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Boards 23' > Respiratory/Cardio > Flashcards

Respiratory/Cardio Flashcards

1
Q

Chinese adult presents with cervical lymphadenopathy gets biopsy and shows pleomorphic keratin-positive epithelial cells in a background of lymphocytes. What disease comes to mind and what is it commonly associated with?

A

Nasopharyngeal carcinoma (squamous cell carcinoma) - malignant tumor of NP; associated with EBV

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2
Q

Most common bug that causes rhinitis (common cold)?

A

RSV according to uWorld

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3
Q

most common cause of acute epiglottis in immunized and non-immunized children?

A

H. influenza b

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4
Q

Laryngotracheobronchitis

A

Croup; inflammation of upper airway; parainfluenza (paramyxovirus) most common cause; presents with hoarse ‘barking’ cough and inspiratory stridor

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5
Q

two major mediators behind pleuritic chest pain from pneumonia?

A

bradykinin and prostaglandin E2, inflammation of lung parenchyma, every time lung stretches with breathing it irritates the pleura and results in pleuritic chest pain

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6
Q

What are the two most common causes of lobar pneumonia?

A

Streptococcus pneumoniae (95%) and Klebsiella pneumoniae

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7
Q
A

lobar pneumonia; commonly caused community acquired pneumonia by streptococcus pneumonia

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8
Q
A

interstitial (atypical) pneumonia

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9
Q
A

interstitial (atypical) pneumonia on biopsy

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10
Q

What is the most common cause of interstitial (atypical) pneumonia?

A

Mycoplasma pneumoniae; typically affects young adults (military recruits/students living in a dormitory); complications include autoimmune hemolytic anemia (IgM) which causes cold hemolytic anemia and erythema multiform; not visible on gram stains due to lack of cell wall

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11
Q

Bug that causes an atypical pneumonia that is seen in veterinarians and farmers and causes a HIGH fever (Q fever)?

A

Coxiella burnetii

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12
Q

Primary TB

A

inhalation of aerosolized Mycobacterium tuberculosis; focal caseating necrosis of lower lobe of lung and hilar lymph nodes; foci undergo fibrosis and calcifications and forms ghon complexes; often asymptomatic but has a positive PPD

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12
Q

Primary TB

A

inhalation of aerosolized Mycobacterium tuberculosis; focal caseating necrosis of lower lobe of lung and hilar lymph nodes; foci undergo fibrosis and calcifications and forms ghon complexes; often asymptomatic but has a positive PPD

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13
Q

Secondary TB commonly arises due to what 2 things?

A

AIDS and aging; primary TB is usually asymptomatic with a positive PPD; but secondary is symptomatic

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14
Q

primary TB v. secondary TB with area of lung affected?

A

1 - lower lobes with Ghon complexes

2- apex of the lung (oxygen tension is highest at the apex)

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15
Q

lung biopsy of pt with secondary TB?

A

caseating granulomas and AFB stain with red acid-fast bacilli

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16
Q
A

AFB stain with red acid-fast bacilli as seen in secondary TB

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17
Q

What is the most common organ affected by TB in systemic spread?

A

kidneys; results in sterile pyuria

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18
Q
A

pulmonary TB; stimulation of CD4 T lymphocytes releasing interferon gamma; form multinucleated Langerhans giant cells; center of the granuloma will be caseating “cheese-like”

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19
Q
A

pulmonary TB; stimulation of CD4 T lymphocytes releasing interferon gamma; form multinucleated Langerhans giant cells; center of the granuloma will be caseating “cheese-like”

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20
Q
A

pink PAS+ globules; built up A1AT in hepatic cells in a pt with A1AT deficiency; results in panacinar emphysema; warn pt against smoking

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21
Q

What is the only pneumoconiosis with increased risk for TB?

A

Silicosis

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22
Q
A

lung biopsy showing asbestosis bodies; long rod-shaped particles with round brown deposits (iron); seen in asbestosis pneumoconiosis

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23
Q
A

air sacs of the lung lined by hyaline membrane as seen in ARDS due to alveolar-capillary damage (leaking)

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24
Q
A

grainy/hazzy appearance of the lung that is characteristic in a neonate with RDS; “diffuse granularity” or “diffuse atelectasis”; decrease type II pneumocystis that produce surfactant

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25
Q
A

adenocarcinoma of the lung; located at the periphery (contrast to central with small and squamous); increased mucus and glands; seen in females nonsmokers

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26
Q
A

normal lung on R; left shows a collapsed lung and thorax full of air as seen in a spontaneous pneumothorax; note that trachea deviates to the side of the collapse

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27
Q
A

thickening of the pleura that encompasses the lung as seen in mesothelioma; malignancy of the pleura; asbestos exposure is a high risk factor; histology: spindle cells; immunohisto: cytokeratins that are calretinin positive and EM will show abundant tonofilaments

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28
Q

Which pathology of the premature newborn is consistent with a continuous murmur and bounding peripheral pulses?

A

Patent ductus arteriosus; left to right shunting increases blood return to the left atrium; decreases systemic vascular resistance; increase in stroke volume and cardiac output causes increased pulse pressure (large differences between diastolic and systolic pressure) leading to bounding pulses

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29
Q

What immune cells are the key players in the formation of lung abscess?

A

neutrophils; they release cytotoxic granules

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30
Q

Which vein has the most de-oxygenated blood?

A

the coronary sinus

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31
Q

NO increases which secondary messenger to promote vasodilation?

A

cGMP

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32
Q

Effects of cocaine on the heart?

A

causes coronary artery vasoconstriction (alpha adrenergic receptors) which leads to decreased coronary O2 supply by also increasing the O2 demand of the heart via tachycardia and increased contractility leading to an acute MI

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33
Q

Changes in ATP level during an acute MI?

A

depleted ATP in cardiac myocytes IMMEDIATELY (w/I seconds); immediately w/I seconds, ischemic MI switch from aerobic to aerobic glycolysis leading to depleted ATP; you can see myofibril relaxation leading to the ventricle not wanting to move (constrict) and a drop in cardiac output

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34
Q

Reversible cell injury (early pathological changes in an MI)

A

cellular and mitochondrial swelling, glycogen depletion and clumping of chromatin (under 20-30 mins)

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35
Q

Irreversible damage

A

mitochondrial vacuolization or membrane rupture (more than 20-30 mins); cells will release their contents - troponin I and CK-MB

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36
Q

Stunned myocardium

A

delay in time before the myocytes become back to normal after reversible injury; viable myocytes do not immediately return to full activity) lasts a few hours to days after reversible myocardia injury (reperfusion)

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37
Q

Reperfusion injury

A

restoring blood flow to ischemic areas can damage it even more; adds more calcium and induces hypercontracture - cells become stuck in a contracted state; also free radicals can build up and induce further damage to surrounding myocytes (more inflammatory cells - destroying other myocytes)

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38
Q

ischemic cardiomyopathy

A

chronic ischemic heart disease leads to progressive heart failure; longterm subclinical ischemia; usually a hx of MI, evidence of “patchy fibrosis” leading to systolic heart failure (contraction phase)

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39
Q

CAD

A

coronary artery disease; atherosclerotic plaque in one or more coronary arteries leading to decreased coronary blood flow and ischemic injury of myocytes

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40
Q

Risk factors for CAD?

A

obesity, smoking, hyperlipidemia

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41
Q

Stable angina

A

FIXED coronary plaques causing >70% stenosis (anything under is asymptomatic) will present with chest pain during exertion or when emotionally stressed; radiates to left arm or jaw; improved with rest and nitroglycerin; lasts under 30 mins; reversible injury

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42
Q

Which zone gets injured first during stenosis of coronary arteries?

A

subendocardial zones (furthest away)

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43
Q

Nitroglycerin

A

increases vasodilation (mostly veins) and decreases venous return to the heart and decreases the preload/workload

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44
Q

recurrent episodes of chest pain that occur at random intervals unrelated to exertion or stress. “Hey doc I get these random chest pains, I’m not really doing anything when it happens, sometimes even at 2am.”

A

vasospastic angina also called prinzmetal angina; smooth muscle hyperactivity in the coronary wall; risk factor of smoking; encourage pt to quit

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45
Q

ACS

A

acute coronary syndrome - umbrella term for three conditions - unstable angina, NSTEMI and STEMI

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46
Q

unstable angina

A

chest pain at rest, needs an immediate work up; high risk for MI

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47
Q

NSTEMI

A

non-ST elevation MI; you can see ST depression (subendocardial injury)

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48
Q

STEMI

A

ST elevation on EKG; very bad occlusion causes a transmural injury (epi, myo and endo) fully occlusive thrombus leading to a full thickness infarct; EKG would show hyperacute T waves with “tombstone” shaped ST segments; negative Q waves and then T waves becomes inverted; watch for a later onset of left bundle branch block LBBB due to non-functioning ventricle (LAD is commonly affected artery)

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49
Q

What are the two types of MI?

A

Non-ST elevation MI = NSTEMI
ST elevation MI = STEMI

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50
Q

What is the most sensitive and specific cardiac enzyme in irreversible cell injury?

A

Tropinin - more sensitive
(stays high for 7-10 days so CK-MB is more specific for 2nd in 3 days or 72 hrs)

Tropinin I - more specific
Tropinin T - more sensitive (has a T)

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51
Q

LAD occlusion MI

A

ischemia of the LV and anterior 2/3rds of the inter ventricular septum and apex; can knock out LV function

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52
Q

s4 heart sound

A

abnormal regardless of patient age; occurs in late diastole “atrial kick” best heard at the apex in a lateral decubitus/recumbent position; associated with LV non compliance (a stiff ventricle); LAD occlusion causing depleted ATP of LV (relaxation); can lead to cardiogenic shock - sudden death!!

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53
Q

RCA occlusion

A

affects the SA and AV nodes (pacemakers of the heart) can lead to bradycardia, heart block and sick sinus syndrome; also supplies the RV, posterior 1/3rd of the interventricular septum and posterior LV; leads II, III and aVF

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54
Q

pt with crushing chest pain, ST elevation on ECG and some lung findings what should you think of?

A

Left sided infarction (commonly LAD is involved)

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55
Q

pt with sudden chest pressure, nausea, bradycardia or heart block what should you think of?

A

Right sided infarction (RCA - gives rise to the posterior descending artery); may also mention JVD; inferior leads of the ECG (II, III and aVF**)

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56
Q

0-4 hours following a MI

A

NORMAL microscopic or gross changes

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57
Q

4-12 hours post MI

A

wavy fibers on histology; dead and non-contractile muscle fibers, edema and punctate hemorrhaging and can start seeing coagulative necrosis

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58
Q

12-24 hours post MI

A

dead cells without nuclei, contraction band necrosis; Ca2+ entering dead cells causing contraction

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59
Q

1-3 days post MI

A

first responders neutrophils are in abundance (infiltrating blue cells); whitish tan; watch for early onset fibrinous pericarditis (only in transmural MI)

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60
Q

your pt is 3 days post MI and onset of chest pain, but the pain is sharp and not dull like how they came in. Pain increases every time the pt swallows or takes a deep breath. Pain is better when the pt leans forward.

A

pleuritic chest pain that is worse on inspiration and better when leaning forward; caused by early onset pericarditis; a couple days post MI due to neutrophils going into the necrotic tissue; usually short lived and relieved with asprin

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61
Q

3-14 days post MI

A

macrophages are predominate; granulation tissue - precursor to scar tissue; watch for ruptures:

  • papillary muscle rupture = mitral regurg happens; holosystolic blowing murmur that radiates to the left axilla; solely supplied by the posterior descending artery
  • septum rupture; supplied by the LAD; immediate R to L shunting (holosystolic murmur)
  • LV free wall rupture; LCA occlusion; can lead to cardiac tamponade - blood collecting in the pericardiac sac; muffled heart sounds, JVD and systemic hypotension
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62
Q

holosystolic blowing murmur that radiates to the left axilla is indicative of what kind of murmur?

A

mitral valve regurgitation (mitral insufficiency); can occur with papillary muscle rupture 3-14 days post MI

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63
Q

the papillary muscle of the LV is solely supplied by which artery?

A

posterior descending artery a branch off the RCA; posterior medially papillary muscles

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64
Q

blood collecting in the pericardiac sac; muffled heart sounds, JVD and systemic hypotension

A

LV free wall rupture 3- 14 days post MI due to a LCA occlusion; cardiac tamponade

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65
Q

after 14 days post MI

A

scar formation; can cause fatal ventricular arrhythmias leading to sudden cardiac death

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66
Q

weeks to month post MI

A

myocardial scar formation can lead to an aneurysm (ballon-like dilation) floppy failing heart balloon

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67
Q

Dressler’s syndrome

A

late onset pericarditis (6 weeks later) pt has pleuritic chest pain; delayed response due to antibodies (IgG) exposed in the pericardium

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68
Q
A

histology of the lung showing hemosiderin-laden macrophages AKA heart failure cells; typically seen with LHF, pul edema causes increased blood to be in the pulmonary circuit and rupture blood vessels causing increased blood into the alveoli and macrophages phagocytosing the RBC and having a buildup of iron.

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69
Q

How can systolic heart failure be assessed?

A

Ejection fraction measures the heart ability to pump (SV/EDV); will be lowered with systolic heart failure (ex dilated cardiomyopathy - all 4 chambers are dilated and pumping ability is decreased)

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70
Q

Ejection fraction measurement?

A

stroke volume divided by the end-diastolic volume (SV/EDV); how effective it the heart is at pumping blood out during systole; normal is 55-80%; pathological under 40%

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71
Q

systolic heart failure

A

heart is unable to contract and pump out blood effectively; emptying problem (ex. dilated cardiomyopathy)

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72
Q

diastolic heart failure

A

the heart is unable to fill appropriately; filling problem (ex. restrictive cardiomyopathy) - reduced ventricular compliance; can pump out blood just fine; heart failure with preserved ejection fraction (55-80%)

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73
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

A

ventricular septum hypertrophy causes diastolic heart failure; the inability to appropriately fill the heart because a big bulky septum in the way

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74
Q

Constrictive pericarditis

A

the pericardium becomes somewhat fibrosis and restricts the heart from filling due to a non-compliant ventricle; can cause diastolic heart failure

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75
Q

eccentric hypertophy

A

caused by VOLUME overload (increased preload) causes a dilated cavity

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76
Q

concentric hypertophy

A

caused by PRESSURE overload (increased afterload) causes a more restricted cavity due to wall thickness

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77
Q

ANP

A

atrial natriuretic peptide (ANP) released by stretched cardiomyocytes in the atria (increased preload); MOA is the decreased afterload by promoting vasodilation (decreases SVR) and decreases preload by promoting salt excretion (natriuresis/diuresis) by decreasing aldosterone and decreased renin

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78
Q

BNP

A

brain natriuretic peptide (BNP) released by stretched cardiomyocytes in the ventricles (increased preload); MOA is the decreased afterload by promoting vasodilation (decreases SVR) and decreases preload by promoting salt excretion (natriuresis/diuresis) by decreasing aldosterone and decreased renin

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79
Q

How does the body try to compensate for low CO?

A

release of EPI to get the sympathetic going (increase HR and increased SVR via vasoconstriction) and activation of RAAS to increase aldosterone release to increase salt and water retention and increased ADH release to retain free water

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80
Q

Orthopnea

A

SOB when laying flat; “hey doc everytime I lay down it feels like I’m drowning” can be due to left heart failure that has backed up into the pulmonary circuit causes pulmonary congestion/edema

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81
Q

paroxysmal noctural dyspnea

A

waking in the middle of the night due to SOB “gasping awake”; can be due to laying flat with left heart failure

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82
Q

bibasilar inspiratory crackles

A

sign of pulmonary edema/congestion caused by left heart failure, blood backflows into the pulmonary circuit and goes into the base of the lungs (crackles - fluid into the interstitium)

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83
Q

chest x-ray findings for left heart failure?

A

diffuse vascular congestion “cephalization” of the pulmonary vessels (pulm vessels more defined compared to normal); fluffy b/l “batwing shaped” opacities and Kerley B lines indicating fluid accumulation between lobes; air bronchograms (dark airways); and an enlarged cardiac silhouette indicating cardiomegaly (takes up more than half of the thorax)

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84
Q

heart sounds in a pt with left heart failure?

A

S3 (S2/S3 gallop) - more common in systolic heart failure (comes right after s2) as blood comes back down from not being able to be ejected from the ventricles

S4 - more common in diastolic heart failure (comes right before S1) as blood is pushed against a stiff wall; occurs during the “atrial kick”

mitral regurg - systolic murmur; due to dilation of the mitral annulus

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85
Q

cor pulmonale

A

right heart failure caused by pulmonary HTN

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86
Q

heart sounds in a pt with right heart failure

A

tricuspid regurg due to dilation of tricuspid annulus; systolic murmur

Kussmaul sign - JVD increases during inspiration seen in RHF

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87
Q

Kussmaul sign

A

JVD increases during inspiration seen in RHF

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88
Q

Which zone of the liver is affected the most in right heart failure?

A

centrilobular zone (zone 3) necrosis due to hepatic venous congestion in RHF; “nutmeg liver”

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89
Q

cardiomyopathies

A

myocardial diseases resulting in cardiac dysfunction; dilated cardiomyopathy is the most common form

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90
Q
A

dilated cardiomyopathy, dilatation of all 4 chambers of the heart; results in a systolic dysfunction (not able to pump/contract appropriately)

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91
Q
A

lymphocytic infiltrated with cardiomyocytes as seen in myocarditis most commonly caused by coxsackie b virus; late complication of dilated cardiomyopathy

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92
Q

What is the most common cause of sudden death in young athletes?

A

ventricular arrhythmias due to hypertrophic cardiomyopathy; diastolic heart failure, inability to fill the lungs results in a decreased CO; genetic mutation in sarcomere proteins (AD inheritance)

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93
Q
A

myofiber hypertrophy with disarray; fibers are not organized neatly in parallel but are going in various directions; histological hallmark in hypertrophic cardiomyopathy

94
Q

What is the histological classic finding in hypertrophic cardiomyopathy?

A

myofiber hypertrophy with disarray; fibers are not organized neatly in parallel but are going in various directions

95
Q

30 yr old pt with flu-like symptoms (fever, runny nose, myalgia) experienced last week and now presents with acute left heart heart failure symptoms what should suspect?

A

pt is too young for heart failure; you should suspect dilated cardiomyopathy caused by acute myocarditis (coxsackie b virus)

96
Q

a holosystolic murmur at the apex of the heart that radiates to the axilla

A

consistent with mitral regurgitation; S3 gallop heart sound “slush3” right after the S2 heart sound of blood coming back down into the ventricles;

97
Q

crescendo - decrescendo systolic murmur best heard at the left sternal border

A

systolic murmur heard in between S1 and S2

98
Q

Positions that increase murmur sounds in HOCM?

A

hypertrophic obstructive cardiomyopathy (HOCM); standing and straining - valsalva and standing decreases preload, higher degree of LVOT obstruction which increases murmur intensity

99
Q

Positions that decrease murmur sounds in HOCM?

A

leg raise (when supine) and squatting increase preload and LV size causes a smaller degree of LVOT obstruction which decreases the murmur intensity; also maneuvers that increase afterload (sustained handgrips) will have a quieter murmur

100
Q

pericarditis

A

inflammation of the pericardium of the heart

101
Q

pt with elevated BUN with chest pain

A

uremia can be a cause of acute pericarditis

102
Q

malignant pericarditis

A

malignancy from another organ (breast, lung) can manifest as pericardial effusion or cardiac tamponade

103
Q

Pericarditis

A

usually idiopathic, but if a causative agent then most likely viral; pt with flu-like/respiratory or GI symptoms last week and now experiences chest pain = think viral pericarditis

104
Q

Symptoms of pericarditis

A

sharp pain in the anterior chest that is provoked by swallowing or deep breath (inspiration) and better when leaning forward = pleuritic chest pain; can hear pericardial friction rub on auscultation; it does NOT disappear when you hold your breath but a pluera friction rub will dissappear when the lungs aren’t moving

105
Q

Pt with pericarditis ECG

A

ST elevations (same as MI); but has more slopping concave shape and “ tombstones” and should be seen in ALL leads not just a few

106
Q

Cardiac tamponade beck’s triad

A

muffled heart sounds, hypotension and JVD - decreased CO increases venous return and RA pressure; can lead to cardiogenic shock (heart that can’t fill, can’t pump)

107
Q

Pulsus paradoxus

A

occurs in cardiac tamponade; increased venous return during inspiration increases RA/RV volume; interventricular septum is pushed into the LV (decreasing chamber size) decreased SV and CO; you will see a >10 mm drop in SBP on inspiration (check radial pulse and it will be undetectable)

108
Q

inspiration has what effect on venous return to the heart?

A

increases; increased RA pressure as well

109
Q

Constrictive pericarditis

A

scarring and fibrosis from the pericarditis can leave the pericardium stiff and non-distensible leading to limited expansion during diastole; shows a prominent Y descent on jugular venous waveform (due to rapid atrial emptying)

110
Q

Which chamber of the heart is most anterior to the chest wall?

A

the right ventricle; it is most likely to be injured to a penetrating trauma that goes through the chest wall at the 4th intercostal space near the sternum on the right side.

111
Q

Which chamber of the heart is located most posterior and lies near the esophagus?

A

the left atrium; if becomes enlarged it can compress the esophagus and cause dysphagia

112
Q

Where would cardiologist like to place an TEE ultrasound to get pictures of the heart?

A

in the esophagus; located between the left atrium of heart and the aorta making it ideal for pictures of the valves and chambers; TEE = transesophogeal echocardiogram

113
Q

90% of people are born with what dominance of the heart?

A

right dominance (10% = left dominant)

114
Q

What is the factor that indicates if someone is R or L dominant in the heart?

A

if the PDA branches off the RCA then they are right dominant (90%)

if the PDA branches off the left circumflex artery then they are left dominant (10%)

PDA supplies inferior wall of the LV

115
Q

Through which vessel does the heart drain?

A

drains to the coronary sinus to the right atrium

116
Q

What major artery does the coronary arteries branch from?

A

the aorta; to supply the heart

117
Q

What are the two major branches of the aorta that supply the heart?

A

the RCA (supplies the right ventricles)

the left main coronary artery - bifurcates into the LAD (supplies the anterior wall of the LV and the interventriulcar septum) and the left circumflex artery (supplies the left lateral wall)

118
Q

When would someone be considered to have a left dominant heart?

A

if the PDA branches from the left circumflex artery

119
Q

What can cause an enlarged or dilated coronary sinus?

A

anything that raises the pressure in the right atrium; the coronary sinus feeds into the right atrium with other venous blood

120
Q

Which vessels supply which walls of the LV?

A

LAD - anterior walls, anterior septum and apex (the words has anterior in it!!)

LCX - lateral wall

PDA - inferior wall, inferior septum (RCA in 90% of people but LCX in 10% of people)

121
Q

Which muscle left ventricle is most vulnerable to ischemia and has the potential to cause a severe mitral regurgitation?

A

the posteriomedial papillary muscle; it only has a single blood supply (RCA in R dominant people 90% and LCX in left dominant people); an interior infarction can lead to rupture of the PM and lead to severe mitral regurg and heart failure

122
Q

Blood supply of the SA and AV nodes/

A

Right coronary artery; SA is on the wall in the RA; AV node is in the interatrial septum

123
Q

the systolic blood pressure is largely determined by what?

A

by stroke volume (EDV-ESV)

124
Q

the diastolic blood pressure is largely determined by what?

A

by TPR (total peripheral resistance); if vasodilator then will fall and have a low DBP; if vasoconstrictor then will not fall low and will be high and have a high DBP

125
Q

pulse pressure

A

the difference between systolic and diastolic pressure (norm pt 120 - 80 = 40 mmHg); should be proportional to SV

126
Q

MAO

A

DBP + 1/3 (SBP-DBP)
DBP + 1/3 (Pulse pressure)

ex. BP 120/80
80 + 1/3 (40) = 93.3 mmHg

127
Q

What are the 4 determinants of CO?

A

preload (more = more CO), after load, contractility and HR (NOT TPR!)

128
Q

Ways to increase preload

A

add volume (blood transfusion or IVF)
slow the HR (allows for more filling)
*constrict the veins (increase venous return to the heart - sym via alpha 1 adrenergic receptors)

129
Q

What are two ways that increase the after load in the LV?

A

when blood pressure is high (chronic HTN pts) - heart has to increase pressure to open the aortic valve to push blood into the aorta (hard to do when the pressure on the other side is high) and when there is aortic stenosis, the valve is narrowed and unable to open fully OR pts with hypertrophic cardiomyopathy

130
Q

How does pulse pressure change with age?

A

increases; also increases in hypertensive pts (increased resistance = decreased compliance = increased in PP)

131
Q

What is the most important baroreceptor?

A

the carotid sinus (CN IX) - senses both low and high blood pressure (unlike the aortic arch (CN X) which only senses high blood pressure)

132
Q

PV loop change in a pt with chronic HTN?

A

increased after load

133
Q

PV loop change in a pt with LV hypertrophy?

A

decreased compliance

134
Q

PV loop in aortic stenosis?

A
135
Q

PV loop in mitral regurgitation

A

isovolumic contraction is disrupted

136
Q

PV loop in aortic regurgitation

A

isovolumic relaxation is disrupted

137
Q

PV loop in mitral stenosis

A
138
Q

S1 and S1 heart sounds on Wigger’s diagram?

A
139
Q

Wigger’s diagram of a pt with aortic stenosis?

A

LV pressure has to get really high to push open the aortic valve (increased after load)

140
Q

Wigger’s diagram of a pt with mitral stenosis?

A
141
Q

Wigger’s diagram of a pt with mitral regurgitation?

A
142
Q

Wigger’s diagram of a pt with aortic regurgitation?

A

very wide pulse pressure which is seen in aortic regurgitation

143
Q

Arteriosclerosis

A

HARDENING of the arteries; common due to long standing HTN; causes changes of hyaline and hyper plastic

144
Q

Atherosclerosis

A

plaque accumulation and lipoproteins (LDL) in the intima layer; involves macrophages (foam cells)!!; narrows artery walls; smooth muscle proliferate in intima PDGF - key factor

145
Q

Which arteries are most affected by atherosclerosis?

A

large elastic arteries - aorta, carotid and iliac arteries and medium-sized arteries - coronary and popliteal in the leg

146
Q

Atheroma growth

A

1st phase - fatty streak; macrophage filled lipids
2nd phase - atherosclerotic plaque; intima thickens and lipids accumulate, usually eccentric
3rd phase - advanced/vulnerable plaques; can rupture and ulcerate

147
Q

Dystrophic calcifications

A

calcification on CT scans with contrast; commonly seen in atheroma as a result of chronic inflammation; on this scan you can see white calcification in the LAD

148
Q

Evolution of EKG changes in a STEMI

A

Q wave indicating that there is an active or prior (even years) MI of the heart

149
Q

Hyperacute T wave on an EKG

A

an early sign in transmural ischemia; seen before the ST elevations

150
Q

poor R wave progression on an EKG?

A

seen in anterior ischemia; R wave increases (progresses) in size in leads V1-V6

151
Q

Which phase of the action potential is slower in AV nodes compared to SA nodes?

A

phase 4 of the Na+ funny channels, takes longer to depolarize the cell; SA is dominant pacemaker of the heart

152
Q

The effects of verapamil and diltiazem on the pacemaker activity of the heart?

A

block L-type ca channels in phase 0; slows the rate of sinus depolarization which slows HR and slows AV node conduction

153
Q

anatomical location of the SA node?

A

right atrial posterolateral wall near the SVC

154
Q

What are the two structures derived from the truncus arteriosus?

A

has the word artery in its name
Aorta and pulmonary artery

155
Q

Derivatives of the sinus venosus?

A

right horn - smooth portion of the right atrium (RIGHT atrium = RIGHT horn)

left horn - coronary sinus (remember that coronary sinus drains blood from the LEFT ventricle)

156
Q

Derivatives of the cardinal veins?

A

SVC (R common cardinal vein and R anterior cardinal vein) and IVC (posterior veins)

157
Q

Two proteins required for cardiac looping in embryology?

A

cilia and dynein; abnomal can result in dextrocardia (heart on the right side of the body)

158
Q

the aorticopulmonary septum is derived from which embryological cells?

A

neural crest cells; helps from the interventricular septum; abnormal formation can cause congenital pathology

159
Q

Ventricular Septal Defect produces what type of murmur?

A

harsh, holosystolic murmur usually involving the tricuspid area - left lower sternal border

160
Q

Atrial Septal Defect produces what type of murmur?

A

systolic ejection murmur with a wide, fixed splitting of S2 due to communication between the left and right atrium making the pulmonic valve close later than the aortic valve

161
Q

The most common type of an ASD?

A

secundum type; defect at the site of the foramen oval/ostium secundum; can form by the septum secunndum being too short or with excessive reabsorption of the septum primum

162
Q

Role of the PDA in utero

A

patent ductus artiosus (PDA) shunts blood from the left pulmonary artery to the aorta in utero and closes after birth to become the ligaments arteriosum

163
Q

the PDA is maintained in utero by high levels of what?

A

prostaglandin E2 (major source in utero provided by the placenta; when the placenta is gone - after birth - then levels go down and is no longer maintained); Alprostadil - prostaglandin E1 analog that is used to maintain the PDA - useful in tetralogy of flow and pulmonary atresia when wanting to deliver blood to the lungs

164
Q

What syndrome is a patent PDA associated with?

A

congenital rubella syndrome (one of the torch infections - watch out for mom who is not vaccinated)

165
Q

PDA murmurs

A

continuous machine-like murmur heard in both systole and diastole; will see a widened pulse pressure and baby will have cyanosis (blue toes and normal fingers)

166
Q

Eisenmenger’s Syndrome

A

when there is an uncorrected ASD, VSD or PDA; the right heart is chronically overloaded causes RV hypertrophy and pulmonary HTN; reverses the l to R shunt to a R to L shunt and the patient will start to display cyanosis, clubbing and polycythemia (very high hematocrit)

167
Q

The 4 abnormalities in Tetralogy of fallot?

A

VSD, rightward deviation of the aortic valve, sub pulmonary stenosis and right ventricular hypertrophy

168
Q

Pathology of the Tetralogy of fallot?

A

abnormal neural crest cell migration leading to deviation of the infundibulum septum AKA conus arteriosus (derivative of the bulbs cordis) leading a connection between the aorta and the right ventricle - causes RV hypertrophy

169
Q

Physiology of Tetralogy of fallot?

A

high resistance to flow from RV to the pulmonary artery (there is subpulmonary stenosis) - reduced pulmonary arterial blood flow; blood is forced to go through VSD into the LV bypassing the lungs - can see severe cyanosis based on severity of obstruction (good thing most babies are born with mild conditions “pink tets”)

170
Q

Murmurs seen in Tetralogy of fallot?

A

Crescendo-decrescendo systolic ejection murmur heard best at the left sternal border with a single S2 and a VSD holosystolic murmur can be heard - rare

171
Q

Murmurs seen in Tetralogy of fallot?

A

Crescendo-decrescendo systolic ejection murmur heard best at the left sternal border with a single S2 and a VSD holosystolic murmur can be heard - rare

172
Q

Classic chest x-ray finding in a pt with Tetralogy of fallot?

A

boot shaped heart; apex is abnormally positioned and RV hypertrophy

173
Q

What position is seen to help improve symptoms in child with Tetralogy of fallot?

A

SQUATTING; increased after load/TPR will resist flow out of the LV; less blood is shunted from RV to LV meaning that more blood will pushed to the lungs

174
Q

Positioning of the great vessels in Transposition of the arteries (TGA)?

A

occurs due to failed spiraling of the aorticopulmonary septum resulting to an anterior aorta

normal - aorta is posterior and to R of pulmonary artery

D-transposition - aorta is ANTERIOR to the pulmonary artery

175
Q

Changes in a patient with hypovolemic shock?

A

there is a hemorrhage/loss of blood; the problem is with decreased blood volume; will be decreased venous return to the heart, decreased right atrium volume/pressure, decreased pulmonary capillary wedge pressure (PCWP) leading to decreased CO and decreased cardiac pressures; the decrease in CO will lead to activation of the sympathetics and RAAS (renin) which will cause increased SVR, ventilation rate and aldosterone (water retention)

176
Q

Pulmonary arterial catheters (PACs)

A

used to diagnose pulmonary HTN; catheter is advanced through RA to RV to pulmonary artery; once lodges in pulmonary artery branch balloon is inflated and obstructs blood flow; pressure measured at the tip is called the pulmonary artery occlusion pressure (PAOP) which closely reflects the LA pressure.

177
Q

Which vessel is used to measure the mixed venous O2 saturation?

A

the pulmonary artery; concentration of O2 after all the venous blood have mixed together in the right atrium

178
Q

Fick’s equation of CO?

A

CO = O2 consumption / Arterial O2 - Venous O2

venous O2 is gathered from the pulmonary artery

179
Q

Cardiogenic Shock

A

low CO with high cardiac pressures; high SVR - sympathetic response; heart is unable to pump from LV to aorta (usually from MI - decreased cardiac contractility) blood pools and transmitted backwards causing an increased PCWP and CVP; decreased CO leads to decreased forward perfusion leading to coronary perfusion

180
Q

Distributive Shock

A

LOW SVR (only shock with low SVR!!) diffuse vasodilation; CO high

181
Q

Primary mechanism of a pleural effusion depending on cause?

A

HF - increased hydrostatic pressure or decreased (transudate)
Nephrotic syndrome - decreased oncotic pressure (transudate)
Infection - increased vascular permeability (exudate)
Malignancy - lymphatic obstruction

182
Q

Physiologic response to high altitude? Plasma volume? Pulmonary arterial resistance? CO?

A
  • decreased plasma volume due to decreased aldosterone (hypoxemia suppresses aldosterone) and increase bicarb excretion
  • hypoxic pulmonary vasoconstriction, shunting leads to increased PAR
  • increased CO (increased HR = increased CO)
183
Q

Intravenous infusion of a patient in septic shock?

A

Isotonic crystalloid 0.9% OR Lactated ringers

184
Q

Airway resistance of the lower respiratory tract?

A
185
Q

Radial traction in emphysema vs pulmonary fibrosis?

A

decreased in emphysema
increased in pulmonary fibrosis - increased outward pulling by surrounding fibrotic tissue

186
Q

3 normal pulmonary physiology changes with age?

A
  1. decreased lung elastin - decreased FVC and increased RV with increased physiological dead space and decreased alveolar surface area
  2. increased chest wall stiffness with decreased diaphragm strength - decreases total system compliance and decreased chest wall compliance, increase A-a gradient and increased V/Q mismatch
187
Q

Pulmonary function testing of CF patient?

A

CF leads to progressive bronchiectasis which is one of the obstructive disorders; decreased - FEV1, FVC and FEV1/FVC with increased RV and TLC (air-trapping)

188
Q

Spirometry of patient with restrictive pulmonary disorder?

A
189
Q

Pulmonary auscultation findings on Physical Examination?

A
190
Q

Loeffler syndrome

A

transient eosinophilic pneumonitis; migration of parasitic roundworms,

191
Q

immunocompromised pt with pneumonia symptoms

A

Coccidioides immitis; a dimorphic fungus that is endemic to US and Mexico; causes lung disease in immunocompetent pts and the immunocompromised; there will be spherules containing endospores on tissue samples

192
Q

Role of beta blockers on the heart

A

reduces HR which lengthens diastolic filling time to increase LV EDV (preload) and reduce LV contractility which decreases the amount of blood ejected during ventricular systole

193
Q

pts w/ long history of asbestos exposure

A

at risk for developing asbestosis, pleural disease and malignancies such as bronchogenic carcinoma and mesothelioma; bronchogenic carcinoma is the most common malignancy in this population although mesothelioma is more specific for asbestos exposure

194
Q

Amniotic fluid markers of maturity during late gestation

A

increased phosphatidylcholine (lecithin) - curve 1 and phosphatidylglycerol and low sphingomyelin - curve 2

195
Q

Elastin metabolism

A

rubber-like property of elastin are due to high content of non polar amino acids and extensive cross-linking (involving lysine) between elastin monomers facilitated by lysyl oxidase; pts w A1AT def can develop early-onset, lower lobe predominant emphysema due to excessive alveolar elastin degradation

196
Q

Flecainide

A

class 1C antiarrhthmic which is a potent Na+ ch blockers that have increased effect at faster HR; effective in tx tachyarrhythmias, but prolongs QRS

196
Q

Flecainide

A

class 1C antiarrhthmic which is a potent Na+ ch blockers that have increased effect at faster HR; effective in tx tachyarrhythmias, but prolongs QRS

197
Q
A

an obstructive lesion in a mainstem bronchus can prevent ventilation of an entire lung, leading to large-volume atelectasis and complete lung collapse; due to an obstruction air becomes trapped and the trachea is pulled toward the affected side

198
Q

Phenylephrine

A

selective alpha-1 agonist w no effect on alpha-2 or beta receptors which causes peripheral vasoconstriction that increases SVR and BP; it has direct effect on the heart stimulates a reflex-mediated decrease in HR and myocardial contractility

199
Q

Post MI ACEi

A

following MI collagen deposition and fibrosis within the infarct region and eccentric hypertrophy of surviving myocytes can lead to progressive LV dilation and worsening contractile dysfunction; ACEi leads to attenuation (reduction)/minimizing LV dilation and helping preserve contractile function

200
Q

MOA of IgE-binding monoclonal antibody agents added for uncontrolled asthma

A

many pts w asthma have high levels of circulating IgE antibodies; agents such as omalizumab bind IgE antibodies and blocks binding to the IgE receptors on mast cells this inhibits proinflammatory substance release by mast cells and markedly reduces airway inflammation

201
Q

Histoplasma capsulatum

A

dimorphic fungus that’s found in soil contaminated w bird or bat droppings (pt exploring caves or cleaning bird cages); immunocompent pt are often asymptomatic but can develop subacute pneumonia w hilarious and mediastinal lymphadenopathy; tissues will should ovoid/round yeast predominately within the intracellular space of macrophages

202
Q

Drug of choice for dyslipidemia

A

HMG-CoA reductase inhibitors (statins) are most effective in lowing LDLs and reducing cardiovascular events (atorvastatin, rosuvastatin and simvastatin)

203
Q

cardiac defect in Turner’s syndrome

A

bicuspid aortic valve disease; aortic ejection sound which is an early systolic, high frequency click best heard over the second interspace

204
Q

Subclavian steal syndrome

A

stenosis of the proximal subclavian artery which leads to reversal of blood flow from the c/l vertebral artery to the I/p vertebral artery; pts have symptoms related to arm ischemia in the affected extremity or vertebrobasilar insufficiency (dizziness)

205
Q

Drug induced lupus erythematosus

A

Exposure to implicated drugs:
Hydralazine
Procainamide
Isoniazid
Minocycline
Quinidine

206
Q

Positive end-expiratory pressure (PEEP)

A

pressurizing the inspired gas reduces the intrapulmonary shunt effect by preparing collapsed alveoli open, displacing extracellular lung fluid and exposing more alveolar SA for gas exchange and O2 uptake

207
Q

Smoking cessation

A

Varenicline is a partial agonist of nicotinic Ach receptors; it can help pts stop using tobacco by reducing withdrawal symptoms and attenuating the rewarding effects of nicotine; the nicotine patch is a full agonist that slowly releases nicotine thus preventing withdrawal symptoms

208
Q

Pulmonary embolism (PE)

A

should be suspected in a pt w recent extended travel and now has acute dyspnea and tachypnea; V/Q scan is preferred diagnostic tool; a perfusion defect without ventilation defect

209
Q

Pulmonary actinomycosis

A

Actinomycosis is a slowly progressive disease caused by gram (+) anaerobic bacteria (actinomyces); usually caused by aspiration which leads to lower lobe consolidation; microscopic findings include filamentous, branching, gram (+) bacteria and sulfur granules

210
Q

V/Q scans for PE

A

use radio tracers to compare the ventilation and blood perfusion in each area of the lung

211
Q

Transudative pleural effusions

A

results from changes in hydrostatic (increased) or oncotic (decreased due to hypoalbuminemia) pressures and are characterized by ow pleural protein and lactate dehydrogenase concentrations as well as normal, monocyte-predominant leukocyte differential

212
Q

fat embolism syndrome (FES)

A

classically presents as triad: respiratory distress, neurological impairment and petechial rash w/I 24-72 hours following a long-bone or pelvic fracture;

213
Q

Pulmonary blastomycosis

A

blastomyces dermatitidis is a dimorphic fungus that causes pulmonary infections in immunoCOMPETENT ppl and should be considered in pts from endemic areas; characterized by granuloma formation; round yeast with thick walls and broad-based budding

214
Q

Bronchopulmonary dysplasia

A

aka chronic lung disease of prematurity; common in premature infants due to arrest of fetal lung development in the saccular stage; histology of the lung tissue shows alveolarization (dilated alveoli w decreased separation) and abnormal vasculogensis (dysmorphic alveolar capillaries)

215
Q

PAH, as vascular complication of systemic sclerosis (CREST)

A

pulmonary arterial HTN (PAH) involves fibroproliferative remodeling of the vessel wall, leading to increased PVR and RHF

216
Q

Community-acquired pneumonia

A

most common cause in both HIV infected and HIV-uninfected is Strep pneumoniae; risk of invasive pneumococcal dz is increased in pts w HIV regardless of CD4 count

217
Q

ARDs

A

acute respiratory distress syndrome involves acute neutrophilic lung inflammation w widespread alveolar damage due to proteases and ROS leading to failure of the vascular barrier and exudative pulmonary edema

218
Q

Acute exacerbation of COPD (bacterial cause)

A

3 most common bacteria during AECOPD are nontypeable Haemophilus influenza, Moraxella catarrhalis and strep pneumoniae

219
Q

Acute exacerbation of COPD (viral cause)

A

3 most common bacteria during AECOPD are: rhinovirus, influenza, and RSV

220
Q

Virulence factor of TB

A

mycobacterium tuberculosis grows in long, serpentine cords due to the presence of cord factor, a surface glycolipid, on the cell wall; main virulence factor - protects the bacteria from digestion by mo and also leads to the formation of caveating granulomas

221
Q

bronchopneumonia due to Nocardia infection

A

a filamentous, branching gram (+) bacteria that is partially acid-fast; commonly causes pneumonia and brain abscesses in immunocompromised pts

222
Q

prone positioning in ARDs

A

used to improve oxygenation via reduced compression of the posterior lung segments where the majority of the alveoli are located; leads to a more evenly distributed ventilation throughout the lungs w reduced intrapulmonary shunting and improved V/Q matching

223
Q

ECG changes with exercise

A

exercise activates beta-1 receptors in the SA node, increasing the frequency of impulse generation and in the AV node, increasing the rate of impulse conduction from the atria to the ventricles; on ECG there is increases frequency of P waves and shortening of the PR interval and RR interval (sinus tachycardia)

224
Q

Digoxin’s effect on HR

A

slows conduction through the AV node via increased parasympathetic tone; enhances efferent ganglionic transmission leading to increased vagal output; also has a positive inotropic effect that can be useful in pts w LV systolic dysfunction

225
Q

ECG effects
of Amiodarone

A

class III anti arrhythmic inhibits the delayed rectifier K+ current (responsible for ventricular repolarization); prolongs QT interval (increases risk of tossed de pointes)

226
Q

which one is tricuspid?

A
227
Q

right-sided brachiocephalic vein obstruction

A

the brachiocephalic veins drains the ipsilateral jugular and subclavian veins; the b/l brachiocephalic veins combine to form the SVC; brachiocephalic vein obstruction causes symptoms similar to those seen in SVC, but only on one side of the body

228
Q

carcinoid syndrome/tumors

A

carcinoid syndrome typically presents w episodic flushing, secretory diarrhea and wheezing; it can lead to pathognomic plaque-like deposits of fibrous tissue on the R-sided endocardium, causing tricuspid regurg and R-sided HF; elevated 24-hr urinary 5-hydroxyindoleactic acid can confirm dx

229
Q

implantable cardioverter defibrillator

A

left ventricular leads in biventricular pacemakers course through the coronary sinus, which resides in the atrioventricular groove on the posterior aspect of the heart

230
Q

Pancoast tumors

A

tumors located in the lung apex (superior sulcus) are called pan coast tumors; invasion of surrounding structures can lead to ipsilateral Horner syndrome, rib destruction, atrophy of hand muscles and pain in the distribution of C8,T1 and T2

231
Q

staining w carbolfuchsin

A

the acid-fast stain identifies organisms that have mycolic acid present in their cell walls, including Mycobacterium and Nocardia species

232
Q

Amyloid

A

cardiac amyloidosis caused by the accumulation of misfiled amyloid fibrils, appears as pink amorphous extracellular material on light microscopy; the ventricular walls becomes stiff and uniformly thickened, leading to impaired diastolic relaxation, a dilated left atrial cavity and progressive left and right sided HF; left ventricular cavity size is typically normal or decreased

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