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My step 1 mnemonics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Allantois - urachus becomes

A

Median umbilical ligament

Urachus is part of allantoic duct between bladder and umbilicus.

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2
Q

Umbilical vein becomes

A

Ligamentum teres hepatis (round ligament)

Contained in falciform ligament.

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3
Q

The most posterior part of the heart?

The most anterior part of the heart?

A

LA

RV

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4
Q

Enlargement of the LA can cause?

A

enlargement can cause dysphagia (due to compression

of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus nerve).

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5
Q

LAD and its branches supply

A

anterior 2/3 of the interventricular septum, anterolateral papillary muscle.

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6
Q

LAD supplies

A

anterior of the intraventricular septum, anterolateral papillary muscle, and the anterior surface of LV. Most commonly occluded.

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7
Q

PDA supplies

A 
AV node (dependent on dominance), posterior 1/3 of interventricu lar septum, posterior 2/3 walls of ventricles, and posteromedial papillary muscle. Right (acute)
marginal artery supplies RV.
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8
Q

RCA supplies

A

SA node (blood supply independent of dominance). Infarcts may cause nodal dysfunction (bradycardia or heart block).

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9
Q

• Right-dominant circulation (?%) = PDA

arises from ?

A

• Right-dominant circulation (85%) = PDA

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10
Q

• Left-dominant circulation (?% ) = PDA arises

from ?

A

• Left-dominant circulation (8% ) = PDA arises

from LCX.

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11
Q

• Codominant circulation (%?) = PDA arises

from?

A

• Codominant circulation (7%) = PDA arises

from both LCX and RCA.

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12
Q

Coronary blood flow peaks in?

A

arises from RCA.

Coronary blood flow peaks in early diastole.

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13
Q

Stroke volume affected by?

A

Contractility (eg, anxiety, exercise)
Preload (eg, early pregnancy)
Afterload

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14
Q

Contractility increased with? (4 things)

A

• Catecholamine stimulation via beta-1 receptor:

  1. Ca2+ channels phosphorylated - inc. Ca2+ entry -> inc. Ca2+-induced Ca2+ release and Ca2+ storage in sarcoplasmic reticulum.
  2. Phospholamban phosphorylation - active Ca2+ ATPase - inc. Ca2+ storage in sarcoplasmic reticulum
  • Inc. intracellular Ca2+
  • dec. extracellular Na+ (dec. activity of Na+/Ca2+ exchanger)
  • Digitalis (blocks Na+/K+ pump - inc. intracellular Na+ -dec.I Na+/Ca2+ exchanger activity - inc. intracellular Ca2+)

Two words: Calcium + Sodium

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15
Q

Afterload approximated by

A

MAP.

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16
Q

Myocardial O2 demand is inc. by:

A
  • Contractility
  • Afterload - proportional to arterial pressure
  • heart Rate
  • Diameter of ventricle ( wall tension)

CARD

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17
Q

Pulse pressure

A

PP directly proportional to SV and inversely proportional to arterial compliance.

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18
Q

Pulse pressure increased in

A

hyperthyroidism
aortic regurgitation,
aortic stiffening (isolated systolic hypertension in the elderly)
obstructive sleep apnea (sympathetic tone)
anemia
exercise(transient).
O-RATES

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19
Q

Pulse pressure decreased in

A

aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF.
ShiFTS

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20
Q

Mean arterial pressure

A

MAP = CO x TPR

MAP (at resting HR) = 2/3 DBP + l/3 SBP = DBP+ 1/3 PP

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21
Q

Inotropy

Inc./dec.

A

Inc. - Catecholamines, digoxin, exercise (DiCE)

Dec. - HF with reduced EF, narcotic overdose, sympathetic inhibition (FaNS)

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22
Q

Venous return

Inc./dec.

A

Inc. - Fluid infusion, sympathetic activity (FS)

Dec. - Acute hemorrhage, spinal anesthesia (FS)

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23
Q

Total peripheral resistance

Inc./dec.

A

Inc. - Vasopressors

Dec. - Exercise, AV shunt

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24
Q

Speed of conduction:

A

Purkinje >atria > ventricles> bundle of His >AV node.

Park At Vent Bun Ave

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25
Q

Torsades de pointes

A

Long QT interval predisposes to torsades de pointes. Caused by dec. K+, Mg2+, Ca2+,
Treatment includes magnesium sulfate.
Mg-i-Ca-K!

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26
Q

Congenital long QT

syndrome

A

Romano-Ward syndrome-autosomal dominant, pure cardiac phenotype (no deafness).

Jervell and Lange-Nielsen syndrome autosomal recessive, sensorineural deafness.

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27
Q

Brugada syndrome

A

Autosomal dominant disorder most common in Asian males.

ECG pattern of pseudo-right bundle

Branch block and ST elevations in V1-V3

Risk of ventricular tachyarrhythmias and SCD. Prevent

SCD with implantable cardioverter-defibrillator (ICD).

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28
Q

Atrial natriuretic

peptide

A

Atria due to volume and pressure

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29
Q

B-type (brain)

natriuretic peptide

A

Ventricles due to tension

Good NPV

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30
Q

Contractility (and SV) dec. with:

5 things

A
  • Beta 1 -blockade (dec. cAMP)
  • HF with systolic dysfunction
  • Acidosis
  • Hypoxia/hypercapnia (dec. Po2 / inc.Pco2)
  • Non-dihydropyridine Ca2+ channel blockers
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31
Q

Peripheral chemoreceptors location and stimulated by?

A

carotid and aortic bodies

are stimulated by:
Dec. Po2 (< 60 mm Hg)
Inc. Pco2
Dec. pH of blood.

3 P’s

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32
Q

Central chemoreceptors location and stimulated by?

A

stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial Co2.

Do not directly respond to Po2.

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33
Q

Cushing reflex triad

A

Triad of hypertension, bradycardia, and respiratory depression

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34
Q

Cushing reflex path-physiology

A

intracranial pressure constricts arterioles -> cerebral ischemia -> inc pCo2 and dec pH -> central reflex sympathetic inc in perfusion pressure (hypertension) -> inc stretch ->peripheral reflex baroreceptor induced bradycardia.

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35
Q

Autoregulation -Skin

FACTORS DETERMINING AUTO REGULATION

A

Sympathetic stimulation most important mechanism for temperature control

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36
Q

Autoregulation - Heart

FACTORS DETERMINING AUTO REGULATION

A

Local metabolites (vasodilatory): Adenosine, NO, Co2, dec. O2

ACON sings to your heart

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37
Q

Autoregulation - Brain

FACTORS DETERMINING AUTO REGULATION

A

Local metabolites (vasodi latory): Co2 (pH)

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38
Q

Autoregulation - Kidneys

FACTORS DETERMINING AUTO REGULATION

A

Myogenic and tubuloglomerular feedback

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39
Q

Autoregulation - Lungs

FACTORS DETERMINING AUTO REGULATION

A

Hypoxia causes vasoconstriction

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40
Q

Autoregulation - Skeletal muscle

FACTORS DETERMINING AUTO REGULATION

A

Local metabolites during exercise: Co2, H+, Adenosine, Lactate, K+ (CHALK)

At rest: sympathetic tone

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41
Q

Persistent truncus arteriosus can also be accompanied by…

A

VSD

42
Q

D-transposition of great vessels can also be accompanied by…

A

VSD, PDA, or patent foramen ovale

43
Q

Tricuspid atresia can also be accompanied by…

A

both ASD and VSD for viability.

44
Q

Tetra logy of Fallot can also be accompanied by…

A

VSD

45
Q

Total anomalous pulmonary venous return can also be accompanied by…

A

ASD and sometimes PDA

46
Q

Ebstein anomaly can also be accompanied by…

A

Right-sided HF
“Atrializing” the ventricle
Regurgitation of the tricuspid valve
Accessory conduction pathways

RARA

47
Q

Ostium Secundum and ostium primum frequency and accompanying defects.

A

Ostium secundum defects most common
and usually an isolated finding; ostium
primum defects rarer and usually occur
with other cardiac anomalies.

48
Q

VSD can be seen with these disorders…

A

Congenital rubella
Down syndrome
Alcohol exposure in utero (fetal alcohol syndrome)
Infant of a diabetic mother

R-DAD

49
Q

Congenital cardiac defect associations - Alcohol exposure in utero (fetal alcohol syndrome)

A

VSD, PDA, ASD, tetralogy of Fallot

Alcohol has it all.

50
Q

Congenital cardiac defect associations - Congenital rubella

A

PDA, pulmonary artery stenosis, septal defects

51
Q

Congenital cardiac defect associations - Down syndrome

A

AV septal defect (endocardial cushion defect),

VSD,ASD

52
Q

Congenital cardiac defect associations - Infant of diabetic mother

A

Transposition of great vessels, VSD

53
Q

Congenital cardiac defect associations - Marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection,

aortic regurgitation

54
Q

Congenital cardiac defect associations - Prenatal lithium exposure

A

Ebstein anomaly

55
Q

Congenital cardiac defect associations - Turner syndrome

A

Bicuspid aortic valve, coarctation of the aorta

56
Q

Congenital cardiac defect associations - Williams syndrome

A

Supravalvular aortic stenosis

57
Q

Congenital cardiac defect associations - 22q 11 syndromes

A

Truncus arteriosus, tetra logy of Fallot

58
Q

Risk factors for thoracic aortic aneurysm and aortic dissection

A

Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (eg, Marfan syndrome).

59
Q

a thoracic aortic aneurysm is associated with…

A

cystic medial degeneration

60
Q

aortic isthmus -

A

proximal descend ing aorta just distal to the origin of the left subclavian artery

61
Q

Myocardial infarction complications

A 
ACT RAPID:
Arrhythmias (SVT, VT, VF)
Congestive cardiac failure
Tamponade/ Thromboembolic disorders
Rupture (ventricle, septum, papillary muscle)
Aneurysm (ventricle)
Pericarditis
Infaction (a second one)
Death/ Dressler's syndrome
62
Q

Atherosclerosis LOCATION

A

Abdominal aorta > coronary artery > popliteal artery > carotid artery .
“After I work out my ABS, I grab a CORONA and POP my collar up to my CAROTID.”

63
Q

Vasospastic (also known as Prinzmetal or Variant)

Triggers

Treatment

A

Triggers include cocaine, alcohol, and triptans.

Treat with Ca2+ channel blockers, nitrates, and smoking cessation (if applicable).

64
Q

Coronary steal syndrome vasodilators used

A

dipyridamole, regadenoson

“two pyramids for my grandson, steal”

65
Q

Myocardial infarction complications timing - Cardiac arrhythmia

A

first 24 hours post-MI.

66
Q

Myocardial infarction complications timing - Postinfarction

fibrinous pericarditis

A

1- 3 days: friction rub.

67
Q

Myocardial infarction complications timing - Papillary muscle rupture

A

2- 7 days

68
Q

Myocardial infarction complications timing - interventricular septal rupture

A

3- 5 days

69
Q

Myocardial infarction complications timing - Ventricular

pseudoaneurysm formation

A

3- 14 days

70
Q

Myocardial infarction complications timing - Ventricular free wall rupture

A

5- 14 days

71
Q

Myocardial infarction complications timing - True ventricular aneurysm

A

2 weeks to several months

72
Q

Myocardial infarction complications timing - Dressler syndrome

A

Several weeks

73
Q

Dilated cardiomyopathy etiologies

include

A

chronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, thyrotoxicosis, peripartum cardiomyopathy.

ABCCCD SHuT uP!

74
Q

Dilated cardiomyopathy treatment

A 
Treatment: BANNDIT
B-blockers
ACE inhibitors
Na+ restriction
Diuretics
Digoxin
ICD  
Transplant (heart)
75
Q

Hypertrophic obstructive cardiomyopathy etiology

A

B-C: 60 - 70% of cases are familial, autosomal dominant (most commonly due to mutations in genes encoding sarcomeric proteins, such as myosin-binding protein C and Beta-myosin heavy chain).

Other causes of concentric LV hypertrophy: chronic HTN, Friedreich ataxia.

76
Q

Hypertrophic obstructive cardiomyopathy Treatment

A

B-C: Treatment: cessation of high-intensity athletics, use of Beta-blocker or non-dihydropyridine Ca2+ channel blockers (eg, verapamil). ICD if the patient is at high risk.

77
Q

Restrictive/infiltrative cardiomyopathy

A 
Sarcoid
Amyloid 
Hemochromatosis
Loffler (hypereosinophilic infiltrate)
fibrosis (post-radiation) and fibro-elastosis (endocardium-young children)
78
Q

Bacterial endocarditis - Acute

A

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

79
Q

Bacterial endocarditis - Subacute

A

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

80
Q

Bacterial endocarditis - negative culture

A

most likely:

Coxiella Brunetti,
Bartonella spp
HACEK (Haemophilus, Aggregatibacter [formerly Actinobacillus], Cardiobacterium, Eikenella, Kingella).
The Mitral valve is most frequently involved.

81
Q

Bacterial endocarditis - Tricuspid valve endocarditis

A

associated with IV drug abuse (don’t “tri” drugs).

Associated with S aureus, Pseudomonas, and Candida.

82
Q

Bacterial endocarditis - other less likely causes

A 
S bovis (gallolyticus) is present in colon cancer,
S epidermidis on prosthetic valves.
83
Q

Bacterial endocarditis - Symptoms

A 
Bacteria FROM JANE
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Na il-bed hemorrhage
Emboli
84
Q

Bacterial endocarditis - nonbacterial

A

(marantic/thrombotic) 2° to malignancy, hypercoagulable state, or lupus.

85
Q

Bacterial endocarditis - Associated with…

A

glomerulonephritis, septic arterial or pulmonary emboli.

86
Q

Rheumatic fever is a consequence of

A

A consequence of pharyngeal infection with group A beta-hemolytic streptococci
“RF from Fatyngitis”

87
Q

Rheumatic fever - heart valves affected

A

affects heart valves- mitral > aortic» tricuspid (high-pressure valves affected most).

88
Q

Rheumatic fever - pathology findings

A 
Aschoff bodies (granuloma with giant cells ), 
Anitschkow cells (enlarged macrophages with an ovoid, wavy, rod-like nucleus), 
Antistreptolysin O (ASO) titers.

AAA’s

89
Q

Acute pericarditis - etiologies and tx

A 
U - uremia 
N - neoplasaia
C - cardiovascular (STEMI/Dressler) + colchicine Tx
A - autoimune
R - radiation
I - infectin (coxsackie B) 
N - NSAIDS Tx
G - Glucocorticoids Tx
90
Q

Myocarditis causes:

A

DART:
D - Drugs (eg, doxorubicin, cocaine)
A - Autoimmune (eg, Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis) “KiSS the skin”
R - Rheumatic fever
T - Toxins (eg, carbon monoxide, black widow venom)

Organisms:
Viruses - adenovirus, Bl9, coxsackie B, HIV, HHV-6 (ABC HH) - lymphocytic infiltrate with focal necrosis.
Parasites - Trypanosoma cruzi, Toxoplasma gondii ( like TT’s)
Bacteria - Borrelia burgdorferi, Mycoplasma pneumoniae. (BuMmer)

91
Q

Cardiac tamponade Findings:

A

Beck triad (hypotension, distended neck veins, distant heart sounds),
Inc. HR
Pulsus paradoxus.
ECG shows low-voltage QRS and electrical alternans.

92
Q

Pulsus paradoxus Seen in

A 
C - croup
A -  asthma
P - pericarditis
O - obstructive sleep apnea
T - tamponade
93
Q

Cyclophosphamide, corticosteroids used for which vasculitides?

A

Wegener - Granulomatosis with polyangiitis

Microscopic polyangiitis

Polyarteritis nodosa

WiMP!

94
Q

Viral hepatitis assosiated with witch vasculitides?

A 
Polyarteritis nodosa (hep B)
Cutaneous small-vessel vasculitis and Mixed cryoglobulinemia (hep C)
95
Q

Behcet syndrome findings

A

Rule of 2:
2 types of ethnic background - of Turkish and Eastern Mediterranean descent.
2 types of ulcer - aphthous ulcers, genital ulcerations
2 viruses - HSV or parvovirus
2 other details - uveitis, erythema nodosum
2 lab findings - Immune complex vasculitis, HLA-B51

96
Q

Cutaneous small-vessel vasculitis causes:

A

after certain medications (allopurinol, penicillin, phenytoin, cephalosporins - sneezing “APPC! - אפצ’י”) or infections (eg, HCV, HIV).

97
Q

Cutaneous small-vessel vasculitis findings

A

Palpable purpura, no visceral involvement.

98
Q

Mixed cryoglobulinemia findings:

A

Triad of palpable purpura, weakness, arthralgias.
May also have peripheral neuropathy and renal disease (eg, glomerulonephritis).
Weak Purrs Join Rentals, Nerds!

99
Q

Mixed cryoglobulinemia Pathology

A

Vasculitis due to mixed lgG and IgA immune complex deposition.

100
Q

immunoglobulin A vasculitis Classic triad:

A

• Skin: palpable purpura on buttocks/legs
• Arthralgias
• Gl: abdominal pain (associated with intussusception)
Painful tummies Join the Purrs!

101
Q

Microscopic polyangiitis presentation and Pathology

A

Presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement.
No granulomas
P-ANCA

102
Q

Drugs that displace digoxin from tissue-binding

sites, and decrease clearance

A

verapamil, amiodarone, quinidine

Quine Amy Vera

My step 1 mnemonics (19 decks)

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