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Boards - Step 1 > First Aid Cardio > Flashcards

First Aid Cardio Flashcards

1
Q

CCB best for

(a) Prevent cerebral vasospasm in subarachnoid hemorrhage
(b) Hypertensive urgency/emergency
(c) AFib/Aflutter
(d) Raynaud’s
(e) HTN

A

CCB used for

(a) Prevention of cerebral vasospasm as complication of SAH = Nimodipine
(b) Hypertensive urgency = Clevidipine
(c) AFib/Flutter = non-dihydropiridines (act on the heart)- Verapamil, Diltiazem
(d) Raynaud’s = dihydropyridines (amlodipine)
(e) HTN- can use either dihydropyridine or non-dihydropyridine

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2
Q

RF for thoracic aortic aneurysm

A

Thoracic aortic aneurysms occur 2/2 medial cystic degeneration which is a vascular pathology of large BVs seen in connective tissue d/o (so Marfans, Ehler-Danlos)

Thoracic aortic aneurysm also historically seen in tertiary syphilis

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3
Q

ABCDEs of drug-induced prolonged QT

A

Drug-induced prolonged QT

Anti-arrthymics: class IA, III
Anti-biotics: macrolides
Anti-Cycotics: Haldol
Anti-depressants: TCAs
Anti-emetics: ondansetron (zofran)
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4
Q

Effect of ACEi and ARBs on preload and afterload

A

ACEi and ARBs both decrease both preload and afterload

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5
Q

Differentiate how receptors in the aortic arch vs. the carotid sinus conveys changes in BP to the CNS

A

Receptors in the aortic arch send signals via the vagus nerve (CN X) to the solitary nucleus of the medulla

Carotid sinus receptors relay messages thru glossopharyngeal nerve (CN IX) to solitary nucleus of the medulla

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6
Q

Which would present w/ earlier cyanosis: R to L or L to R cardiac shunts

A

R to L shunt (5 Ts of cyanosis) present earlier than L to R shunt (ex: VSD)

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7
Q

Takayasu arteritis

(a) Populaiton
(b) Clinical presentation
(c) Vessel affected

A

Takayasu arteritis = large vessel granulomatous vasculitis MC affecting aorta and its branches

(a) See in young (under 40 yo) Asian F
(b) Also called pulselessness disease b/c of weak upper extremity pulses
(c) Also called aortic arch syndrome

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8
Q

Differentiate the physiology of systolic vs. diastolic HF

A

Systolic HF is due to weakness of contraction (inotropic deficit) while diastolic dysfunction is due to reduced compliance due to myocardial hypertrophy

Systolic = can't properly contract
Disastolic = can't properly relax
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9
Q

2 main indications of digoxin

A

Digoxin (positive inotrope and reduces HR) indications

  1. HF/LV dysfunction
  2. AFib b/c reduces AV nodal conduction and depresses AV node
    - so reduces ventricular rate in AFib
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10
Q

How does hand grip change murmurs?

A

Hand grip increases afterload

  • increases most murmurs (AS, MR)
  • decreases HOCM murmur
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11
Q

Locate the infarct (and which artery is involved) if you see ST elevations or Q waves in the following

(a) V1-V2
(b) V3-V4
(c) V5-V6
(d) I, aVL
(e) II, III, aVF

A

Location of infarct

(a) Anteroseptal (LAD)
(b) Anteroapical (distal LAD)
(c) Anterolateral (LAD or LCx)
(d) Lateral (LCx)
(e) Inferiorly (RCA)

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12
Q

Name 4 systolic murmurs

A

4 systolic murmurs = AS, MR, VSD, MVP

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13
Q

Blood test lab value helpful in diagnosing heart failure

A

BNP (brain naturitic peptide)- released by ventricular myocytes in response to high wall tension, functions to promote diuresis by kidneys

Very good negative predictive value for HF (so if not elevated, can r/o HF)

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14
Q

Kawasaki disease

(a) What population?
(b) Clinical features

A

Kawasaki disease = medium vessel vasculitis

(a) Children under 4 yo, Asian
(b) Clinically: CRASH and burn
- Conjunctivitis- classically limbic sparing
- Rash
- Adenopathy- cervical
- Strawberry tongue
- Hand/foot changes- edema/erythema
- burn b/c fever for 5/7+ days

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15
Q

Describe the quality of the murmur heard in mitral stenosis

A

Mitral stenosis = late diastolic murmur following opening snap

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16
Q

Explain physiologic S2 splitting

A

S2 splits into A2 and P2 physiologically w/ inspiration b/c inspiration drops intrathoracic pressure which increases venous return

Increased venous return = more blood in the right heart, more time needed for RV to empty => delayed pulmonic closure

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17
Q

Describe how an untreated L to R shunt over time can cause late onset clubbing (Eisenmengers)

A

Eisenmengers = untreated L to R shunt causes eventual R to L shunt => late-onset cyanosis, clubbing, polycythemia

L to R shunt increases blood flow into pulm vasculature => pulm HTN => RVH => R to L shunt

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18
Q

Drug to decrease mortality in CAD pts

A

Statins (HMG CoA reductase)

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19
Q

Child 1 wk s/p URi p/w belly pain and red rash on buttocks and legs

(a) Dx
(b) Mechanism of disease

A

(a) HSP = Henoch-Schonlein purpura
- Clinical triad: skin-palpable purpura on butt/legs, arthralgias, abd pain
- following URI
- associated w/ IgA nephropathy => blood/protein in urine

(b) IgA complex deposition

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20
Q

What is the most common coronary artery to get occluded?

A

LAD (widow makerrrr)

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21
Q

Lab values to check in pt on amiodarone

A

Amiodarone is a dirty antiarrhythmic, w/ features of all 4 classes of drug (but is technically class III b/c it’s a K+ channel blocker)

Monitor 2 lab values: TFTs and LFTs q6 mo
-and EKG at baseline

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22
Q

What makes S1 and S2?

A

S1 = closing of AV valves (tricuspid and mitral)

S2 = closing of aortic and pulmonic valves

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23
Q

Key to management of cardiac glycoside toxicity

A

Management of glycoside toxicity

  • pacer or management of any arrhythmias
  • gradually normalize K+
  • -Anti-dig Fab fragments = Dig-specific antibody
  • Mg2+
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24
Q

Types of shock where skin is cold and clammy

A

Skin is cold and clammy in most shock (cardiogenic, hypovolemic)

Skin is warm/dry in distributive = neurogenic/anaphylactic

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25
Q

What is coarctation of the aorta?

(a) Location of defect
(b) Associated conditions
(c) CXR finding
(d) Clinical findings

A

Coarctation of the aorta = critical narrowing of the aorta

(a) Often juxtaductally (near the ductus arteriosus)
(b) Associated w/ bicuspid aortic valve and Turners syndrome
(c) CXR: rib notching, collaterals expand and erode ribs
(d) HTN in arms, weak delayed pulse w/ low BP in legs (brachial-femoral delay)

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26
Q

Name the 4 parts of Tetrology of Fallot

A

PROV

  • Pulmonary infundibular stenosis
  • RVH
  • Overriding aorta
  • VSD
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27
Q

Embryologic cause of

(a) persistent truncus arteriosus
(b) transposition of the great vessels
(c) tetrology of fallot

A

Embryology (gahhh Rindler no)

(a) Persistent truncus from failure of truncus division from lack of aorticopulmonary septum formation
(b) TGA due to failure of the aorticopulmonary septum to spiral
(c) ToF from anterosuperior displacement of the infundibular septum

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28
Q

How long after MI do you expect

(a) Neutrophils vs. macrophages to come on the scene
(b) Free wall rupture
(c) Dressler syndrome

A

Post-MI

(a) Neutrophils come first (w/in 4-12 hrs), then macrophages later around 3 days
(b) Highest risk of free wall rupture at 3-10 days
(c) Dressler syndrome (autoimmune post-MI pericarditis) several weeks post-MI

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29
Q

Ductus arteriosus

(a) How to keep open
(b) How to shut

A

Ductus arteriosus

(a) Keep open w/ prostaglandin E2
“kEEp opEn w/ E2”

(b) Shut w/ indomethacin (NSAID)

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30
Q

Function of ANP

A

ANP (atrial naturitic peptide) functions to promote diuresis in the setting of high blood volume and atrial volume

  • released by atrial myocytes in responseto high volume and high atrial pressures
  • causes vasodilation and decreased Na+ reabsorption in kidney => promoting diuresis
  • contributes to aldo escape mechanism (aldo high but still diures)
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31
Q

Name the 4 locations of fetal erythropoiesis

A

“young liver synthesizes blood”

Yolk sac for first 3-8 weeks
Liver from 6 weeks to birth
Spleen from 10-28 weeks of life
Bone marrow from 18 weeks to adulthood

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32
Q

What does it mean to be right heart dominant?

A

PDA (posterior descending artery/interventricular artery) arises from the right carotid artery- 85% of the population

While 8% are L. dominant where the PDA arises from the LCx

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33
Q

Describe coronary steal syndrome and how it explains pharmacologic stress tests

A

Coronary steal syndrome: at rest the post-stenotic arterial segment is maximally dilated, so upon administrating vasodilator (dipyridamole, regadenoson) blood is actually shunted towards already well perfused areas of the heart, causing loss of flow to the areas that need it (and just can’t dilate anymore b/c already maximally dilated at rest)

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34
Q

What embryologic structure gives rise to the ascending aorta

A

Truncus arteriosus => ascending aorta and pulmonary trunk

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35
Q

VSD

(a) Describe the quality of the murmur
(b) Location of the murmur

A

VSD

(a) Harsh holosystolic murmur
(b) Typically heard loudest at the tricuspid area

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36
Q

MC primary cardiac tumor in

(a) Adults
(b) Children

A

MC primary cardiac tumors in

(a) Adults = myxomas- usually in the LA

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37
Q

Rheumatic fever

(a) Early vs. late valvular finding
(b) Tx
(c) Major criteria

A

Rheumatic fever

(a) Early lesion is MR, late lesion is MS
(b) Penicillin
(c) Major criteria = JO(heart shaped)NES for clinical findings of rheuamtic fever

Joints- migrating polyarthritis
Cardiac
Nodules in skin (subcutaneous)

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38
Q

What do the following embryologic structures become

(a) Allantois
(b) Ductus arteriosus
(c) Foramen ovale
(d) Notochord
(e) Umbilical arteries
(f) Umbilical vein

A

Embryologic derivatives

(a) AllaNtois => urachus (connects bladder and umbilicus) => mediaN umbilical ligament
(b) Ductus arteriosus => ligamentum arteriosum
(c) Foramen ovale => fossa ovalis
(d) Notochord => nucleus pulposis btwn vertebrae
(e) UmbilicaL arteries => mediaL umbilical ligament
(f) Umbilical vein => falciform ligament

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39
Q

Differentiate effects of venodilators vs. vasodilators on preload and afterload

A

vEnodilators (ex: nitroglycerin) decrease prEload
-explains why to not give pts w/ inferior MI sublingual nitro, b/c they’re preload dependent to maintain CO

vAsodilators (hydrAlAzine) decrease Afterload

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40
Q

What is isovolumetric relaxation?

A

Isovolumetric relaxation = time between when pulmonic/aortic valves close and the AV valves open

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41
Q

Name the mechanism of the classes of antiarrhythmis

(a) I
(b) II
(c) III
(d) IV

A

Antiarrhtyhmics

(a) I = Na+ channel blockers, reduces the slope of phase 0
(b) II = beta-blockers, reduces slope of phase 4, reduces SA and AV node activity
(c) III = K+ channel blockers

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42
Q

Mitral valve prolapse

(a) Describe the quality of the murmur
(b) Location of the murmur

A

MVP

(a) Late systolic crescendo murmur w/ midsystolic click
(b) Over the apex, heard best just before S2

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43
Q

Bacterial endoarditis

(a) Most frequently involved valve
(b) Valve associated w/ IV drug use

A

(a) Mitral- almost most frequently involved in rheumatic fever
(b) “dont TRI drugs”- tricuspid valve vegetations associated w/ IVDU

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44
Q

Differentiate S3 and S4

(a) Timing
(b) Implications

A

S3 happens in early diastole

  • indicates elevated filling pressures (HF, MR) and in dilated ventricles
  • can be normal in children and pregnant F

S4 happens in late diastole

  • indicates high atrial pressure and ventricular hypertrophy
  • LA pushing against a stiff LV wall
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45
Q

How does inspiration change heart sounds?

A

Inspiration decreases intrathoracic pressure => increases venous return => increases preload so increases right sided heart sounds (like S1)

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46
Q

Clinical manifestations of bacterial endocarditis

“FROM JAME”

A

FROM JANE

Fever
Roth spots = round white spots on retina surrounded by hemorrhage
Osler nodes = tender raised lesions on finger or toe pads
Murmur- of new onset
Janeway lesions = small, painless, erythematous lesions on palm or soles
Anemia
Nail-bed (splinter) hemorrhage
Emboli (septic arterial or pulmonary)

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47
Q

Define

(a) HTN
(b) Hypertensive urgency
(c) Hypertensive emergency

A

(a) HTN = over 140, over 90
(b) hypertensive surgery: severe HTN (over 180, over 120) w/o e/o end organ damage
(c) Over 180, over 120 w/ evidence of end organ damage
- stroke, MI, retinal hemorrhage, papilledema, encephalopathy, aortic dissection, eclampsia

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48
Q

What is the Starling curve?

A

Starling curve = compares preload to cardiac output/SV

So at any given preload, how much of it will the heart output
-shows how HF will have much lower CO at a given preload

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49
Q

Name some positive inotropes

A

Inotropes increase contractility

  • Digoxin (Na/K channel blocker) increases contractility by increasing intracellular Ca2+
  • Catecholamines (Dopamine, epi, norepi)
  • exercise
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50
Q

What is Brugada syndrome?

(a) EKG pattern
(b) Risk
(c) Prevention

A

Brugada syndrome = aut dom d/o w/ characteristic EKG and increased risk of sudden cardiac death from VF
-MC in asian males

(a) EKG: pseudo-right bundle branch block w/ ST elevations in V1-V3
(b) Risk = sudden cardiac death
(c) ICD = implantable cardioverter-defibrillator

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51
Q

Name 2 etiologies of wide S2 splitting

A

Wide S2 splitting caused by things that delay closure of the pulmonic valve

  • pulmonic stenosis
  • RBBB
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52
Q

Differentiate baroreceptors and chemoreceptors

A

Both are located at the carotid body (swelling at the bifurcation of common carotid artery) and in the aortic arch

Baroreceptors repsond to stretch (carotid massage, pressure due to elevated ICP) while chemoreceptors respond to change in pCO2 and pH (and peripherally to low pO2)

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53
Q

Differentiate the 4 types of AV block

A

1st degree block = benign, prolongation of PR interval to over 200 ms

2nd degree

  • Mobitz Type I (Wenckebach): progressive lengthening of PR interval until dropped beat, regularly irregular
  • Mobitz Type II: dropped beats not preceded by PR prolongation, may progress to 3rd degree so often tx w/ pacemaker

3rd degree = presence of P-waves and QRS complexes but completely independent of each other

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54
Q

What is a J point on EKG?

A

J point = junction btwn the end of the QRS and the start of the ST segment

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55
Q

Unique feature of pulmonary vasculature

A

Pulmonary vasculature is the one place that vasoconstricts in response to hypoxia

  • high CO2 in brain/heart causes vasodilation, while in lungs high CO2 causes vasoconstriction so that only well-ventilated areas are perfused
  • selective vasoconstriction to make the best V/Q match
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56
Q

Which lipid lowering agent increases the risk of cholesterol gallstones

A

Fibrates (best at reducing TG) can cause cholesterol galstones

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57
Q

Name 3 shunts found in utero not found in the fetus

A
  1. Ductus venosus connecting umbilical vein to IVC
  2. Foramen ovale connecting RA and LA
    - bypass the lungs
  3. Ductus arteriosus shunts from pulmonary artery (R. heart) into the descending aorta
    - 2/2 high fetal pulmonary artery resistance
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58
Q

Describe the quality of the murmur heard in aortic regurgitation

A

Aortic regurg = early diastolic decrescendo murmur, high pitched

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59
Q

Predictor of mortality in cardiac glycoside activity

A

In digoxin toxicity, hyperkalemia (presence and degree) determines prognosis and is associated to mortality

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60
Q

Tetrology of fallot

(a) most important factor for prognostic determination
(b) CXR finding
(c) Classic clinical feature
(d) Response to squatting
(e) Tx

A

ToF

(a) Degree of pulmonary stenosis determines prognosis
(b) Boot shaped heart 2/2 RVH
(c) Tet spells (blue spells) where baby hugs knees into chest (squatting to increase SVR)
(d) Squatting improves cyanosis b/c increases SVR and decreases the R to L shunt
(e) Tx is early surgical correction

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61
Q

Name the congenital heart defect(s) associated w/ the following d/o

(a) Fetal alcohol syndrome
(b) Congenital rubella
(c) Down syndrome
(d) Maternal diabetes

A

(a) FAS => VSD, ASD, ToF, PDA
(b) Congenital rubella => pulmonary artery stenosis and patent ductus
(c) Down => endocardial cushion defect (causing AV septal defect)
(d) Maternal diabetes => transposition of great vessels

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62
Q

Name 3 places in the body where lipid-laiden histiocytes are MC to deposit 2/2 hyperlipidemia

A

Xanthomas = lipid-laiden histiocytes deposit in nodules/plauqes

  • skin, especially eyelides (xanthelomas)
  • also in the cornea, causing earlier onset of corneal arcus (rim around cornea)
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63
Q

Main features of cardiac glycoside toxicity

A

Cardiac glycoside (digoxin) toxicity

  • -cardiac arrhythmias (really can cause any)
  • -electrolyte abnormalities: mainly hyperkalemia
  • visual changes
  • cholinergic: nausea/vom/dio
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64
Q

Etiologies of right HF

A

MC cause of R HF is left HF

R HF w/o L HF = cor pulmonale- due to pulm HTN and other lung pathology

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65
Q

Differentiate physiologic cardiac action potential from pacemaker action potential

A

Talking physiologic pacemaker (not external) so like SA and AV node

Similar (obvs) except for fast-gated Na+ channels (responsible for rapid depolarization in step 0) are permanently inactivated
-phase 0 done by opening of voltage-gated Ca2+ channels => slow conduction velocity used by AV node to delay transmission from A to V

Then Ca2+ inactivated and K+ activated (same as non-pacemaker regions)
Stage 4 is a slow spontaneous depolarization (upstroke)
-slope of this stage 4 at the SA node determines HR

66
Q

3 clinical manifestations of aortic stenosis

A

AS- SAD
syncope
angina
dyspnea on exertion

67
Q

Bacteria implicated in endocarditis and

(a) acute rapid onset w/ no previously abnormal valves
(b) congenitally abnormal or diseased valve w/ gradual onset
(c) colon cancer
(d) prosthetic valves
(e) after dental procedure

A

Bacterial endocarditis

(a) Acute, staph aureus
- high virulence
(b) Gradual onset on diseased valve (subacute)- strep viridans
(c) Colon cancer- think strep bovis (gallolyticus)
(d) Prosthetic valve- staph epidermis
(e) Post-dental procedure = strep viridans => subacute

68
Q

How is cardiac output maintained

(a) Early in exercise
(b) Later in exercise

A

Cardiac output

(a) Early in exercise both stroke volume and HR increase to maintain
(b) Then SV plateaus and elevated HR maintains CO the rest of exercise

69
Q

What can cause fixed S2 splitting?

A

Fixed S2 splitting (aka doesn’t change w/ inspiration) caused by ASD, b/c left to right shunt makes pulmonic valve close super delayed regardless

70
Q

Name some negative inotropes

A

Negative inotropes = decrease cardiac contractility (thereby decrease myocoardial O2 demand)

  • Beta1-blockers transiently (atenolol, metoprolol) by reducing cAMP
  • loss of cardiac tissue: like infarction seen in MI
  • non-dihydropyridine CCB = Verapamil, Diltiazam
  • Acidosis (elevated PCO2)
71
Q

Differentiate microscopic polyangiitis from eosinophilic granulomatosis w/ polyangiitis

A

Both are p-ANCA small vessel vasculitides

Microscopic polyangiitis = no granulomas, mostly lung kidney and skin involvement

Eosinophilic granulomatosis w/ polyangiitis = asthma/sinusitis, skin nodules or purpura, granulomatosis and IgE
-mechanism = IgE deposition

72
Q

Mitral regurgitation

(a) Describe the quality of the murmur
(b) Location of the murmur
(c) Most common cause

A

MR

(a) Holosystolic high pitched blowing murmur
(b) Heard best at the apex radiating towards the axilla
(c) MC cause = MI (ischemic heart disease)

73
Q

EKG findings of Prinzmetal angina

A

Prinzmetal angina = coronary vasospasm, CP at rest not due to occlusion

EKG shows transient ST elevations

74
Q

Name 2 etiologies of paradoxically split S2

A

Paradoxically split S2 means the split goes away w/ inspiration, really P2 coming before A2 w/ inspiration
Caused by things that delay closure of aortic valve
-aortic stenosis
-LBBB

75
Q

MC cause of

(a) aortic regurg
(b) mitral stenosis

A

MC cause of

(a) Aortic regurg = bicuspid aortic valve, aortic root dilation, endocarditis
(b) MS 2/2 RF

76
Q

Polyarteritis nodosa

(a) What is it? Vessels affected?
(b) Associated condition
(c) Classic finding on renal arteriogram
(d) Tx in addition to corticosteroids

A

Polyarteritis nodosa = medium-vessel vasculitis

(a) Medium vessel vasculitis affecting mostly renal and visceral vessels, sparing pulmonary vasculature
(b) Around 30% of pts have chronic HepB
(c) Rosary appearance of renal arteries b/c of tons of small renal aneurysms strung like beads
(d) In addition to corticosteroids, tx w/ immunosupression (cyclophosphamide) b/c it’s immune complex mediated

77
Q

Mechanism of digoxin

A

Digoxin = cardiac glycoside = Na/K ATPase inhibitor

  1. Indirectly inhibits Na/Ca2+ exchanger to increase intracellular calcium => positive inotrope
  2. stimulates vagus nerve => reduces HR
78
Q

Recombinant form of what natural peptide is useful in tx of HF

A

Recombinant form of BNP (released by ventricular myocytes in response to high wall tension to promote diuresis by kidneys) is available in the tx of HF

79
Q

Differentiate clinical signs of L vs. R heart failure

A

LHF- orthopnea, PND, pulmonary edema
-fluid backs up into lungs

RHF- JVD, hepatomegaly, peripheral edema

80
Q

Kawasaki disease

(a) What is it?
(b) Tx
(c) Coronary complication

A

Kawasaki disease

(a) Medium vessel vasculitis of children under 4 yo p/w fever for multiple days
(b) Tx = IVIG and aspirin
(c) Risk of coronary artery aneurysm

81
Q

ANP vs. BNP

(a) Where are they released from?
(b) Function

A

ANP vs. BNP

(a) ANP from atrial myocytes (in response to high atrial pressure and high blood volume), BNP from ventricular myocytes (in response to high wall tension)
(b) Both function to cause vasodilation and reduce renal Na+ reabsorption => promote diuresis (ex: elevated in HF)

82
Q

Differentiate Romano-Ward syndrome from Jervell/Lange-Nielson syndrome

A

Both are congenital ion channel defects that cause congenital long QT syndrome => increased risk of sudden cardiac death

Romano-Ward: aut dom, pure cardiac phenotype (no deafness)
Jervell/Lange-Nielson: aut rec, sensorineural hearing loss

83
Q

What is Kussmal’s sign (not breathing…)

(a) Associated conditions

A

Kussmal’s sign - paradoxical increase in JVD w/ inspiration (usually JVD decreases w/ inspiration)
-occurs b/c there is an obstruction preventing RV filling

(a) RA/RV tumors, constrictive pericarditis, restrictive cardiomyopathy

84
Q

Differentiate granulomatosis w/ polyangiitis from microscopic polyangiitis

A

Granulomatosis w/ polyangiitis = c-ANCA small vessel vasculitis involving kidneys, upper and lower airways

Microscopic polyangiitis = p-ANCA small vessel vasculitis involving kidneys, lung, and skin (w/o nasopharyngeal involvement)
-no granulomas

85
Q

MC

(a) congenital heart defect
(b) cause of early childhood cyanosis

A

MC

(a) Congenital heart defect = VSD
(b) Cause of earlihood cyanosis = ToF

86
Q

Temporal arteritis

(a) Clinical presentation
(b) Vessels MC affected
(c) Tx and why to tx fast
(d) Associated condition
(e) Pathology on biopsy

A

Temporal arteritis = large vessel vasculitis

(a) Unilateral headache and ipsilateral jaw claudication
(b) Carotid artery and its branches (temporal artery, opthalmic artery)
(c) Tx w/ corticosteroids before temporal artery biopsy comes back b/c want to prevent vision loss 2/2 opthalmic artery occlusion
(d) Associated w/ polymyalgia rheumatica (pain of girdles- shoulder and hips/pelvis)
(e) Focal granulomatous inflammation

87
Q

Name the 5 T’s that cause blue baby

A

5 T’s (use fingers 1 through 5)

  1. Truncus arteriosus- persistence of single vessel comprising of aortic and pulmonic trunk
  2. Transposition of the great vessels
  3. Tricuspid atresia
  4. Tetrology of Fallot
  5. TAPVR = total anomalous pulmonary venous return- pulmonary veins drain into the r. heart
88
Q

What is isovolumetric contraction?

A

Isovolumetric contraction = the period between the time that the mitral valve closes and the aortic/pulmonic valve opens
-first little bit of systolic

89
Q

Mechanism of CCBs in tx of HTN

A

CCBs block voltage-dependent L-type calcium channels of cardiac and smooth muscle to decrease contractility

90
Q

Relationship of pulse pressure to

(a) Stroke volume
(b) arterial compliance
(c) Aortic valve function
(d) thyroid hormone levels

A

Pulse pressure = SBP - DBP

(a) directly proportional to stroke volume
(b) inversely proportional to arterial compliance
- more elastic vessels causes narrower pulse pressure

(c) Aortic stenosis causes narrowing of pulse pressure, while aortic insufficiency/stiffening (w/ age)
(d) Hyperthyroid can cause widened pulse pressure

91
Q

Cherry hemangioma vs. strawberry hemangioma

A

Both are benign capillary hemangiomas, but just dif age groups

Cherry hemangiomas in the elderly, incidence increases w/ age

Strawberry hemangiomas in infancy, regress spontaneously by ages 5-8

92
Q

Differentiate the two categories of CCB

A

Dihydropyridines act on vascular smooth muscle: amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

Non-dihydropyridines act on the heart: verapamil, diltiazem

93
Q

Name 2 large vessel vasculitides

A

Large vessel vasculitides = temporal/giant cell arteritis and Takayusu arteritis

94
Q

Cushings triad

A

HTN, bradycardia, respiratory depresison

95
Q

Describe 2 things that happen to fetal circulation w/ the first breath

A
  1. Reduced resistance of the pulmonary vasculature causes increased LA pressure => closing of the foramen ovale (now the fossa ovalis)
  2. High O2 (from respiration) and decreased prostaglandins (from placental separation) closes ductus arteriosus
    - now the ligamentum arteriosum
96
Q

HF tx

(a) Symptomatic
(b) Decrease mortality

A

Tx of HF

(a) For symptomatic tx only: diuretics
(b) Drugs that have mortality benefit =

97
Q

What is the funny current?

A

Funny current is the current thru funny channels on cardiac pacemaker cells- slightly different type of conduction potential that causes spontaneous depolarization
-spontaneous depolarization during diastole to create the funny current, forming a natural pacemaker

98
Q

Define sudden cardiac death and name some causes

A

SCD = death from cardiac cause w/in 1 hour of symptom onset

Etiologies

  • arrhythmia
  • large obstruction
  • congenital: long-QT, Brugada (channelopathies)
  • HOCM
99
Q

Local metabolites of the

(a) Heart
(b) Brain

that help maintain blood flow during low perfusion states

A

Local metabolites to increase perfusion (autoregulation), aka local factors that cause vasodilation

(a) Heart- adenosine, NO, CO2, hypoxia

(b) Brain- CO2
- this is why hyperventilation (CO2 to 30) temporarily causes vasoconstriction in attempt to reduce ICP

100
Q

Give a brief overview of atherosclerotic plaque formation

A

Pathophysiology of atherosclerotic plaque: macrophages eat up LDL and turn into foam cells and form fatty streaks, PDGF and FGF attract smooth muscle cells which deposit proliferate and form fibrous plaque over cholesterol deposits

101
Q

Hydralazine

(a) Mechanism
(b) Indications
(c) Why often coadministered w/ beta-blocker

A

Hydralazine

(a) Smooth muscle relaxation (vasodilation) viaincrease in cGMP
- Vasodilates arterioles much more than veins => reduces afterload
(b) Used for severe HTN (and safe in pregnancy) and HF tx
(c) Prevents reflex tachycardia seen w/ beta-blockers

102
Q

What is pulsus paradoxus?

(a) Seen in what?

A

Pulsus paradoxus = drop in systolic BP of 10 or more mmHg during inspiration

(a) Seen in cardiac tamponade, asthma, OSA, pericarditis, croup

103
Q

What does a T wave represent on EKG?

A

T wave is ventricular repolarization
-expect it to be in the same direction as the QRS (unless there is a bundle branch block)

Inverted T waves (as in in a different direction than the QRS w/o BBB) may indicate recent MI

104
Q

Keys to treating HTN in pts w/ DM

A

ARB/ACEis help prevent diabetic neuropathy

105
Q

Differentiate peripheral vs. central chemoreceptors for BP

A

Central chemoreceptors respond to changes in pH and pCO2 in the brain
-so not directly, but these reflex body arterial pO2

Peripheral chemoreceptors respond to change in pH, pCO2, and very low pO2 (under 60 mmHg)

106
Q

Describe how baroreceptors are involved in the following

(a) Response to carotid massage
(b) Cushings reflex

A

Baroreceptors

(a) Carotid massage increases pressure on the carotid baroreceptors which increases firing, increasing the refractory period and slowing HR
- basically know it slows HR

(b) Cushing’s triad (HTN, bradycardia, respiratory depression): elevated ICP vasoconstricts cerebral vasculature => ischemia which activates central reflexive increase in sympathetic tone (hence the HTN)
- this HTN then increases stretch on the baroreceptors => bradycardia

107
Q

How to treat HTN in HF

A
  • diuretics for symptoms
  • ACEi and ARBs to decrease mortality
  • beta-blockers cautiously, only in compensated (not acute) HF
108
Q

Describe what ion is in charge of causing cardiac myocyte contraction

A

Ultimately it is intracellular calcium that stimulates calcium release from SR that causes contraction

109
Q

First line anti-anginals

(a) Physiology

A

Anti-angina = nitrate plus beta-blocker

(a) Act to decrease myocardial oxygen demand

110
Q

Describe the pathway of blood from placenta to fetal heart

A

Blood leaves the placenta out the umbilical vein, then into ductus venosus (only present embryologically, allows bypass of portal circulation) into the IVC

So umbilical vein –> ductus venosus –> IVC

111
Q

What embryologic structure gives rise to the valves of the heart

A

Endocardial cushions

112
Q

Differentiate physiology of nitrates vs. hydralazine

A

Both vasodilate

  • nitrates vasodilate veins over arteries => reduce preload
  • hydralazine vasodilates arteries over veins => reduces afterload
113
Q

What is the ST segment on EKG?

A

ST segment = ventricles are depolarized, haven’t started to repolarize yet

Segments don’t include waves while intervals do

114
Q

Risk factor for Ebstein’s anomaly

A

Mothers taking Lithium in first trimester

115
Q

EF value in systolic vs. diastolic HF

A

EF is normal in diastolic, but reduced (under 55%) in systolic HF

116
Q

Small vessel vasculitides

(a) c-ANCA
(b) p-ANCA

A

Small vessel vasculitides

(a) c-ANCA = granulomatosis w/ polyangiitis
(b) p-ANCA = both microscopic polyangiitis and eosinophilic granulomatosis w/ polyangiitis

117
Q

Differentiate the components of embryonic, fetal, and adult Hgb

A 
Embryonic = zeta2epsilon2
Fetal = alpha2gamma2
Adult = alpha2beta2

“Alpha always, gamma goes and becomes beta”

118
Q

Treatment of

(a) Afib
(b) Aflutter
(c) Vfib

A

Tx

(a) Afib:
rate control: beta-block, no-dihy CCB, digoxin
rhythm control w/ class Ic and III antiarrhythmics
anticoagulate w/ warfarin
(b) Aflutter- same tx as Afib or definitive therapy of catheter ablation
(c) Vfib- defibrillate immediately

119
Q

How does valsalva change murmurs?

A

Valsalva decreases preload

  • decreases most murmurs (AS, MR)
  • increases HOCM murmur
120
Q

Dx if you hear pericardial friction rub

(a) 1-3 days post-MI
(b) 3 weeks post-MI

A

Pericardial friction rub post-MI

(a) 1-3 days = postinfarction fibrinous pericarditis
(b) 3 weeks = Dressler syndrome = autoimmune phenomenon causing fibrinous pericarditis

121
Q

Name the congenital heart defect(s) associated w/ the following d/o

(a) Marfan syndrome
(b) Lithium exposure
(c) Turner syndrome
(d) Williams syndrome
(e) 22q11 syndromes

A

(a) Marfan => MVP, thoracic aortic aneurysm, aortic insufficiency
(b) Lithium exposure => Ebstein anomaly (severe TR)
(c) Turner => coarctation of aorta, bicuspid aortic valve
(d) Williams => supravalvular aortic stenosis
(e) 22q11 syndromes => truncus arteriosus, ToF

122
Q

Of the 3 types of cardiomyopathies (dilated, hypertrophic, restrictive) which is associated w/

(a) systolic dysfunction
(b) S3
(c) S4
(d) chronic EtOH/chronic abuse
(e) Doxorubicin toxicity
(f) Sarcoidosis
(g) Amyloidosis
(h) Friedreich ataxia
(i) B1 deficiency

A

90% of cardiomyopathies are dilated (so majorly the most common)

(a) Systolic dysfunction seen in dilated, while diastolic dysfunction seen in hypertrophic and restrictive
(b) S3 heard in dilated
(c) S4 heard in hypetrophic
(d) EtOh/Cocaine => dilated
(e) Doxorubicin (amikacin, chemo drug) => dilated
(f) Sarcoidosis => usually restrictive but can cause dilated
(g) Amyloid => restrictive
(h) Friedreich ataxia => hypertrophic
(i) Wet beriberi => dilated

123
Q

Wolff-Parkinson-White

(a) What is it?
(b) EKG pattern
(c) Risk

A

WPW

(a) Ventricular pre-excitation, presence of abberant fast accessory pathway from the A to V (bundle of Kent) that bypass the rate-slowing by the AV node
(b) Ventricles depolarize earlier => characteristic delta wave (concave upward slope of P to R), widened QRS, shortened PR
(c) Can result in reentry circuit => supraventricular tachycardia

124
Q

Clinical findings of end organ damage in hypertensive emergency

A

Signs of end organ damage

  • Neuro: encephalopathy, stroke
  • HEENT: papilledema, retinal hemorrhage
  • CV: MI, aortic dissection
  • Renal: kidney injury
  • eclampsia
125
Q

Formula for MAP

A

MAP = 2/3(diastole) + 1/3(systole)

126
Q

Antiarrhythmic that is best for

(a) post-MI ventricular tachycardia
(b) Digitalis induced arrhythmias
(c) diagnose and abolish SVT short-term
(d) Afib rate control

A

Antiarrhtyhmic for

(a) post-MI ventricular arrythmias = Class IBs (Na+ channel blockers) = Lidocaine, Mexiletine
(b) Digitalis induced arrhtyhmias = Mg2+, Class IBs
(c) Diagnose and abolish SVT = adenosine, very short acting (like 15 seconds)

(d) AFib rate control- lots of options
- beta-blockers (class II)
- CCBs (class IV)

127
Q

What is Ebstein’s anomaly

A

Inferiorly displaced tricuspid valve, causes severe tricuspid regurgitation (backflow into the RA)

128
Q

Aortic stenosis

(a) Describe the quality of the murmur
(b) Location of the murmur
(c) Associated physical exam finding

A

Aortic stenosis

(a) Holosystolic crescendo- decrescendo ejection murmur
(b) Heard best at RUSB (base of the heart), radiating to the carotids
(c) Pulsus parvus et tardus = pulse weak and w/ delayed peak

129
Q

Statins

(a) Mechanism of action
(b) Lab value to monitor
(c) Effect on LDL, HDL, and TG
(d) Clinical side effect

A

Statins = lipid lowering agent

(a) HMG CoA reductase inhibitor to reduce precursor production into cholesterol in hepatocytes
(b) Monitor LFTs, can cause hepatotoxicity
(c) Great at reducing LDL, increase HDL, reduces TG
- yay to all 3
(d) Myopathy
- especially when taken w/ fibrates or niacin

130
Q

Which cyanotic congenital heart lesions require VSD

A

Out of the 5 cyanotic heart lesions

  1. Truncus arteriosus usually w/ VSD
  2. Transposition of the great vessels REQUIRES shunt (VSD, PDA, PFO)
  3. Tricuspid atresia- requires both ASD and VSD for viability
  4. Tetrology of fallot- has VSD
  5. TAPVR often ASD (not VSD)
131
Q

Explain how LA enlargement could cause

(a) dysphagia
(b) hoarseness

A

(a) LA is just anterior to the esophagus => esophageal compression
(b) left recurrent larygneal nerve compression

132
Q

Name 2 causes of U-waves on EKG

A

U waves = waves after T wave before P wave

Caused by hypokalemia and bradycardia

133
Q

Tx of Raynaud’s phenomenon

A

CCB b/c it’s arteriolar vasospasm

134
Q

Risk factors for prolonged QT

A

RF for prolonged QT

  • tons of drugs (macrolides, haldol, zofran)
  • hypomag and hypophs
135
Q

Describe 4 mechanisms by which edema can occur given capillary pressure, interstitial fluid pressure, plasma colloid osmotic pressure, and interstitial fluid colloid osmotic pressure

A

Edema = excess fluid outflow out of capillaries into the interstitium

  • increased capillary pressure: HF
  • loss of plasma proteins (reduced plasma colloid osmotic pressure): nephrotic syndrome, liver failure
  • increase in capillary permeability: toxins, infections,burns
  • increase in intertitial fluid colloid osmotic pressure (pulls fluid out of capillaries) such as in lymphatic blockage
136
Q

Cardiac tamponade

(a) Clinical findings
(b) EKG finding

A

Cardiac tamponade

(a) Beck’s triad = muffled heart sounds, JVD, hypotension
(b) EKG: electrical alternans and low-voltage QRS

137
Q

MC heart tumor

A

Mets

138
Q

Nitroprusside

(a) Mechanism
(b) Indication
(c) Risk

A

Nitroprusside

(a) Direct release of NO causes increase in cGMP
(b) Hypertensive emergency
(c) Risk of cyanide poisoning b/c releases cyanide

139
Q

How does rapid squatting change murmurs?

A

Rapid squatting increases preload

  • increases most murmurs (AS, MR)
  • decreases HOCM
140
Q

What is congenital long QT syndrome?

(a) Why it’s concerning

A

Congenital long QT syndrome = inherited ion channel defect causing disorder of myocardial repolarization => increased risk of sudden cardiac death due to torsades de pointes (polymorphic VT)

141
Q

35 yo heavy smoker w/ Raynaud’s phenomenon and auto-amputation of 2 toes

(a) Possible dx
(b) Mechanism of disease

A

(a) Dx = Buerger disease = Thromboangiitis obliterans = medium vessel vasculitis seen in smokers
(b) Recurring progressive inflammation and clotting in hands/feet => gangrene, autoamputation

Tx = smoking cessation

142
Q

What are angiosarcomas?

A

Angiosarcomas = malignant tumors of vasculature, can be of the walls of blood vessels or lymphatic vessels
-often aggressive and hard to treat

143
Q

What two arrhythmias indicate tx w/ Mg2+

A

Give Mg2+ in Torsades de pointes and digoxin toxicity

144
Q

PDA

(a) Quality of murmur
(b) Location of murmur
(c) 2 MC etiologies

A

Patent ductus

(a) Machine like continuous murmur loudest at S2
(b) Best heard at the L infraclavicular area

145
Q

Differentiate ASD from PFO

A

ASD = actual lack of atrial septal tissue

PFO = failure to fuse

146
Q

Differentiate function of troponin I and CK-MB as cardiac markers

A

Troponin I elevates after 4 hrs, remains elevated for 7-10 days. Most specific marker b/c only released by cardiac myocytes

CK-MB elevated after 6-12 hrs and normalizes w/in 48 hrs. Not as specific b/c also can be released by skeletal muscle, but good for marker of reinfarction b/c normalizes much faster

147
Q

Acute pericarditis

(a) Clinical features
(b) Physical exam finding
(c) EKG findings
(d) MC cause

A

Acute pericarditis

(a) Pain worse w/ inspiration, improves on sitting up and leaning forward
(b) Pericardial rub
(c) Classically- diffuse ST elevations w/ PR
(d) MC cause = idiopathic, which then is assumed to be viral

148
Q

Describe the EKG findings of

(a) Afib
(b) Aflutter
(c) Vfib

A

EKG findings

(a) Afib- irregularly irregular sporadic baseline w/ no discrete P waves
(b) Aflutter- rapid identical atrial depolarizations giving appearance of sawtooth
(c) Vfib- completely erratic w/ no identifiable waves

149
Q

Differentiate EKG findings of

(a) transmural
(b) subendocardial infarcts

A

EKG findings

(a) Transmural infarct = ST elevations, Q waves
(b) Subendocardial infarcts (less than 50% of the ventricular wall infarcted) = ST depression

150
Q

What is torsades de pointes?

A

Tosades de pointes = polymorphic ventricular tachycardia (waves all look dif, fast HR with wide QRS)

Dangerous b/c can turn into Vfib => sudden cardiac death

151
Q

Describe phases 0 through 4 of a myocardial action potential

A

Myocardial action potential

Phase 0 = INa = opening of voltage-gated Na+ channels to go from -85mV to +10ish

Phase 1 = initial repolarization, Na+ channels inactivated and voltage-gated K+ channels begin to open

Phase 2 = Ica and Ik) Plateau, Ca2+ influx thru voltage-gated Ca2+ channels balances K+ efflux
-Ca2+ influx triggers Ca2+ release from SR and myocyte contraction

Phase 3 = IK = rapid repolarization- quickly drops from 0mv back down to -85 2/2 massive K+ efflux due to opening of voltage-gated slow K+ and closure of voltage-gated Ca2+

Phase 4 = resting potential, high K+ permeability through K+ channels

152
Q

AV node

(a) Exact location
(b) Blood supply
(c) Duration and significance of conduction delay

A

AV node

(a) Posterior inferior part of the intra-atrial septum
(b) Usually supplied by the RCA
(c) Conduction delay of about 100ms to allow for ventricular filling

153
Q

Why don’t we see atrial repolarization on EKG?

A

Masked by QRS (ventricular depol)

154
Q

Possible etiologies of mitral valve prolapse

A

MVP

  • myxomatous degeneration: primary or secondary to CT disease (Marfans, Ehlers-Danlos)
  • RF
  • chordae rupture
155
Q

Duration of

(a) QRS interval
(b) PR interval

A

Duration of

(a) Ventricular depolarization = 120 ms or shorter (so 3 small boxes)
(b) PR interval- time from start to atrial depol to start of ventricular depol (start of P wave to start of Q) under 200ms

156
Q

Describe paradoxical emboli and their cause

A

Cause = PFO = patent foramen ovale- foramen secundum not completely covered by the septum secundum

When venous clot ends up in the arterial circulation (so out the aorta by getting shunted RA to LA) instead of in the lungs

157
Q

What is PCWP used to approximate?

(a) Name a disease state where PCWP > LV diastolic pressure

A

PCWP used to approximate LA pressure
-measured w/ Swan-Ganz catheter

(a) Mitral stenosis

158
Q

Most common etiologies of aortic stenosis

A

AS

  • calcification w/ age
  • bicuspid aortic valve
159
Q

When does coronary blood flow peak?

A

Coronary blood flow peaks in early diastole

-heart relaxes so less mechanical pressures on the arteries so they can fill

160
Q

Why is ASD often seen in TAPVR?

A

TAPVR = total anamalous pulmonary venous return where the pulmonary veins drain freshly oxygenated blood into the RA (instead of the LA)
-so need ASD to shunt oxygenated blood to the left heart

161
Q

What percent of HTN is secondary?

(a) Name two causes of secondary HTN

A

10% of HTN is secondary

(a) 2 big causes
- renal artery disease: stenosis, fibromuscular dysplasia (vasculopathy)
- pheo
- primary hyperaldosteronosim

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