Digoxin is also used because it has important parasympathetic effects, on the AV node)

Answer 18

**Radiofrequency Ablation therapy** (aka rhizotomy) which is a type of minimally invasive procedure that uses heat to destroy abnormal tissue

Answer 19

Atrial fibrillation | (more common as age increases)

Answer 20

all cardiac diseases can lead to AF non-cardiac reasons = drugs, alcohol, acute respiratory infections, hyperthyroidism, hormonal diseases

Answer 21

many supraventricular foci, especially at the junction of pulmonary veins

Answer 22

**PSVT** doesn't show the P waves because the QRS complex covers them due to the atrial and ventricles contracting simultaneously. (there technically IS a P wave) **Atrial fibrillation** doesn't have P waves because the atrial doesn't contract (no atrial depolarization), it vibrates instead because of the many activations foci.

Answer 23

False, the condition has varying heart rates. In AF young patients the AV node may conduct many impulses and cause tachycardia, but in AF older patients, the conductivity is reduced and the heart rate may be normal or reduced. (so the only things that confirm AF is irregular R-R's and no P waves, heart rate doesn't play a factor)

Answer 24

blood clots forming in the atria (because they don't contract) that can cause infractions or strokes

Answer 25

Valvular Atrial Fibrillation is when a patient who has _Atrial Fibrillation as well as Mitral valve stenosis_. (both those conditions cause blood to stay in the atria- very high risk of stroke) ## Footnote **Give anticoagulants**

Answer 26

b. Nonvalvular Atrial Fibrillation

Answer 27

b. Nonvalvular Atrial Fibrillation (in Valvular you immediately give anticoagulants)

Answer 28

yes, in males if above 1 then you give

Answer 29

150bpm (300 atrial circuit rate and 2:1 AV physiological block)

Answer 30

no, for women it should be above 2 to administer anticoagulants

Answer 31

Ventricular Tachycardia, with a capture beat (a normal looking SA beat). The ventricles are causing SA suppression, and the capture beat is evidence that the SA node is still functioning and can depolarize the heart.

Answer 32

false, it is regular but the AV node may very in its conductivity. So it can conduct 2 to 1 then change to 4 to 1, which would make the rate appear irregular- that's why we can't use it. (diagnose because of saw tooth appearance only, and it's commonly 150bpm)

Answer 33

ventricular tachycardia, the circles indicate P waves when the SA node was able to depolarize the atria (but it wasn't able to continue down the pathway to the AV node and bundle)

Answer 34

a. atrial flutter | (that's why they give 50J initially)

Answer 35

wide QRS no P waves tachycardia

Answer 36

polymorphic ventricular tachycardia, also called torsades de pointes

Answer 37

ventricular fibrillation

Answer 38

both second degree heart blocks ## Footnote Mobitz I= (PR interval prolonging + QRS missing) Mobitz II= (PR interval constant + a QRS missing)

Answer 39

people with structural heart disease (ex/ **ischemic heart disease**- most likely) and cardiomyopathy patients

Answer 40

b. 1b Lidocaine IV Mexilitine

Answer 41

a. 1a Procainamide IV Quinidine

Answer 42

WPW syndrome/AVRT ## Footnote When an accessory pathway is present, the sinus node action potential can pass through the bypass tract before the AV node, resulting in the ventricles becoming rapidly depolarized. This is termed “pre-excitation” and results in a **shortened PR** interval on the ECG. The typical ECG finding of WPW is **a short PR interval and a “delta wave.“** A delta wave is slurring of the upstroke of the QRS complex. This occurs because the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.

Answer 43

Delta wave is a **slurred upstroke in the QRS complex** often associated with a short PR interval. It is most commonly associated with (due to) **pre-excitation** syndrome such as Wolff-Parkinson-White syndrome.

Answer 44

c. 1c Flecainide Propafenone

Answer 45

1. shock 'em with 100J 2. pharmacological therapy (Procainamide, Sotalol, Lidocaine, Amiodarone) 3. give magnesium sulfate if polymorphic VT 4. correct contributing conditions

Answer 46

Adenosine/Amiodarone Beta Blockers Calcium Blockers (Verapamil, Diltiazem) Digoxin (ABCD)

Answer 47

Beta Blockers Amiodarone Lidocaine Sotalol (BALS)

Answer 48

A condition in which there is an extra electrical pathway in the heart.The most common **mechanism** of tachycardia in patients with WPW is called atrioventricular reentrant tachycardia **(AVRT)**

Answer 49

**Control Rate** with Beta Blockers, Calcium Channel Blockers, Digoxin **Control Rhythm** (AF to Sinus rhythm) with either Electrical or Pharmacological methods. pharma= Propafenone, Flecanide, Amiodarone Or treat permanently with Ablation therapy

Answer 50

sustained= 30 secs or more non-sustained= less than 30 seconds

Answer 51

Paroxysmal nocturnal dyspnea or paroxysmal nocturnal dyspnoea (PND) is an attack of severe shortness of breath and coughing that generally occur at night. It usually awakens the person from sleep, and may be quite frightening.

Answer 52

cold and dry means they have hypoperfusion but are not congested. Give them epinephrine to increase the cardiac output.

Answer 53

they're congested. give diuretics. (if cold and wet, give both diuretics and epinephrine)

Answer 54

Pulmonary edema due to left ventricle systolic dysfunction **Kerley b lines** are seen, indicates interstitial pulmonary edema.

Answer 55

a dilated heart

Answer 56

false, not always. If the systolic dysfunction is acute, the heart may not have has enough time to enlarge

Answer 57

Natriuretic Peptides are high in **heart failure**. They're released with the atrial pressure is high and its dilated, they act to reduce the BP. (by natriuresis- the excretion of sodium by the kidneys)

Answer 58

**anemia**, high HR due to low RBC's delivering oxygen **hyperthyroidism**, can increase the metabolic rate so drastically that the body can't keep up and thus increases HR

Answer 59

Echocardiography classify it into heart failure with reduced ejection fraction OR with sustained ejection fraction

Answer 60

50-75% Ejection Fraction= SV/EDV

Answer 61

They have a filling issue and not a contraction error, so can minimally help them bu giving diuretics, controlling blood pressure, and heart rate.

Answer 62

reduced ejection fraction= dilated cardiomyopathy sustained ejection fraction= Left ventricular hypertrophy

Answer 63

SNS is activated and epinephrine is released to so it increases SV and HR via **beta receptors**. This aids the heart initially, but epinephrine is toxic to myocardial tissue

Answer 64

due to the low CO and reduced renal perfusion, renin is released to increase the BP and volume. This acts to improve the CO initially, but then the volume increases the afterload, which decreases CO furthur.

Answer 65

1- ACE inhibitor→ stop angII synthesis, increase bradykinin 2- angiotensin receptor blocker (ARB's)→ stop the effects of angII by blocking its receptors (AT1) 3- Mineralocorticoid Receptor Antagonist (MRA)→ stop aldosterone from retaining Na and water

Answer 66

false, they act to improve the symptoms (the neurohormonal antagonists are the ones improving survival)

Answer 67

drugs that only improve symptoms (digoxin and diuretics), you give as little as possible

Answer 68

Neurohormonal Antagonists | (they decrease death)

Answer 69

Black Americans (increases their survival rate more)

Answer 70

use angiotensin receptor blockers if ACE inhibitors are intolerated

Answer 71

ACE inhibitors beta-blockers MRA (mineralocorticoid antagonists) (the first 2 are given, then if symptoms persist, MRA's also given)

Answer 72

false, there are four that can be used: bisoprolol, carvedilol, nebivolol, metoprolol succinate XL

Answer 73

give ARNI, a new class of drugs called angiotensin receptor neprilysin inhibitor

Answer 74

made up of Valsartan/Sacubitril Valsartan= angiotensin receptor blocker Sacubitril= neprilysin inhibitor

Answer 75

The natriuretic peptide system and RAAS system Valsartan= angiotensin receptor blocker (↓vasoconstriction) Sacubitril= neprilysin inhibitor neprilysin is an enzyme that deactivates brain natriuretic peptide (BNP; which decreases BP). So if we stop the degradation of BNP we enhance its action.

Answer 76

30 minutes

Answer 77

ST segment elevation myocardial infarction most commonly occurs when thrombus formation results in **complete occlusion** of a major epicardial coronary vessel.

Answer 78

chest pain (severe pressure)

Answer 79

retrosternal Ulnar aspect of left arm Neck Jaw Epigastrium Back (interscapular)

Answer 80

true (ex/ of someone who only has jaw pain)

Answer 81

false, women have a higher chance of having unusual symptoms

Answer 82

unstable angina= less than 30 minutes MI= more than 30 min, severe, high troponin

Answer 83

unstable angina (crescendo angina- escalating angina- and the fact that she has pain while resting indicates this)

Answer 84

chest wall pain/ MSK pain/ costochondritis

Answer 85

aortic dissection

Answer 86

chest wall pain | (MSK)

Answer 87

acute pericarditis

Answer 88

false, 1/3 have a normal ECG (even MI patients may initially present with normal ECG- we treat them and keep checking ECG till we see abnormality)

Answer 89

Modern assays can detect troponins as early as 3-4 hours after onset of myocardial damage. **(the note says 4-6 hours)** **stays elevated for 2 weeks** (this is why we use it to _confirm_ the diagnosis)

Answer 90

elevated troponin levels + _one_ of the following things motion abnormality, myocardial viability, ischemia signs, ST-segment or Q wave abnormalities, thrombus

Answer 91

Renal failure, pulmonary causes, burns, **s**evere illness, **s**troke, **s**ubarachnoid hemorrhage, **s**epsis

Answer 92

Dual Antiplatelet Therapy (Aspirin + P2Y12inhibitors Clopidogrel) this is to prepare the artery for reperfusion

Answer 93

Percutaneous coronary intervention (**PCI** or angioplasty with stent) if that's not possible then fibrinolysis therapy/ thrombolytic therapy

Answer 94

use the Fibrinolytic therapy (aka thrombolytic therapy) Why? the PCI is the best treatment but it must be done within 2 hours- if thats not possible fibrinolytic therapy is the way to go.

Answer 95

travel the five hours for a PCI facility. fibrinolytic therapy is absolutely contraindicated.

Answer 96

stroke or intracranial hemorrhage of unknown cause ischemic stroke less than 6 months ago recent head trauma (1 month) recent GI bleeds noncompressible punctures aortic dissection bleeding disorders

Answer 97

Dual Antiplatelet therapy + Parenteral anticoagulation

Answer 98

if the STEMI went on for 12 hours, the fibrinolytic therapy won't do anything. PCI is the only option.

Answer 99

ACE inhibitor= to treat aldosterone antagonist= secondary prevention drug (if we keep the ejection fraction this low, remodeling will occur to compensate.)

Answer 100

myocardial infarctions that in a Q wave forming on the 12-lead ECG once the infarction is completed. Many **Q-wave infarctions are often non-transmural**, and conversely, transmurality may occur in the absence of Q-waves.

Answer 101

elevated creatinine= renal impairment (maybe due to renal failure, which will increase the risk of MI) elevated glucose= indicates necrosis (higher MI risk)

Answer 102

primary risk prevention is preventing high risk patients from getting the first cardiovascular attack. secondary risk prevention is for patients who already had a cardiovascular attack- we want to prevent further attacks from occurring

Answer 103

low risk =5% or less high risk= 20% or more

Answer 104

false, salt is still a necessary nutrient

Answer 105

false, exercise reduces the risk of cardiovascular disease independently on its affect on weight

Answer 106

b. secondary

Answer 107

aspirin + statin

Answer 108

beta blocker ACEI aldosterone antagonist (Give these when CAD established + less that 40% EF)

Answer 109

aspirin can't be used for primary prevention (due to bleeding risk) statins are used when the patient has an intermediate or high risk (ex/ high LDL + diabetes)

Answer 110

1- left ventricle ejection fraction 35% or less 2- is on optimal medical therapy (OMT) to increase the ejection fraction 3- NYHA Class II or III 4- nonischemic dilated cardiomyopathy

Answer 111

no, you have to wait for at least 40 days after the MI because the ejection fraction may improve with time. If you measure the ejection fraction again after 40 days and it's still below 35%, an ICD is an appropriate secondary prevention.

Answer 112

anticoagulant (atria not contracting, so blood may pool and coagulate in them- then leaving the heart and embolizing in the body)

Answer 113

embolic stroke

Answer 114

- patients who have artificial heart valves - patients who have Valvular Atrial Fibrillation (atrial fibrillation and mitral stenosis)

Answer 115

Atrial Fibrillation with mitral stenosis

Answer 116

the most commonly utilized method to predict thromboembolic risk in atrial fibrillation (stroke risk)

Answer 117

both! but in stable coronary artery disease, the mismatch occurs slowly while in ACS it happens suddenly

Answer 118

fibrous cap= thinner the cap, more vulnerable to rupture lipid pool size= bigger pool size, more vulnerable to rupture more inflammatory cells, the more vulnerable to rupture

Answer 119

mitral regurgitation→ increase contractility→ increases the hearts demand for blood

Answer 120

hypertension → increasing systolic wall tension→ increases demand

Answer 121

a. imaging techniques (imaging techniques based on **perfusion, metabolism or wall motion** are more sensitive)

Answer 122

history! "It is possible to make a confident diagnosis on the basis of history alone"

Answer 123

1-5 minutes

Answer 124

atypical angina (2/3 of the three characteristics)

Answer 125

1. substernal chest pain (quality= heavy, duration=1-5min) 2. provoked by exertion 3. relieved by rest or nitroglycerin

Answer 126

Aortic Stenosis + Hypertrophic Cardiomyopathy both cause obstruction of flow to outside of the ventricle, causing non CAD angina

Answer 127

patients with stable CAD often have normal physical exams and ECG's That's why we do **functional tests**- to provoke cardiac ischemia by stressing the patient. We also have **anatomical tests** (ex/angiography) so we can see the arteries

Answer 128

LVEF is the strongest predictor of long-term survival as **LVEF declines, mortality increases** (Patient with an LVEF \<50% is already at high risk for CV death)

Answer 129

1. Patients with an intermediate pretest probability of IHD (not a high probability- if high then we don't need the test) 2. No major ECG changes or LBBB 3. Are able to exercise

Answer 130

in normal patients= after exercise BP increase ischemic heart= BP decreases because heart doesn't have strength to contract and raise BP

Answer 131

CT angiography= its **less invasive**, so its done for patients with low/intermediate likelihood of CAD- when you're **not certain** Catheter coronary angiography= **more invasive** and involves catheterization, do it when patient has **high CAD risk** or taking optimal medical therapy (OMT) *fails*

Answer 132

1-Risk stratification by clinical evaluation. 2-Risk stratification by ventricular function. **(echocardiogram)** 3-Risk stratification by response to stress testing. 4-Risk stratification by coronary anatomy. **(angiography)**

Answer 133

stress imaging St ress Imaging has advantages over conventional Exercise ECG Test because it can be done even if there are **resting ECG abnormalities** **(**exercise ECG test is done if ECG is normal\*\*\*\*)

Answer 134

1. can be done even with ECG abnormalities 2. can be used if patient can't exercise 3. better sensitivity and specificity 4. can quantify and localise ischemia areas

Answer 135

heart muscle tissue with a good blood flow will emit more gamma rays than areas with a poor blood flow or damaged tissue. So his heart has a good blood supply.

Answer 136

with rest all areas get O2= complete horseshoe with stress= the apex isn't getting enough blood

Answer 137

areas of the heart are given numbers (divided into segments), and when patient is exercising we see how each segment moves. (bad movement means ishemia) hypokinetic means not moving well akinetic means not moving at all

Answer 138

• Nitrates by decreasing systemic will tension

Answer 139

they both **decrease demand** of blood by increasing heart rate and contractility

Answer 140

give OMT (optimal medical therapy) if resistant, revascularize by PCI or CABG

Answer 141

As first-line treatment in patients with : Left main coronary artery disease (50% stenosis or more ). Multivessel disease with severe or extensive ischemia. Left ventricular dysfunction with EF of 35–50

Answer 142

internal mammary artery saphenous vein

Answer 143

higher pain threshold silent episodes reflect less severe ischmia defect in pain preception

Answer 144

managed as angina

Answer 145

false, LA adapts to the larger volume by **dilating**, which increases its **compliance**. This remodeling helps to limit the increases in LA pressure initially- but after a while it can't keep up and pulmonary congestion occurs.

Answer 146

It undergos Calcification

Answer 147

Rheumatic Fever, Trauma, infective endocarditis

Answer 148

Ischemia, LV dilatation

Answer 149

mitral regurgitation→blood leaks from LV to RV→RV has higher pressure→RV dilates to compensate→LV volume overload→ hyperdynamic LV→progressive LV dilation→ to heart failure

Answer 150

**left atrial pressure**= increases because the regurgitated blood causes an increase in volume; since its acute, the right atrium has no time to dilate (to compensate) **ejection fraction**= it increases due to the increase in total stroke volume. The regurgitated blood causes an increase in preload, leading to a hyperdynamic state-\>SV increase

Answer 151

**left atrial pressure=** it's *_slightly_* elevated. The left atria had time to dilate and accommodate the regurgitated blood, leading to a decrease in pressure (**LAP is less than LAP in acute regurg.**) **ejection fraction=** high because the heart is pumping harder to provide adequate blood to body-\> high total stroke volume -\> high EF

Answer 152

**left atrial pressure=** high because the atria dilated to it's max **ejection fraction=** low because the ventricle is dilated further due to the high pressure and now has a weak pump

Answer 153

Echocardiogram

Answer 154

Valve repair= artificial annulus (stop dilation) + stitch leaflets to repair them (this is the preferred surgery) Valve replacement= remove old and put a new artificial valve

Answer 155

due to stenosis, the blood gradient has to be high between atria and ventricle for the blood to pass through the stenotic valve. higher gradient means increased velocity, and that also means turbulent flow. this has a mosaic appearance in echo.

Answer 156

when patient is **S**ymptomatic and if the valve infection **S**evere (2 conditions)

Answer 157

The ECG in mitral stenosis is often normal early in disease. The most common finding is left atrial enlargement **(p-mitrale)**(however this finding disappears if the patient enters atrial fibrillation\*\*) Right heart strain may produce findings of **right axis deviation** (and _right ventricular hypertrophy_) ## Footnote **\*\*=**valve stenosis is linked to a higher risk for atrial fibrillation

Answer 158

Diuretics, ACE-I, warfarin (AF)

Answer 159

Rheumatic fever (99%)

Answer 160

5cm squared (has to get to 2 to produce symptoms; if 1cm or smaller then its severe mitral stenosis)

Answer 161

Mitral stenosis= only L atria Mitral regurgitation= both LV and LA

Answer 162

warfarin, control heart rate

Answer 163

by relieving the obstruction via **Trans-septal balloon valvotomy** OR **Mitral valve replacement**

Answer 164

The valve obstruction does not allow CO to increase during exercise

Answer 165

stenosis causes left ventricular hypertophy→thick wall more susceptible to ischemia→ arrythmias→ heart failure

Answer 166

developed countries

Answer 167

similar to those for vascular atherosclerosis: elevated LDL cholesterol, diabetes , smoking, hypertension

Answer 168

False, Calcific aortic stenosis has a 50 % increased risk of cardiovascular death and myocardial infarction **even in the absence of valve obstruction**

Answer 169

false, it's non-invasive (done by catheter)

Answer 170

false, Usually functions normally in childhood. the abnormal structure causes stress which leads to calcifications later on (40's+)

Answer 171

true 4:1 ratio

Answer 172

**Medial degeneration** (damages connective tissue and results in the breakdown or destruction) **Aortic aneurysm** **Aortic Dissection** (rare)

Answer 173

Rheumatic valve disease (can involve all left heart) (If mitral stenosis **alone**—\> mitral valve disease)

Answer 174

the symptoms are the best indicator no symptoms= good prognosis symptoms=dismal prognosis

Answer 175

1. chest pain * no blood in aorta, no blood in coronary arteries 2. syncope * no blood reaching brain 3. dyspnea * indicates heart failure= the worst symptom

Answer 176

mean pressure gradient the higher it is, the more severe the stenosis

Answer 177

Marfan syndrome: **beta-blockers** (may slow aortic root dilatation) Hypertension, LV dysfunction when surgery is contraindicated or LV dysfunction persists: **ACE, ARB**

Answer 178

no medical treatment, just replace the valve via" ## Footnote **Transcatheter Aortic-Valve Implantation (TAVI)**

Answer 179

adjust lifestyle (no vigorous physical activity) observe clinically and by echo prophylaxis for rheumatic fever (penicillin) and infective endocarditis (good hygine)

Answer 180

1. age-related (degenerative) aortic dilation 2. cystic medial necrosis of the aorta (Marfan’s)\*\*\* 3. Syphilitic aortitis 4. Ankylosing spondylitis ## Footnote \*\*\* cystic medial necrosis= accumulation of basophilic ground substance in the media with cyst-like lesions

Answer 181

for Cardiac Output to be maintained, total volume pumped into aorta must increase, leading to **_LV dilatation_**

Answer 182

aortic stenosis→ hypertrophy aortic regurgitation→ dilation

Answer 183

Mitral regurgitation and aortic stenosis—\> systolic murmurs Mitral stenosis and aortic regurgitation—\> diastolic murmurs

Answer 184

aortic regurgitation= prominent carotid pulsations aortic stenosis= low/little carotid pulsations

Answer 185

**Symptomatic + severe** —\> surgery Either repair or replacement but *mostly replacement.*

Answer 186

metabolically inactive myocardium (not dead, so if you improve the circulation to it, it gets activated)

Answer 187

used to prevent **ventricular arrhythmia** (the most common cause of sudden death). So we give them to patients with a reduced ejection fraction *(below 35%)* because we want to reduce the chance of sudden cardiac death. (the device senses **ventricular arrhythmia** and sends a shock to the heart)

Answer 188

For patient with electrical dissociation (ex/ right or left bundle branch block). So when the ventricles aren't contracting at the same time, the CO and ejection fraction decreased. This therapy makes the heart a new conduction system via wires. This is only used when conventional therapy fails and the ejection fraction is less than 25% or QRS complex is wide.

Clinical Medicine Review Q's (same Q's but via subject) Flashcards

Clinical aspects of hypertension (1-23) Cardiac arrhythmias (24-87) Heart failure (88-119) Acute coronary syndromes (120-148) Prevention of cardiovascular disease (149-163) Chronic ischemia (164-197) Valvular heart disease (198-247)