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*First Aid in Brainscape* > Steve Colbert's Cardiac Comedy Clues > Flashcards

Steve Colbert's Cardiac Comedy Clues Flashcards

1
Q

What does this embryonic structure grow into: Truncus arteriosus

A

Ascending aorta and pulmonary trunk

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2
Q

What does this embryonic structure grow into: Bulbus cordis

A

Smooth parts (outflow tract) of left and right ventricles

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3
Q

What does this embryonic structure grow into: Primitive atria

A

Trabeculated part of left and right atria

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4
Q

What does this embryonic structure grow into: Primitive ventricle

A

Trabeculated part of left and right ventricles

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5
Q

What does this embryonic structure grow into: Primitive pulmonary vein

A

smooth part of left atrium

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6
Q

What does this embryonic structure grow into: Left horn of sinus venosus (SV)

A

Coronary sinus

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7
Q

What does this embryonic structure grow into: right horn of SV

A

smooth part of right atrium

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8
Q

What does this embryonic structure grow into: Right common cardinal vein and right anterior cardinal vein

A

SVC

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9
Q

Heart embryo morphogenesis

A

first functional organ to develop in vertebrate embryos; beats spontaneously by 4th week

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10
Q

Cardiac looping in embryo

A

primary heart tube loops to establish left-right polarity; begins in week 4 of gestation; defect in left right dynein (involved in R/L asymmetry) can lead to dextrocardia, as seen in Kartagener syndrome (primary ciliary dyskinesia)

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11
Q

Walk through the steps of the separation of the heart chambers in embryo

A

1) Septum primum grows toward endocardial cushions, narrowing foramen primum; 2) Foramen secundum forms in septim primum (foramen primum disappears); 3) Septim secundum maintains R to L shunt; 4) Septum secundum expands and covers most of the foramen secundum. THe residual Foramen is the foramen ovale; 5) Remaining portion of septum primum forms valve of foramen ovale; 6) Septum secundum and septum primum fuse to form the atrial septum; 7) formane ovale usually closes soon after birth because of increase LA pressure.

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12
Q

Patent foramen ovale

A

caused by failure of septum primum and septum secundum to fuse after birth; most are left untreated; can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation), similar to those resulting from an ASD

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13
Q

Walk through the steps of ventricle formation in ventricles

A

1) muscular ventricles septum forms. Opening is called interventricular foramen. 2) Aorticopulmonary septim rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular setpum. 3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of the interventricular septum.

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14
Q

Ventricular septal defect (VSD)

A

most commonly occurs in the membranous septum; acyanotic at birth due to L to R shunt

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15
Q

Outflow tract formation in embryo

A

Truncus arteriosus rotates; neural crest and endocardial cell migrations leading to truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum leading to the ascending aorta and pulmonary trunk

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16
Q

Conotruncal abnormalities

A

Transposition of great vessels; Tetralogy of fallot; Persistent truncus arteriosus

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17
Q

Valve development: Aortic/pulmonary

A

derived from endocardial cushions of outflow tract

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18
Q

Valve development: Mitral/tricuspid

A

Derived from fused endocardial cushions of the AV canal

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19
Q

Ebstein anomlay

A

Displaced valves from abnormal development

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20
Q

Fetal erythropoiesis

A

Yolk sac (3 to 8 weeks); Liver (6 weeks to brith); Spleen (10-28 weeks); Bone marrow (18 weeks to adult); “Young Liver Synthesizes Blood”

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21
Q

Hemoglobin development

A

Fetal hemoglobin=HbF (alpha2Gamma2);
Adult hemoglobin=HbA (alpha2beta2);
HbF has higher O2 affinity for oxygen due to less avid binding of 2,3 BPG;

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22
Q

Fetal circulation;

A

Blood entering fetus through the umbilical vein is conducted via the ductus venous into the IVC to bypass the hepatic circulation; Oxygenated Blood from IVC goes through heart and is shunted through foramen ovale; Deoxygenated blood entering the RA from the SVC goes into the RA into the RV into the main PA into the patent ductus arteriousus into the descending aorta

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23
Q

At birth the infant takes its first breath then:

A

the resistance in pulmonary vasculature decreases leading to an increase in left atrial pressure vs right atrial pressure; foramen ovale closes (now called fossa ovalis; increase in O2 (from respiration) and decrease in PGE (from placental separation) leads to closure of ductus arteriosus

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24
Q

fetal-postnatal derivatives: umbilical vein turns into

A

ligamentum teres hepatis; contained in falciform ligament

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25
Q

fetal-postnatal derivatives: umbilical arteries turns into

A

Medial umbilical ligaments

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26
Q

fetal-postnatal derivatives: Ductus arteriosus turns into

A

Ligamentum arteriosum

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27
Q

fetal-postnatal derivatives: Dustus venosus turns into

A

Ligamentum venosum

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28
Q

fetal-postnatal derivatives: Foramen ovale turns into

A

fossa

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29
Q

fetal-postnatal derivatives: Allantois turns into

A

Urachus-median umbilical ligament; the urachus is the part of the allantoic duct between the bladder and the umbilicus. Urachal cyst or sinus is a remnant

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30
Q

fetal-postnatal derivatives: Notochord turns into

A

Nucleus pulposus of intervertebral disc

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31
Q

SA and AV nodes are usually supplied by what artery

A

Right Carotid Artery; Infract may cause nodal dysfunction (bradycardia or heart block)

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32
Q

Right dominant heart circulation

A

85% of people are this way; PDA arises from RCA

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33
Q

Left dominant heart circulation

A

8% of people are this way; PDA arises form LCX (left circumflex coronary artery)

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34
Q

Co-dominant heart circulation

A

7% of people are this way; PDA arises from both the LCX and RCA

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35
Q

Coronary artery occlusion normally occurs in the

A

LAD (Left Anterior Descending artery)

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36
Q

When is is coronary blood flow at its highest point (systole or diastole)

A

Highest at early diastole

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37
Q

The most posterior part of the heart is the Left atrium; enlargement of this can cause

A

Dysphagia (compression of esophagus); or hoarseness (compression of left recurrent laryngeal nerve, a branch of the vagus)

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38
Q

Left circumflex artery (LCX) supplies

A

lateral and posterior walls of left ventricle

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39
Q

Left anterior descending artery (LAD) supplies

A

anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle

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40
Q

Posterior Descending/Interventricular artery (PDA) supples the

A

posterior 1/3 of interventricular septum and posterior walls of ventricles

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41
Q

Acute marginal artery supplies the

A

Right ventricle

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42
Q

Formula for Cardiac output

A

CO=stroke volume x HR

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43
Q

Fick principle equation

A

CO=(rate of O2 consumption)/arterial O2 content-Venous O2 content)

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44
Q

Mean arterial pressure equation

A

MAP= CO x TPR; or MAP= 2/3 diastolic + 1/3 systolic

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45
Q

Pulse pressure equation

A

pulse pressure= systolic- diastolic pressure; Pulse pressure is proportional to SV, inversely proportional to arterial compliance

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46
Q

Stroke volume equation

A

SV= EDV-ESV

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47
Q

When you exercise how is Cardiac output maintained

A

Early stages of exercise: CO is maintained by increase HR and SV; during late exercise CO is maintained by increase HR only (SV plateaus)

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48
Q

When you increase HR your diastolic goes down which leads to

A

decreased CO

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49
Q

When do you see increased Pulse Pressure

A

in hyperthyroidism; aortic regurgitation; arteriosclerosis; obstructive sleep apnea (increase sympathetic tone), exercise (transient)

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50
Q

when do you see decreased pulse pressure

A

in aortic stenosis; cardiogenic shock; cardiac tamponade; and advanced heart failure

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51
Q

Stroke Volume: what affects it

A

SV affected by contractility, afterload, and preload (SV CAP); increased SV when increased contactility, increased preload, or decreased afterload

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52
Q

Way to calculate total peripheral resistance

A

TPR=(MAP-right Atrial pressure)/CO

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53
Q

Contractility of the heart (and SV) is increased by

A

Catecholamines (increased activity of Ca2+ pump in SR); increased intracellular Calcium; decreased extracellular Na (decreased activity of the Na/Ca exchanger; Digitalis (blocks Na/K pump which decreases Na/Ca exchanger which increases intracellular Calcium

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54
Q

Contractility of the heart (and SV) is decreased by

A

beta1 blockade (decreased cAMP); Heart failure with systolic dysfunction; acidosis; hypoxia/hypercapnea; non-dihydropyridine calcium channel blockers

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55
Q

Myocardial O2 demand is increased by

A

increased afterload; increased contractility; increased HR; increased ventricular diameter

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56
Q

Preload

A

preload approximated by ventricular EDV; depends on venous tone and circulating blood volume; Venodilators decrease preload (nitro)

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57
Q

Afterload

A

approximated by MAP; relation of LV size and afterload called Laplace’s law: Wall tension= (pressure X radius)/ 2X wall thickness); LV compensates for increased afterload by thickening (hypertrophy) to decrease wall tension; Vasodilators decrease afterload (hydralazine); ACE inhibitors and ARBs decreases afterload and preload; chronic HTN increases MAP causing LV hypertrophy

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58
Q

Ejection fraction

A

EF=SV/EDV= (EDV-ESV)/EDV; left ventricular EF is an index of ventricular contractility; normal EF is 55% or greater; decreased EF in systolic heart failure; EF is normal in diastolic heart failure

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59
Q

Artery Venous fistula causes

A

increased HR, increased SV, increased CO, increased mixed venous O2 content; decreased systemic resistance; decreased diastolic BP

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60
Q

Starling curve is a theory that says what

A

force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload); increased contractility with catecholamines, digoxin; decreased contractility with loss of myocardium (e.g. MI), beta blockers, Calcium channel blockers, dilated cardiomyopathy

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61
Q

When is viscosity of blood changes

A

increased viscosity in: polycythemia, hyperproteinemic states (e.g. MS), and hereditary spherocytosis;
decreased viscosity in: anemia

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62
Q

Inotropy

A

is the measure of the force of contraction; positive inotrope would be catecholamines and digoxin; negative inotrope would be uncompensated heart failure, narcotic overdose

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63
Q

Venous return on cardiac and vascular function curves

A

Changes in circulating volume or venous tone leads to altered RA pressure for a give CO. Mean systemic pressure (x-intercept) changes with volume/venous tone; Fluid infusion and sympathetic activity increase venous return; acute hemorrhage, spinal anesthesia decreases venous return

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64
Q

Total peripheral resistance

A

Changes in TPR lead to altered CO at a given RA pressure, however, mean systemic pressure is unchanged; Vasopressor increase TPR; Exercise, AV shunt decrease TPR

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65
Q

S1 heart sounds

A

mitral and tricuspid valve closure. Loudest at mitral area

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66
Q

S2 heart sounds

A

aortic and pulmonary valve closure; loudest at left sternal border.

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67
Q

S3 heart sounds

A

in early diastole during rapid ventricular filling phase. Associated with increase filling pressure (e.g. mitral regurgitation, CHF) and more common in dilated ventricles (but normal in children and pregnant women).

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68
Q

S4 heart sounds

A

“atrial kick” in late diastole. high atrial pressure. Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall

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69
Q

Jugular venous pulse: has 5 distinct waves

A

A wave-atrial contraction;
C wave-RV contraction (closed tricuspid valve bulging into atrium);
X descent-atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction. Absent in tricuspid regurgitation.absent in tricuspid regurgitation;
V wave- increased right atrial pressure due to filling against closed tricuspid valve;
Y descent-blood flow from RA to RV

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70
Q

Normal splitting of S2: caused by what

A

Inspiration leads to drop in intrathoracic pressure which increases venous return to the RV leading to increased RV stroke volume leading to increased RV ejection time causing delayed closure of pulmonic valve. Decreased pulmonary impedance (increased capacity or the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve

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71
Q

Wide splitting of S2: what causes it

A

Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block). delay in RV emptying causes delayed pulmonic sound (regardless of breath). an exaggeration of normal splitting

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72
Q

Fixed splitting of S2: caused by

A

Seen in ASD. ADS leads to left to Right shunt causing increased RA and RV volumes causing increased flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed

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73
Q

Paradoxical splitting of S2: caused by

A

Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block). normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2, thereby paradoxically eliminating the split

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74
Q

When listening to the heart what does the following due to change the heart’s function: inspiration

A

increases intensity of right heart sounds

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75
Q

When listening to the heart what does the following due to change the heart’s function: Valsalva (phase II), standing (decrease venous return)

A

Decreases intensity of most murmur (including AS);
Increase intensity of hypertrophic cardiomyopathy murmur;
MVPL decrease murmur intensity, earlier onset of click/murmur

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76
Q

When listening to the heart what does the following due to change the heart’s function: Hand grip

A

Increases intensity of MR, AR, VSD murmurs;
Decrease intensity of AS, hypertrophic cardiomyopathy murmurs;
MVP: increase murmur intensity, later onset of click/murmur

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77
Q

When listening to the heart what does the following due to change the heart’s function: Rapid squatting (increased venous return, preload, and afterload with prolonged squatting)

A

Decrease intensity of hypertrophic cardiomyopathy murmur;
Increase intensity of AS murmur;
MCP: increase murmur, later onset of click/murmur

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78
Q

Describe the sound of a mitral/tricuspid regurg murmur

A

Holosystolic, high pitched blowing murmur;
Mitral: is loudest at apex, radiates to axilla, enhanced by maneuvers that increase TPR (squats and hand grips). MR is often due to ischemic heart disease, MVP, or LV dilation;
Tricuspid: loudest at tricuspid area and radiates to right sternal border. Enhanced by maneuvers that increase RA return (e.g. inspiration). TR commonly caused by RV dilation. Rheumatic fever and infective endocarditis can cause either MR or TR

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79
Q

Describe the sound of an Aortic stenosis

A

Crescendo-decrescendo systolic ejection murmur. LV&raquo_space; aortic pressure during systole. Loudest at heart base; radiates to carotids. “Pulsus parvus et tardus” (pulses are weak with a delayed peak). Can lead to syncope, angina, and dyspnea on exertion. Often due to age-related calcific aortic stenosis or bicuspid aortic valve.

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80
Q

Ventral septal defect makes what sounds

A

Holosystolic, harsh murmur. Loudest at the tricuspid area, accentuated by hand grip due to increased afterload

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81
Q

Mitral valve prolapse sounds like what

A

Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae). Most frequent valvular lesion. Best heard over the apex. Loudest just before S2. Usually benign. Can predispose to infective endocarditis. Can be caused my myxomatous degeneration, rheumatic fever, or chordae rupture. Occurs earlier with maneuvers that decrease venous return (e.g. standing or Valsalva).

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82
Q

Aortic regurgitation sounds like

A

High-pitched blowing early diastolic decrescendo murmur. Wide pulse pressure when chronic, can present with bounding pulses and head bobbing. often due to aortic root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever. Increased murmur with hand grip. Vasodilators decrease intensity of murmur. Large stroke volume, heard lower left sternal border

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83
Q

Mitral stenosis sounds like

A

Floowins opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fused leaflet tips). Delayed rumbling late diastolic murmur; Decreased interval between S2 and OS correlates with increased severity. LA&raquo_space; LV pressure during diastole. Often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation. Enhanced by maneuvers that increase LA return (e.g. expiration)

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84
Q

PDA sounds like

A

Continuous machine like murmur. Loudest at S2. Often due to congenital rubella or prematurity. Best heard at left infraclavicular area

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85
Q

Ventricular action potentials: phases

A

Phase 0= rapid upstroke and depolarization- voltage gated Na channels open;
Phase 1= initial repolarization, inactivation of voltage gated Na channels, Voltage gated K start to open;
Phase 2= plateau- Calcium influx through voltage gated Ca channels balances K efflux. Ca influx triggers Ca release from SR and myocyte contraction.
Phase 3= rapid repolarization- Massive K efflux due to opening of voltage gated slow K channels and closure of voltage gated Ca channels
Phase 4= resting potential-High K permeability through K channels

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86
Q

Pacemaker action potential: differences between ventricular action potential and pacemaker

A

Occurs in the SA and AV nodes. Key differences from the ventricular action potential include;
Phase 0=upstroke-opening of voltage gated Ca channels. fast voltage gated Na channels are permanently inactivated because of the less negative resting voltage of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission form the atria to ventricles;
Phase 3: inactivation of Ca channels and increased activation of K channels leading to K influx;
Phase 4: Slow diastolic repolarization; Na conductance from funny channels increases. accounts for the automaticity of AV and SA nodes.

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87
Q

ECG: P wave

A

atrial depolarization; atrial repolarization blocked by QRS complex

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88
Q

ECG: PR interval

A

conduction delay through the AV node (about 200 msec)

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89
Q

ECG: QRS complex

A

ventricular depolarization: normally

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90
Q

ECG: QT interval

A

mechanical contraction of the ventricles

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91
Q

ECG: T wave

A

ventricular repolarization: T wave inversion may indicate previous MI

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92
Q

ECG: ST segment

A

isoelectric, ventricular depolarization

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93
Q

ECG: U wave

A

caused by hypokalemia, bradycardia

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94
Q

Heart conduction pathway

A

SA node to the atria to the AV node to the common bundle to the bundle branches to the purkinje fibers to the ventricles

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95
Q

Speed of different conduction fibers through the heart

A

Purkinje; atria; ventricles; AV node

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96
Q

Pacemaker speed in the heart:

A

SA node is fastest pacemaker> AV> Bundle of his/purkinje/ventricles

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97
Q

AV node delay

A

AV node delay is about 100 msec and atrioventricular delay; allows time for ventricular filling

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98
Q

Torsades de pointes

A

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation; long QT interval predisposes to torsades de pointes. Caused by drugs, decreased K, decreased Mg, other abnormalities. Treatment includes magnesium sulfate

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99
Q

Torsades de pointes is caused by what meds

A

Some Risky Meds Can Prolong QT; Sotalol, Risperidone, Macrolides, Chloroquine, Protease inhibitors, Quinidine; Thiazides

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100
Q

Congenital long QT syndrome

A

Inherited disorder of myocardial repolarization, typically due to ion channel defects; increased risk of sudden cardiac death due to torsades de pointes, Includes: Romano Ward syndrome and Jervell and Lange-Nielson Syndrome

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101
Q

Romano-Ward syndrome

A

congenital long QT syndrome: autosomal dominant, pure cardiac phenotypes (no deafness)

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102
Q

Jervell and Lange-Nielsen syndrome

A

Congenital long QT syndrome: autosomal recessive recessive, sensorineural deafness

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103
Q

Wolff Parkinson White syndrome

A

Most common type of ventricular pre-excitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. As a result, ventricles begin to depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG. May result in reentry circuit leading to supraventricular tachycardia; if you give WPW syndrome patient digoxin they get V fib

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104
Q

Atrial fibrillation

A

Chaotic and erratic baseline (irregularly irregular) with no discrete waves in between irregularly spaced QRS complexes. Can result in atrial stasis and lead to thromboembolitic stroke. Treatment includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion

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105
Q

Atrial flutter

A

a rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the sawtooth appearance of the flutter waves. Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics. Rate control: Beta blocker or calcium channel blocker. Definitive treatment is catheter ablation

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106
Q

Ventricular fibrillation

A

A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.

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107
Q

AV block: 1st degree

A

The PR interval is prolonged (> 200 msec). Benign and asymptomatic. No treatment required

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108
Q

AV block: 2nd degree, Mobitz type I (wenckebach)

A

Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). Usually asymptomatic.

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109
Q

AV block: 2nd degree, Motitz type 2

A

Dropped beats that are not preceded by a change in the length of the PR interval (as in type I) it is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response. May progress to 3rd degree heart block. Treated with pacemaker

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110
Q

AV block: 3rd degree

A

The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves beat no relation to the QRS complexes. the atrial rate is faster than the ventricular rate. Usually treated with pacemaker. Lyme disease can result in 3rd degree heart block.

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111
Q

Atrial natriuretic peptide

A

Released from atrial myocytes in response to increase blood volume and atrial pressure. Causes vasodilation and decreased Na reabsorption at the renal collecting tubule. Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to “aldosterone escape” mechanism

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112
Q

B-type (brain) natriuretic peptide

A

released form ventricular myocytes in response to increase tension. Similar physiologic action to ANP, with longer half life. BNP blood test used for diagnosing heart failure (Very good negative predictive value). Available in recombinant form (nesiritide) for treatment of heart failure.

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113
Q

During V-FIB the heart stops pumping out blood and the systemic blood pressures do what

A

all blood pressures equalize in the body: RA=venous=arterial and so on

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114
Q

Preventricular contraction (PVC)

A

Less end diastolic volume, no pave, no atrial contraction

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115
Q

The aortic arch receptors transmit signal using the

A

vagus nerve to the solitary nucleus of medulla (responds only to increased BP)

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116
Q

The Carotid sinus receptors transmit signal using the

A

glossopharyngeal nerve to the solitary nucleus of the medulla (responds to decreased and increased BP)

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117
Q

Baroreceptor mechanism when you have hypotension

A

hypotension leads to decreased arterial pressure causing decreased stretch leading to decreased afferent baroreceptor firing causing increased efferent sympathetic firing and decreased efferent parasympathetic stimulation leading to vasoconstriction, increased HR, increased contractility, increased BP;
important in the response to severe hemorrhage

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118
Q

Mechanism of carotid massage

A

increased pressure on carotid sinus leads to increased stretch and therefore increased afferent baroreceptor firing causing increased AV node refractory period leading to decreased HR

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119
Q

Baroreceptors and Cushing syndrome: mechanism of that

A

Increased intracranial pressure constricts arterioles which leads to cerebral ischemia and reflex sympathetic output in perfusion pressure (HTN) causing increased stretch and reflex baroreceptor induced bradycardia

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120
Q

Chemoreceptors: Peripheral

A

Carotid and aortic bodies are stimulated by decrease Po2 (

121
Q

Chemoreceptors: Central

A

Are stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Does not directly respond to O2.

122
Q

Which organ gets 100% of the bodies cardiac output (not the heart you smarty pants)

A

The lungs!

123
Q

Which organ has the largest share of systemic cardiac output

A

liver

124
Q

Which organ has the highest blood flow per gram of tissue

A

kidney

125
Q

what is pulmonary capillary wedge pressure used for?

A

is a good approximation of left atrial pressure. In mitral stenosis PCWP is greater than LV diastolic pressure; measured by Swan Ganz catheter

126
Q

Normal pressure in RA

A
127
Q

Normal RV pressure

A

25/5 mmHg

128
Q

normal pulmonary blood pressure

A

25/10 mmHg

129
Q

normal LA pressure

A
130
Q

Normal LV pressure

A

130/10 mmHg

131
Q

Normal Aorta blood pressure

A

130/90 mmHg

132
Q

Factors that influence autoregulation in the heart

A

Local metabolites (vasodilatory): CO2, adenosine, NO

133
Q

What is autoregulation referring to

A

how blood flow to an organ is maintained constant over a wide range of perfusion pressures

134
Q

Factors that influence autoregulation in the brain

A

Local metabolites (vasodilatory): CO2 (pH)

135
Q

Factors that influence autoregulation in the Kidneys

A

myogenic and tubuloglomerular feedback

136
Q

Factors that influence autoregulation in the Lungs

A

hypoxia causes vasoconstriction (ONLY ORGAN TO DO THIS, normally a blood vessel with dilate when hypoxic)

137
Q

Factors that influence autoregulation in the skeletal muscles

A

local metabolites: lactate, adenosine, K, H, CO2

138
Q

Factors that influence autoregulation in the Skin

A

sympathetic stimulation most important mechanism-temperature control

139
Q

Edema is excess fluid outflow into the interstitium: this is caused by different factors including

A

Increased capillary pressure (heart failure);
Decreased plasma proteins (nephrotic syndrome, liver failure);
Increased capillary pressure (toxins, infections, burns)
Increased interstitial colloid osmotic pressure (lymphatic blockage)

140
Q

Right to Left shunts: when are they present, what are the types

A

Present at birth or shortly after, usually require emergency surgery or maintenance of PDA;
5 T’s: 1) Truncus arteriosus (1 vessel), 2) Transposition (2 vessels) 3) TRIcuspid atresia (3=tri) 4) TETRAlogy of Fallot (4=tetra) 5) TAPVR (5 letters)

141
Q

Persistent truncus arteriosus

A

Failure of truncus arteriosus to divide into pulmonary trunk and aorta; most patients have accompanying VSD which increases pulmonary pressure; associated with 22q11 (Digeorge); conotruncal ridges fail to develop; R to L shunt

142
Q

D-transposition of great vessels

A

Aorta leaves RV (anterior) and the pulmonary trunk leaves LV (posterior) leading to separation of pulmonic and systemic circulation. Will die unless shunt is present (like PDA, VSD or patent foramen ovale); due to aoritcopulmonary septum to spiral; without surgery you die; associated with maternal diabetes; 1/3 of x rays will show eggs on a string appearance; R to L shunt

143
Q

Tricuspid atresia

A

absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability; R to L shunt

144
Q

Tetralogy of Fallot

A

Caused by antereosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis.
1) pulmonary infundibular stenosis (most important determinant for prognosis)
2) RV hypertrophy (boot shaped heart on x ray)
3) Overriding Aorta
4) VSD; Pulmonary stenosis forces R to L shunt across VSD;
Squatting increases SVR, decreases R to L shunt and improves cyanosis

145
Q

Total anomalous pulmonary venous return

A

Pulmonary veins drain into the right heart circulation (SVC, coronary sinus, etc); associated with ASD and sometimes PDA to allow for R to L shunting to maintain CO

146
Q

Bicuspid aortic valve

A

Asymptomatic until adult; hear systolic click and there is a systolic ejection murmur @ right upper sternal border which radiates to carotids

147
Q

Ventral septal defect

A

Most common congenital cardiac defect;
Asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life;
Most self resolve; larger lesions may lead to LV overload and heart failure; L to R shunt

148
Q

Atrial septal defect

A

defect in the interarterial septum; loud S1; side, fixed split S2; Usually occurs in septum secundum; septum primum defects usually occur with no other abnormalities;
Symptoms range from none to heart failure; distinct from patent foramen ovale in that septa are missing tissue rather than unfused; usually presents as exercise intolerance; L to R shunt

149
Q

Patent ductus arteriosus

A

If fetal period shunt is R to L; in neonatal where you have decreased lung resistance shunt becomes L to R and you get progressive RVH and/or LVH and heart failure;
Get a persistent machine like murmur; Patency maintained by PGE synthesis and low O2 tension (give indomethacin to close, PGE (alprostadil to keep open); Uncorrected PDA can lead to cyanosis in lower extremities

150
Q

Eisenmenger syndrome

A

Uncorrect L to R shunt (VSD, ASD, PDA) leads to increased pulmonary blood flow causing pathogenic remodeling of vasculature leading to pulmonary arteriolar HTN. RVH occurs and then shunt becomes R to L. Causes late cyanosis, clubbing, and polycythemia

151
Q

Coarctation of the aorta is associated with

A

Bicuspid aortic valve

152
Q

Coarctation of the aorta: infantile type

A

Associated with PDA; aorta narrowing is proximal to insertion of ductus arteriosus (preductal). Associated with Turner syndrome. Can present with closure of the ductus arteriosus (reverse it with PGE2)

153
Q

Coarctation of the aorta: Adult type

A

Aorta narrowing is distal to ligamentum arteriosum (postductal). Associated with notching of the ribs AKA scalloping (collateral circulation), HTN in upper extremities, and weak, delayed pulses in lower extremities; Patient will c/o leg pain while exercising

154
Q

What cardiac abnormality is associated with: 22q11

A

Truncus arteriosus, tetralogy of fallot

155
Q

What cardiac abnormality is associated with: Down syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

156
Q

What cardiac abnormality is associated with: Congenital rubella

A

PDA, Septal defects, pulmonary stenosis

157
Q

What cardiac abnormality is associated with: Turner syndrome

A

Bicuspid aortic valve coarctation of the aorta (preductal or infantile form)

158
Q

What cardiac abnormality is associated with: Marfan Syndrome

A

Mitral Valve prolapse; Thoracic aortic aneurysm and dissection, Aortic regurgitation

159
Q

What cardiac abnormality is associated with: Infant of diabetic mother

A

Transposition of the great vessels

160
Q

HTN: Risk factors

A

increased age, obesity, diabetes, smoking, genetics, blacks > white > asian

161
Q

HTN: features of it

A

90% of HTN is primary (essential) and is related to increased CO and TPR; remaining 10% is secondary to renal disease including fibromuscular dysplasia in young people/

162
Q

Hypertensive emergency

A

Severe HTN (180/120 or greater) with evidence of acute, ongoing target organ damage (e.g. papilledema, mental status changes)

163
Q

HTN predisposes you to

A

Atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, and aortic dissection; if long standing HTN then you get decreased blood flow in end organ damage and decreased number of arterioles

164
Q

Fibromuscular dysplasia

A

narrowing of the lumen (thickening of the wall) in medium and large vessels. Unknown cause.
Targets renal arteries and cerebral vessels; leads to stroke, TIA, headache; hear bilateral bruits on abdominal exam leading to decrease kidney function

165
Q

Sudden cardiac death

A

has to be no abnormalities and no drug use;

Long QT; Brugada syndrome; Catecholaminergic polymorphic ventricular tachycardia

166
Q

Hyperlipidemia signs: what can you see on physical exam (massive hyperlipidemia)

A

Xanthomas: plaques or nodules composed of lipid laden histiocytes in the skin, especially the eyelids (xanthelasma);
Tendinous Xanthomas are lipid deposits in tendons, especially Achilles (usually sign of familial hyperlipidemia);
Corneal arcus: lipid deposits in cornea, appears early in life with hypercholesterolemia. common in elderly (arcus senilis)

167
Q

Mockenburg arteriosclerosis

A

Mock it, nobody cares;
uncommon, calcification in the media of the arteries, especially radial or ulnar, usually benign; pipestem arteries on x ray; does not obstruct blood flow; intima not involved

168
Q

Arteriolosclerosis

A

common, two types. 1) hyaline (thickening of small arteries in essential HTN or diabetes) and 2) hyperplastic (onion skin as seen in severe HTN)

169
Q

Atherosclerosis is a disease of what

A

Disease of elastic arteries and large and medium size muscular arteries

170
Q

what are the risk factors for atherosclerosis

A

Modifiable: smoking, hyperlipidemia, HTN, diabetes
Nonmodifiable: age, sex (Males and postmenopausal women have increased chance), and family history

171
Q

Disease progression of atherosclerosis

A

inflammation is important in the disease process;
Endothelial cell dysfunction gives macrophages and LDL a place to enter leading to foam cell formation which eventually turns into fatty streaks. Smooth muscle cell migration (PDGF and FGF), proliferation, and extracellular matrix deposition leads to fibrous plaques and complex atheromas

172
Q

Complications of atherosclerosis

A

Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

173
Q

Location of atherosclerosis

A

Abdominal Aorta > coronary artery > popliteal artery > carotid artery

174
Q

Aortic aneurysm

A

localized pathologic dilation of the aorta. May cause pain, which is a sign of leaking, dissection, or imminent rupture

175
Q

Abdominal aortic aneurysm

A

associated with atherosclerosis. Occurs more frequently in HTN male smokers > 50 years old

176
Q

Thoracic aortic aneurysm

A

Associated with cystic medial degeneration due to HTN (old patients) or Marfan (younger patients). Also tertiary syphilis (obliterative endarteritis of the vasa vasorum)

177
Q

Aortic dissection

A

Longitudinal intraluminal tear forming a false lumen. Associated with HTN, bicuspid aortic valve, and inherited connective tissue disorders (Marfan). Can present as tearing chest pain, of sudden onset, radiating to the back +/- markedly unequal BP in different arms. CXR shows mediastinal widening.
False lumen can be limited to the ascending aorta, propagate from the ascending aorta, or propagate from the descending aorta.
Can result in cardiac tamponade, aortic rupture, and death

178
Q

Angina: what is it

A

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necoris.

179
Q

Angina: what are the types

A 
Stable: usually secondary to atherosclerosis; exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest.
Variant Type (Prinzmetal): occurs at rest secondary to coronary artery spasm; transient ST elevation on ECG; triggers include tobacco, cocaine, triptans. Treat with Ca channel blocker, nitrates, and stop smoking
Unstable/Crescendo: Thrombosis with incomplete coronary artery occlusion; ST depression on ECG (increased frequency or intensity of chest pain; any chest pain at rest)
180
Q

Coronary steel syndrome

A

Distal to coronary stenosis, vessels are maximally dilated at rest. Administration of vasodilators (dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well perfused areas leading to decreased flow and ischemia in the post-stenotic region. Principle behind stress tests.

181
Q

Myocardial infarction

A

most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis. If transmural ECG will show ST elevation, if subendocardial ECG may show ST depression. Cardio biomarkers (Troponin I, CK-MB) are diagnostic.

182
Q

Sudden cardiac death

A

Death from cardiac causes within 1 hour of symptoms, most commonly due to a lethal arrhythmia (like V fib). Associated with CAD, cardiomyopathy, and hereditary ion channelopathies

183
Q

Chronic ischemic heart disease

A

progressive onset of CHF over years due to chronic ischemic myocardial damage.

184
Q

What are the most common carotid arteries to occlude

A

LAD > RCA > Circumflex

185
Q

Morphologic changes in heart after a heart attack: 0-4 hours

A

no gross or microscopic changes; complications to look for would be arrhythmias, HF cardiogenic shock, death

186
Q

Morphologic changes in heart after a heart attack: 4-12 hours

A

Grossly you will start to see infarcted area, dark mottling, looks pale with tetrazolium stain;
Microscopically: Early coagulative necrosis, release of necrotic cell contents into blood stream, edema, hemorrhage, wavy;
complications to look for would be arrhythmias, HF, cardiogenic shock, death

187
Q

Morphologic changes in heart after a heart attack: 12-24 hours

A

Grossly you will start to see infarcted area, dark mottling, looks pale with tetrazolium stain;
Microscope you see: neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage);
Complications to look out for: Arrhythmias, HF, cardiogenic shock, death

188
Q

Morphologic changes in heart after a heart attack: 1-3 days

A

Grossly you see hyperemia;
Microscope shows: extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation w/ neutrophils
Complications: Fibrinous pericarditis (presents as friction rub and chest pain)

189
Q

Morphologic changes in heart after a heart attack: 3 to 14 days

A

grossly: hyperemic borders, central yellow-brown softening, maximally soft and yellow at day 10;
Microscopic findings: Macrophages, then granulation tissue at margins
Complications: free wall rupture leading to a tamponade; papillary muscle rupture leading to mitral regurgitation; inter-ventricular septal rupture due to macrophage mediated structural degradation. LV pseudoaneurysm (mural thrombosis plugs hole in myocardium which leads to “time bomb”

190
Q

Morphologic changes in heart after a heart attack: 2 weeks to several months

A

grossly you see gray white scar, recanalized artery;
microscope you see: contracted scar complete;
Complications: dressler syndrome, HF, arrhythmias, true ventricular aneurysm (outward bulge during contraction, “dyskinesia or akinesia”)

191
Q

How do you diagnose a MI

A

in first 6 hours ECG is gold standard which shows ST elevation in STEMI and acute transmural infarct, ST depression in subendocardial infarcts, and pathologic Q waves (evolving or old transmural infarct)
Cardiac troponin I is elevated after 4 hours and stays up for 7 to 10 days (most specific marker);
CK-MB is predominantly found in mycardium but is also found in skeletal muscle. Useful in diagnosing reinfarction following MI because levels drop to normal after 48 hours

192
Q

Types of infarcts

A

Transural infarcts: increase infarcts, affects entire wall, ST elevation on ECG, Q waves
Subendocardial infarcts: Due to ischemic necrosis

193
Q

ECG Diagnosis of MI, what leads will show this type of infarct: Anterior Wall (LAD)

A

V1-V4

194
Q

ECG Diagnosis of MI, what leads will show this type of infarct: Anteroseptal (LAD)

A

V1-V2

195
Q

ECG Diagnosis of MI, what leads will show this type of infarct: Anterolateral (LAD and LCX)

A

V4-V6

196
Q

ECG Diagnosis of MI, what leads will show this type of infarct: Lateral wall (LCX)

A

I, aVL

197
Q

ECG Diagnosis of MI, what leads will show this type of infarct: Inferior wall (RCA)

A

II, III, aVF

198
Q

Dressler syndrome

A

autoimmune reaction after an MI. Attacks the fibrinous pericarditis (4-6 weeks post MI);
Fever, positional substernal chest pain, loud friction rub, Diffuse ST elevations

199
Q

Dilated Cardiomyopathies: Causes

A

Most common type of cardiomyopathy; often idiopathic or congenital; known causes include Alcohol abuse, wet Beriberi, Coxsackie B virus, Cocaine, Chagas, Doxorubicin toxicity, hemocrhomatosis and peripartum cardiomyopathy

200
Q

Dilated cardiomyopathies: Findings and treatments

A

Findings: Heart failure, S3, dilated heart on echo, balloon appearance of heart on CXR, systolic dysfunction (decreased ejection fraction and contractility)
Treatment: Na restriction, ACE inhibitors, Beta blockers, diuretics, digozin, implantable cardioverter defibrillator, heart transplant (goal is to decrease BP, HR, and heart workload)

201
Q

Hypertrophic cardiomyopathies

A

60 to 70% are familial, autosomal dominant (commonly a beta myosin heavy chain mutation). Rarely can be associated with Friedreich ataxia. Causes sudden death in athletes, due to ventricular arrhythmia.
Findings: S4, systolic murmur, diastolic dysfunction (preserved EF or increased EF)
Treatment: stop strenuous activity, use beta blockers or non dihydropyridine Ca channel blockers (verapamil). ICD if patient is high risk.

202
Q

What is the mechanism of obstructive cardiomyopathies

A

a subset of hypertrophic; hypertrophied septum too close to anterior mitral leaflet causing outflow obstruction leading to dyspnea, possible syncope

203
Q

Restrictive/infiltrative cardiomyopathies

A

Major causes are sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy can also occur);
Get diastolic dysfunction. Can have low voltage ECG even though you have thick myocardium (especially amyloid)

204
Q

CHF

A

Clinical syndrome of cardiac pump dysfunction. Symptoms include dyspnea, orthopnea, and fatigue, signs include rales, JVD, and pitting edema.

205
Q

CHF: systolic dysfunction

A

Low EF, poor contractility, often secondary to ischemic heart disease or DCM.

206
Q

CHF: diastolic dysfunction

A

preserved or increased EF, normal contractility, impaired relaxation, decreased compliance (S4 sound),

207
Q

CHF: right heart failure

A

usually secondary to left heart failure; isolated right heart failure usually due to cor pulmonale

208
Q

CHF: Treatments

A

ACE inhibitors, beta blockers (except in acute decompensated HF), angiotensin II receptor blockers, and spironolactone decrease mortality. Thiazide and loop diuretics are for symptomatic relief. Hydralazine with nitro therapy improves both symptoms and mortality in some patients.

209
Q

CHF: hemosiderin laden macrophages

A

AKA heart failure cells. Blood backs up in lungs increases pressure, RBCs lead out, macrophages eat them, macrophages fill with iron from RBCs.

210
Q

Hepatomegaly from heart failure

A

due to Right heart failure; increased central venous pressure causing increased resistance to portal flow. see nutmeg liver and can progress to “cardiac cirrhosis”

211
Q

Jugular venous distension measures

A

measures central venous pressure (which is a reflection of RA pressure and not volume). Great than 4 cm and you have a problem.

212
Q

Bacterial Endocarditis: symptoms, valves involved, complications

A

Fever (most common symptom), new murmur, Roth spots (round white spots on retina surrounded by hemorrhage), Osler nodes (tender raised lesions on finger or toe pads), Janeway lesions (small, painless, erythematous lesions on palm and sole), anemia, splinter hemorrhages on nail bed. Multiple blood cultures necessary for diagnosis;
Mitral valve is most frequently involved, Tricuspid think IV drug abuse;
Chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

213
Q

Acute Bacterial Endocarditis: what bug

A

S. aureus (high virulence), Large vegetations on previously on previously normal valves. Rapid onset.

214
Q

Subacute bacterial endocarditis: what bug

A

Viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset.

215
Q

Culture negative endocarditis: what bugs

A

Most likely Coxiella burnetti and Bartonella spp.

216
Q

What are roth spots

A

Type III Hypersensitivity causes emboli, retinal hemorrhage

217
Q

What are Osler nodes

A

Type III hypersensitivity causes emboli; painful red raised lesions found on hands and feet

218
Q

What are Janeway Lesions

A

Emboli, not immune mediated; non tender red lesions on hands and feet

219
Q

What are Nail-bed hemorrhage

A

Emboli, not immune mediated; blood clots that happen under the nails due to small vessels

220
Q

Rheumatic fever

A 
consequence of Beta hemolysis strep. Early deaths due to myocarditis, Late sequelae includes rheumatic heart disease, which affects heart valves Mitral > Aortic >> tricuspid (high pressure valves), Early lesion is mitral valve regurgitation. Late lesion is mitral stenosis. Associated with Aschoff bodies (granuloma with giant cells), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod like nucleus), Increase ASO titer;
Immune mediated (Type II) not a direct effect of bacteria, Antibodies to M protein react with heart valve cells
221
Q

Rheumatic FEVERSS stands for

A

Fever, Erythema marginatum, Valvular damage (vegetation and fibrosis), increased Esr, Red-hot joints (migratory polyarthritis), Subcutaneous nodules, St. Vitus’ dance (Sydenham chorea)

222
Q

Acute pericaridits

A

Commonly presents with sharp pain, aggravated by inspiration, relieved by sitting up and leaning forward, friction rub, ECG shows widespread ST elevation and/or PR depression; 3 types Fibrinous, Serous, Suppurative/Purulent

223
Q

Acute pericarditis: Fibrinous type

A

Caused by Dressler syndrome, uremia, radiation. Presents with loud friction rub.

224
Q

Acute pericarditis: Serous type

A

Viral pericarditis (often resolves spontaneously); noninfectious inflammatory diseases (e.g. rheumatoid arthritis, SLE)

225
Q

Acute pericarditis: Suppurative/Purulent type

A

Usually caused by bacterial infections (e.g. pneumococcus, Streptococcus). Rare now with antibiotics.

226
Q

Cardiac Tamponade

A

Compression of heart by fluid in pericardium, leading to decreased CO. Equilibration of diastolic pressures in all 4 chambers. Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), increased HR, pulsus paradoxus, Kussmaul sign, ECG shows low voltage QRS and electric alternans (due to “swinging” movement of heart in large effusions

227
Q

What is pulsus paradoxus

A

Decrease in amplitude of systolic blood pressure by >10 mmHg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup

228
Q

Syphilitic heart disease

A

Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilation of the aorta and valve ring;
May see calcification of the aortic root and ascending aortic arch. leads to tree bark appearance of the aorta.

229
Q

Cardiac tumors are mostly

A

most common heart tumor is a metastasis (e.g. melanoma, lymphoma), but it is still rare.

230
Q

Cardiac tumors: Myxoma

A

Most common primary cardiac tumor in adults. 90% occur in atria (mostly left atrium). Myxomas are usually described as a ball valve obstruction in the left atrium (Associated with multiple syncopal episodes)

231
Q

Cardiac tumors: Rhabdomyomas

A

Most frequent primary cardiac tumor in children (associated with tuberous sclerosis)

232
Q

Kussmaul signs

A

Increased in JVP on inspiration instead of normal decrease;
Inspiration leads to negative intrathoracic pressure not transmitted to heart causing impaired filling of right ventricle leading to blood backs up into venae cavae causing JVD. May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.

233
Q

Raynaud phenomenon

A

Decreased blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress. Most often in the fingers and toes. Called raynaud disease when primary (idiopathic), Raynaud syndrome when secondary to a disease process such as mixed connective tissue disease, SLE, CREST syndrome.

234
Q

Strawberry hemangioma

A

benign capillary hemangioma of infancy. Appears in the first few weeks of life (1/200 births); grows rapidly and regresses spontaneously at 5-8 years old.

235
Q

Cherry hemangioma

A

Benign capillary hemangioma of the elderly. Does not regress. Frequency increase with age.

236
Q

Pyogenic granuloma

A

Polypoid capillary hemangioma that can ulcerate and bleed. Associated with trauma and pregnancy.

237
Q

Cystic hygroma

A

Cavernous lymphangioma of the neck. Associated with turners syndrome.

238
Q

Glomus tumor

A

Benign, painful, red-blue tumor under fingernails. Arises from modified muscle cells of glomus body.

239
Q

Bacillary angiomatosis

A

Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections. Frequently mistaken for Kapose sarcoma.

240
Q

Angiosarcoma

A

Rare blood vessel malignancy typically occuring in the head, neck, and breast areas. Usually in elderly sun exposed areas. Associated with radiation therapy and arsenic exposure. Very aggressive and difficult to resect due to delay in diagnosis.

241
Q

Lymphangiosarcoma

A

Lymphatic malignancy associated with persistent lymphedema (e.g. post radical mastectomy)

242
Q

Kaposi sarcoma

A

Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Frequently mistaken for bacillary angiomatosis

243
Q

Temporal (Giant cell arteritis)

A

Generally elderly females; Unilateral headache (temporal artery), jaw claudication.
May lead to irreversible blindness due to opthalmic artery occlusion.
Associated with polymyalgia rheumatica;
Focal granulomatous inflammation (do biopsy, may not see it because it is focal) leads to increased ESR, usually affects branches of the aorta,
Treat with high dose corticosteroids

244
Q

Takayasu arteritis

A

think asian females

245
Q

polyarteritis nodosa

A

young adults; Associated with Hep B (30%) and C, Fever, weight loss, malaise and headache. GI symptoms of melena and abdominal pain. HTN, neuro dysfunction, cutaneous eruptions, renal damage. See increased ESR and CRP. Typically involves renal and visceral vessels but spares lungs. Immune complex mediated. Transmural inflammation of arterial wall with fibrinoid necrosis (likes muscular arterioles). tons of micro-aneurysms. Treat with corticosteroids and cyclophosphamide.

246
Q

Kawasaki Disease

A

Asian kids

247
Q

Buerger disease (thromboangiitis obliterans)

A

Heavy smokers, males,

248
Q

Granulomatosis with polyangiitis

A

weCener disease. Upper respiratory tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis. Lower respiratory tract: hemoptysis, cough, dyspnea. Renal: hematuria, red cell casts.
Triad is: Focal necrotizing vasculitis, Necrotizing granulomas in the lungs and upper airway, Necrotizing glomerulonephritis.
Diagnose with PR3-ANCA/c-ANCA (anti-proteinase 3), CXR shows large nodular densities.
Treat with cyclophosphamide and corticosteroids

249
Q

Microscopic polyangitis

A

Necrotizing vasculitis commonly involving the lungs, kidneys, skin with pauci-immune glomerulonephritis and palpable purpura. Presentation similar to granulomatosis with polyangiitis but with NO nasal involvement.
No granulomas, MPO-ANCA/p-ANCA (anti-myeloperoxidase). Treat with cyclophosphamide and corticosteroids.

250
Q

Churg-Strauss syndrome

A

Asthma, sinusitis, palpable purpura, peripheral neuropathy (e.g. wrist/foot drop). Can also involve the heart, GI, kidneys (pauci-immune glomerulonephritis).
Granulomatous, necrotizing vasculitis with eosinophilia.
MPO-ANCA/p-ANCA (anti-myeloperoxidase), increased IgE

251
Q

Henoch-Schonlein purpura

A

Most common childhood systemic vasculitis, follows URIs; Classic triad: Skin (palpable purpura on butt/legs), Arthralgias, GI (abdominal pain, melena, multiple lesions of same age).
Vasculitis secondary to IgA complex deposition. Associated with IgA nephropathy.

252
Q

Treatment for primary essential HTN

A

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), Calcium channel blockers

253
Q

Treatment for HTN with CHF

A

Diuretics, ACE inhibitors/ARBs, beta blockers (must be compensated CHF), aldosterone antagonists

254
Q

HTN with diabetes

A

ACE inhibitors, ARBs, calcium channel blockers, diuretics, beta blockers, alpha blockers (ACEs and ARBs are kidney protective)

255
Q

Calcium channel blockers: names, mechanism

A

Dihydropyridines (-dipines, amlodipine, nimodipine, nifidipine); non-dihydropyridines (diltiazem, verapamil);
Mechanism: block voltage gaited L type Ca channels of cardiac and smooth muscle causing reduced muscle contractility.
Targets for smooth muscle: amlodipine=nifidipine > diltiazem > verapamil
Target for heart: verapamil > Diltiazem > amlodipine=nifedipine

256
Q

Calcium channel blockers: clinical use

A

Dihydropyridine (-dipines, except nimodipine): HTN, angina (including prinzmental), Raynaud
non-dihydropyridine (verapamil, diltiazem): HTN, angina, atrial fib/flutter
Nimodipine: Subarachnoid hemorrhage (prevents cerebral vasospasm)

257
Q

Calcium channel blockers: side effects

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation.

258
Q

Hydralazine

A

mechanism: increases cGMP causing smooth muscle relaxation. Vasodilates arteries > veins (kinda opposite of nitro); afterload reduction;
Uses: severe HTN, CHF. 1st line for HTN in pregnancy, with methyldopa. co-administered with beta blocker to prevent reflex tachycardia.
Toxicity: compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus like syndrome.

259
Q

Hypertensive emergency: treatment

A

Commonly used drugs are nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam.

260
Q

Nitroprusside

A

short acting; increases cGMP via direct release of NO. Can cause cyanide toxicity; used for hypertensive emergency

261
Q

Fenoldopam

A

Dopamine D1 receptor agonist: coronary, peripheral, renal, and splenic vasodilation. decreased BP and increased natriuresis. Used in hypertensive emergencies.

262
Q

Nitroglycerin, isosorbide dinitrate

A

Mechanism: vasodilate by increased NO in vascular smooth muscle causing increased cGMP and smooth muscle relaxation. dilates veins&raquo_space; arteries. Decreases preload.
Uses: angina, acute coronary syndrome, pulmonary edema
Toxicity: reflex tachycardia (treat with beta blockers), hypotension, flushing, headacne

263
Q

What is Monday disease in industrial exposure to Nitroglycerin?

A

Development of tolerance for the vasodilating effects during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon re-exposure

264
Q

What do nitrates do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2

A

End-diastolic pressure decreases, blood pressure decreases, contractility increases (reflex), heart rate increases (reflex), ejection time (Decreases), MVO2 (Decreases)

265
Q

What do beta blockers do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2

A

End-diastolic pressure (increase), blood pressure (decreases), contractility (decrease), heart rate (decreases), ejection time (increases), MVO2 (decrease)

266
Q

What do nitrates + beta blockers do to cardiac function measurements: End-diastolic pressure, blood pressure, contractility, heart rate, ejection time, MVO2

A

End-diastolic pressure (no effect or decreased), blood pressure (Decrease), contractility(no effect), heart rate (decreased), ejection time (no effect), MVO2 (massive decrease)

267
Q

HMG-CoA reductase inhibitors

A

-statins; massively decrease LDL, decrease triglycerides, increase HDL; inhibit conversion of HMG-CoA to mevalonate which is a cholesterol precursor;
Side effects: Hepatotoxicity (increases LFTs), rhabdomyolysis (esp. when used with fibrates and niacin)

268
Q

Niacin (Vit B3)

A

decreased LDL, really increase HDL (why we give it), decrease triglycerides; inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis;
Side effects: red flushed face which in decreased by taking aspirin, hyperglycemia (acanthosis nigricans), hyperuricemia (gout)

269
Q

Bile acid resins

A

(Chole-) cholestyramine, colestipol, colesevelam; Big LDL decrease; prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more; Patients hate it, tastes bad, GI problems, cholesterol gall stones, decreased fat soluble vitamin absorption

270
Q

Fibrates

A

(-fibrate), clofibrate, bezafibrate, fenofibrate, gemfibrozil; decreases LDL, increases HDL, massive decrease in triglycerides; upregulates LPL leading to increased TG clearance; activates PPAR-alpha to induce HDL synthesis.
Side effects: myositis (increased risk with concurrent statins), hepatotoxicity (increased LFT), cholesterol gallstones

271
Q

Cardiac glycosides (digoxin): mechanism and uses

A

Direct inhibition of Na/K ATPase, leading to inhibition of Na/Ca exchanger, increased intracellular Ca levels, positive inotrope. Stimulates vagus nerve causing decreased HR.
Used for CHF (increases contractility); atrial fib (decreased conduction at AV node and depression at SA node)

272
Q

Digoxin toxicity

A

Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision; ECG shows increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block/
Can lead to hyperkalemia which indicates poor prognosis.
Factors predisposing to toxicity: renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K binding site on Na/K ATPase), verapamil, amiodarone, quinidine (decreased digoxin clearance; displaces digoxin from tissue binding sites). Don’t give with K wasting diuretics.

273
Q

Digoxin antidote

A

Slowly normalize the K levels, cardiac pacer, antidigoxin Fab fragments, Mg2+

274
Q

Na channel blockers Class IA: name them

A

Quinidine, Procainamide, Disopyramide “the Queen Proclaims Diso’s pyramid”

275
Q

Na channel blockers Class IA: Mechanism and use

A

Mechanism: Increase AP duration, increased effective refractory period.
Uses: Both atrial and ventricular arrhthmias, especially re-enterant and ectopic SVT and VT

276
Q

Na channel blockers Class IA: Toxicity

A

Conchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), Heart failure (disopyramide), thrombocytopenia, torsades de pointes due to increased QT interval

277
Q

Na channel blockers Class IB: Names

A

Lidocaine, mexiletine, Phenytoin can also fall into this category.

278
Q

Na channel blockers Class IB: Mechanism, uses

A

Mechanism: decreases AP duration, Preferentially affects ischemic or depolarized purkinje and ventricular tissue.
Uses: acute ventricular arrhythmias (Especially post MI), digitalis induced arrhythmias, 1B is Best post MI

279
Q

Na channel blockers Class IB: Toxicity

A

CNS stimulation/depression; cardiovascular depression

280
Q

Na channel blockers Class IC: Names

A

Flecainide, Propafenone (Can i have Fries Please)

281
Q

Na channel blockers Class IC: Mechanism and uses

A

Mechanism: Significantly prolongs refractory period in AV node, minimal effect on AP duration;
Uses: SVTs, including atrial fib. Only used as last resort in refractory VT

282
Q

Na channel blockers Class IC: Toxicity

A

Proarrhythmic; 1C is Contraindicated post MI and ischemic heart disease.

283
Q

Na channel blockers Class 1: Give me an overview of what they do

A

Slow or block conduction (especially in depolarized cells). Decrease slope of phase 0 and increased threshold for firing in pacemaker cells. Are state dependent (act more on depolarized cells so they will target tachycardic areas); Hyperkalemia causes increased toxicity for all Type 1 drugs.

284
Q

Antiarrhythmics Type II (Beta blockers): names

A

-olol (and carvedilol)

285
Q

Antiarrhythmics Type II (Beta blockers): Mechanism

A

Decrease SA and AV node activity by decreasing cAMP, and Ca currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV especially sensitive, increases PR interval. Esmolol is very short acting

286
Q

Antiarrhythmics Type II (Beta blockers): Clinical uses

A

SVT, slowing ventricular rate during atrial flutter and fibrillation

287
Q

Antiarrhythmics Type II (Beta blockers): Toxicity

A

Impotence, Makes COPD and asthma worse, heart block, bradycardia, sedation, sleep alterations. May mask the signs of hypoglycemia. Metoprolol can cause dyslipidemia, Propranolol can cause vasospasm in Prinzmetal angina. Contraindicated in cocaine users (unopposed alpha receptor agonist activity), treat overdose with glucagon

288
Q

Beta blockers can cause heart block: how will this normally present on ECG

A

ECG may show mobitz type II AV block (Some P waves will not be followed by QRS, but every QRS has a P wave before it)

289
Q

Antiarrhythmics Type III K channel blockers: names

A

Amiodarone (has class 1, 2, 3, and 4 effects), Ibutilide, Dofetilide, Sotalol (AIDS)

290
Q

Antiarrhythmics Type III K channel blockers: Mechanism

A

Increase AP duration, Increase ESR. Used only when other antiarrythmics fail. Increases QT interval.

291
Q

Antiarrhythmics Type III K channel blockers: Clinical use

A

Atrial Fib, atrial flutter, Ventricular tachycardia (amiodarone, sotalol)

292
Q

Antiarrhythmics Type III K channel blockers: Toxicity

A

Sotalol: Torsades de pointes, excessive Beta blockade;
Ibutilide: Torsades de pointes;
Amiodarone: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine), corneal deposits, skin deposits (blue/gray), resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF

293
Q

Antiarrhythmics Type IV Calcium channel blockers: Names

A

Verapamil, Diltiazem (non-dihydropyridines)

294
Q

Antiarrhythmics Type IV Calcium channel blockers: Mechanism, uses

A

Mechanism: decrease conduction velocity, increase ERP, increase PR interval;
Uses: Prevention of nodal arrhythmias (e.g. SVT), rate control in atrial fib.

295
Q

Antiarrhythmics Type IV Calcium channel blockers: Toxicity

A

Constipation, flushing, edema, CHF, AV block, sinus node depression

296
Q

Adenosine

A

Anti-arrythmic;
Increases K outside of cells leading to hyperpolarization and decreased Ca entering cell. Drug of choice for diagnosing and treating supraventricular tachycardia. Very short acting (15 seconds). Adverse effects are hypotension, chest pain, and flushing. Effects blocked by theophylline and caffeine

297
Q

Mg2+ as an anti-arrythmic

A

Effective in torsades de pointes and digoxin toxicity.

298
Q

What does the heart do when you have severe anemia

A

The decrease hemoglobin and decrease hematrocrit (hematocit is more important) cause decrease viscosity of blood. You get decreased peripheral resistance. The heart has increased HR, Stroke Volume, Pulse Pressure, and CO. you may get high output cardiac failure.

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