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Cardiology > Cardio- Pathology (FA) > Flashcards

Cardio- Pathology (FA) Flashcards

1
Q

Right to Left Shunts- 12345 + E

A
  1. Truncus arteriosus
  2. Transposition of great vessels
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. TAPVR (total anomalous pulmonary venous return)
    Ebstein anomaly

Often have underlying VSD, ASD, PDA, to make it to term (these are kept open until surgery is possible)

EaRLy cyanosis (blue babies) see immediately after birth

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2
Q

Truncus arteriosus

A

Truncus arteriosus does not appropriately divide into pulmonary trunk and aorta

Babies that make it to term often have VSD

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3
Q

D transposition of great vessels

A

Failure of aorticopulmonary septum to spiral

Causes RV to send blood to aorta and LV to send blood to pulmonary artery

S&S: immediate cyanosis, continuous machine-like murmur b/w scapulae (because of PDA shunt?)

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4
Q

D transposition risk factors (1)

A

Pregnant women with diabetes (increased risk of birthing infants with arteriovenous malformations

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5
Q

Tricuspid atresia

A

Tricuspid valve does not form and RV is hypo plastic

Requires ASD AND VSD in order to be viable

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6
Q

Tetralogy of Fallot- PROV

A

PROV

Pulmonary valve stenosis (degree determines prognosis)
Right ventricular hypertrophy
Overiding aorta
VSD

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7
Q

Tetralogy of Fallot- cause and tx

A

Due to anterosuperior displacement of infundibular septum

Tx: surgery

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8
Q

Tetralogy of Fallot- exacerbation and compensation

A

Exacerbation: “tet” spells caused by crying, fever, exercise (due to increased RV outflow obstruction/ stenosis)

Compensation: Squatting; increases systemic resistance (after load), causes shunting of blood from left to right through VSD, to allow more blood to get through pulmonary circulation and get oxygenated

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9
Q

TAPVR- Total anomalous pulmonary venous return

A

Pulmonary veins drain into right heart circulation

Associated with ASD and/or PDA to allow for right to left shunting to maintain CO

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10
Q

Ebstein anomaly

A

“Atrialization” of the right ventricle due to downward displacement of the tricuspid valve

Associated with lithium exposure in utero

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11
Q

Left to right shunts

A

Late cyanosis (LateR cyanosis)

Frequency: VSD > ASD > PDA

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12
Q

VSD- cause

A

Most common congenital cardiac defect

Can result from failed fusion of superior and inferior endocardial cushions

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13
Q

VSD- S&S

A

Asymptomatic at birth
May manifest weeks later or remain asymptomatic throughout life
Often self resolve

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14
Q

VSD- identification

A

The larger the VSD, the quieter the murmur
Harsh, holosystolic murmur (loudest near tricuspid area)

O2 saturation will be higher in the RV and pulm artery than normal

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15
Q

ASD- cause

A

Osteum secundum defects (not to be confused with patent foramen oval- which has a similar presentation, but is due to incomplete fusion of atrial septum primum and secundum)

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16
Q

ASD- S&S

A

Symptoms range from none to HF

Can cause persistent pulmonary HTN (due to increased flow through pulmonic valve into pulmonary artery)

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17
Q

ASD- identification

A

Diastolic murmur- increased flow through tricuspid valve)

Fixed, wide splitting of the S2 (due to increased flow to RA causing delayed closing of the pulmonic valve regardless of inspiration vs. expiration

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18
Q

Patent ductus arteriosus

A

In fetal period- normal; R –> L shunt to allow blood flow from PA to aorta

Normally closes soon after birth because of increased pO2 in aorta, but increased pulmonary resistance can cause a decrease in oxygen tension (partial pressure) in the aorta that prevents closure (due to production of prostaglandins)

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19
Q

PDA- S&S and identification

A

Late cyanosis (lower extremities will be blue)

IDed: continuous, machine-like murmur in left infraclavicular area

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20
Q

PDA- tx

A

Indomethacin (NSAID): inhibits PGE synthesis and closes PDA (can cause premature closure in mom’s who take it during pregnancy

Prostaglandins (E1 and E2) kEEp PDA open (may be necessary to do this until surgery can be performed)

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21
Q

PDA- RF

A

congenital rubella

in mom, characterized by non-immunized mom presenting with fever, arthralgia, lymphadenopathy, and rash that spreads from limbs to trunk

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22
Q

Eisenmenger syndrome

A

Result of uncorrected left to right shunt (VSD, ASD, and PDA)

Chronically increased pulmonary blood flow cause muscularization of the PA (progressively increased resistance) and eventually reverses the direction of the shunt (to R –> L)

This is super dangerous and is irreversible; therefore fix left to right shunt early before this happens

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23
Q

Eisenmenger syndrome- S&S

A

Digital clubbing (caused by heart and lung conditions that decrease O2 supply to tissue- chronic hypoxia)
Late cyanosis
Polycythemia
Right ventricular hypertrophy

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24
Q

Hypoxia vs. hypoxemia

A

Hypoxia: low O2 in tissue

Hypoxemia: low arterial pO2 (if arterial oxygen supply is low, can cause hypoxia)

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25
Q

Coarctation of aorta

A

Characterized by constriction of the aorta (generally near the ductus arteriosus- “juxtaductal”)

Associated with Turner (preductal coarctation)- Turner pts also associated with bicuspid aortic valve

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26
Q

Coarctation of aorta- S&S

A

Difference in pressure between upper and lower extremities

HTN in upper extremities
Weak femoral/ lower extremity pulses

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27
Q

Coarctation of aorta- complications

A

Long-term can cause notching (prominent base) of the ribs due to collateral circulation that is established

Also can cause HF, cerebral hemorrhage (due to berry aneurysm formation), aortic rupture, and endocarditis

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28
Q

Cardiac defects associated with alcohol

A

All L–> R shunts (VSD, ASD, PDA) + Tetralogy of Fallot

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29
Q

Cardiac defects associated with congenital rubella

A

PDA, pulmonary artery stenosis, septal defects

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30
Q

Cardiac defects associated with Down Syndrome

A

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

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31
Q

Cardiac defects associated with diabetic mother

A

Transposition of great vessels

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32
Q

Cardiac defects associated with Marfan

A

MVP, thoracic aortic aneurysm and dissection, aortic regurg

33
Q

Cardiac defects associated with lithium in utero

A

Ebstein anomaly (tricuspid moved down in RV)

34
Q

Cardiac defects associated with Turner

A

Coarctation of aorta, bicuspid aortic valve

35
Q

Cardiac defects associated with Williams

A

Supravalvular aortic stenosis

36
Q

Cardiac defects associated with 22q11 syndromes

A

Truncus arteriosus, Tetralogy of Fallot

37
Q

Quick aside: what are the ToRCHES infections

A 
Toxoplasmosis
Rubella
Cytomegalovirus
Herpes Simplex (HSV)/ HIV
Syphillis
Plus there are some others like Listeria, etc.
38
Q

Hypertension- definition (Sys/Dias pressures)

A

Systolic > 140

Diastolic > 90

39
Q

HTN- RFs

A

Age, obesity, diabetes, physical inactivity, salt intake, alcohol, FH

AA > Caucasian > Asian

40
Q

HTN- Features

A

90%- primary (essential) and related to increased CO

10%- renovascular (e.g. fibrovascular dysplasia- string of beads; seen in younger women), hyperaldo

41
Q

Hypertensive urgency defn

A

Severe HTN; high BP, but no end-organ damage
Sys > 180mmHg
Dias > 120mmHg

42
Q

Hypertensive emergency defn

A

Severe HTN (> 210/120??) with end-organ damage

End-organ damage characterized by: retinal hemorrhage (flame sign), encephalopathy, stroke, papilledema (swelling of optic disk), MI, HF, aortic dissection, kidney injury, preeclampsia, hemolytic anemia

43
Q

Hypertensive emergency tx

A

Sodium nitroprusside (vasodilator)

44
Q

HTN predisposes to:

A

CAD, LVH, HF, AF, aortic dissection and aneurysm (vs. just aneurysm for atherosclerosis), CKD, retinopathy

45
Q

Hyperlipidemia- xanthomas

A

plaques or nodules composed of lipid-laden histiocytes in skin (e.g. eyelids)

46
Q

Hyperlipidemia- tendinous xanthoma

A

Lipid deposits in tendon (especially Achilles- seen in familial hypercholesterolemia- w/ defective LDL receptor)

47
Q

Corneal arcus

A

Lipid deposits in cornea

Seen in elderly, but can also be seen with familial hypercholesterolemia

48
Q

Arteriosclerosis- defn

A

Hardening of the arteries

Arterial wall thickening and loss of elasticity

49
Q

Arteriolosclerosis- defn (hyaline vs. hyperplastic)

A

Hardening of small arteries and arterioles

Two types- hyaline and hyperplastic
Hyaline (deposition of hyaline (pink)): thickening of vessel walls in essential HTN or DM
Hyperplastic (increase in smooth muscle cells): “onion-skinning” in severe HTN with proliferation of SMCs

50
Q

Monckeberg sclerosis (medial calcific sclerosis)

A

Affects medium-sized arteries
Calcification of internal elastic lamina and media of arteries; does NOT affect intima
“Pipe-stem” on X-ray (not to be confused to string of beads sign seen with fibrous dysplasia)

51
Q

Atherosclerosis- defn

A

Disease of elastic arteries and large and medium-sized muscular arteries

A form of arteriosclerosis- caused by buildup of cholesterol plaques

52
Q

Atherosclerosis- most common locations

A

Abdominal aorta > Coronary a. > Popliteal a. > Carotid a.

53
Q

Atherosclerosis- characteristics

A

Eccentric intimal thickening with fibrous cap, smooth muscle proliferation, macrophage/ foam cell infiltrate, lipid-filled core

54
Q

Atherosclerosis- S&S

A

Angina, claudication, arterial ulcers (e.g. ulcers on toes), renal artery stenosis

55
Q

Atherosclerosis- RFs (modifiable and non-modifiable)

A

Modifiable: smoking, HTN, hyperlipidemia, diabetes

Non-modifiable: age, gender (men and post-menopausal women), FH

56
Q

Atherosclerosis- progression

A

Begins with ENDOTHELIAL INJURY/ DYSFUNCTION

Endothelial injury –> macrophages and LDL accumulate –> Foam cells form –> Fatty streaks –> SMC migration from media to intima (involves platelet derived growth factor and fibroblast growth factor) –> proliferation –> ECM deposition –> fibrous plaque (cap) –> complex atheromas (accumulated in tunica INTIMA of artery walls)

57
Q

Atherosclerosis- complications

A

Aneurysms- (not dissections- this is bigger risk with HTN), ischemia, infarct, nephropathy (renal artery stenosis), peripheral vascular disease, thrombus, emboli

58
Q

Aneurysm- defn

A

Localized pathologic dilatation of all three layers of the arterial wall (intima, media, and adventitia)

59
Q

Aortic dissection vs. aneurysm- S&S

A

Aneurysm: back/ abdominal pain, palpable pulsatile abdominal mass, bruit

Dissection: chest pain, pain RADIATING to back, unequal BP between arms

60
Q

Aneurysm- RF

A

Abdominal: Tobacco use, increased age, male sex, family history

Thoracic: HTN, bicuspid aortic valve, connective tissue disease/ myxomatous degeneration (Marfans), tertiary syphillis (affects vasa vasorum- arteries that supply blood to aorta)

61
Q

Traumatic aortic rupture

A

Due to trauma/ deceleration injury

Most often affects aortic isthmus (proximal descending artery, distal to the left subclavian– where ligamentum afteriosum resides)

62
Q

Aortic dissection- defn

A

Longitudinal intimal tear forming false lumen (between intima and media)

CXR: shows mediastinal widening

63
Q

Aortic dissection- RF

A

Same as thoracic aneurysm RF: HTN, bicuspid aortic valve, connective tissue disease (e.g. Marfan)

64
Q

Aortic dissection- Stanford type A (proximal)

A

Proximal– involves Ascending aorta; may result in aortic regurg or cardiac tamponade

Tx: surgery

65
Q

Aortic dissection- Stanford type B (distal)

A

Distal– involves Descending aorta (no ascending aorta involvement); generally near subclavian artery

Tx: beta blockers and vasodilators

66
Q

Ischemic heart disease manifestations (5)

A 
Angina
Coronary steal syndrome
Sudden cardiac death
Chronic ischemic heart disease
Myocardial infarction
67
Q

Angina (3 subtypes)

A

Stable: generally due to atherosclerosis; resolves with rest or nitroglycerin

Variant (Prinzmetal): coronary artery spasms; transient ST elevations; triggered by tobacco, cocaine, triptans (often unknown though); tx with CCBs, nitrates, and smoking cessation

Unstable: generally > 75% occlusion; may show ST depression or T-wave inversion on ECG, but NO elevation of cardiac biomarkers

68
Q

Coronary steal syndrome

A

Distal to coronary stenosis

Administration of vasodilators dilates normal vessels and shunts blood toward well-perfused areas and decreases blood flow to post-stenotic regions (vasodilation + path of least resistance leads to worsening ischemia of stenotic vessels)

Pharmacologic stress tests are rooted on this (use dipyridamole, regadenoson)

69
Q

Sudden cardiac death

A

Death occurs within 1 hr of cardiac symptoms

generally due to lethal arrhythmia

RF: CAD (70%), cardomyopathy, ion channel probs

Tx: implantable cardioverter-defibrillator

70
Q

Chronic ischemia heart disease

A

progressive HF over many years due to chronic ischemic myocardial damage

71
Q

Myocardial infarction- STEMI vs. NSTEMI

A

Both have increase in cardiac biomarkers (CK-MB (early), troponin (longer-lasting))

STEMI: ST-elevation; transmural (full thickness) infarct; may show Q waves

NSTEMI: No ST-elevation; sub-endocardial infarcts (inner 1/3 most susceptible to ischemia); may see ST depression on ECG

72
Q

Hibernating myocardium

A

Decreased blood flow at rest causes dysfunction of heart (e.g. LV)–> partially or completely reversible with coronary revascularization

73
Q

MI- vessels most commonly affected

A

LAD (anterior LV) > RCA (anterior RA and RV) > circumflex (lateral and posterior LV)

74
Q

MI- S&S

A

Angina, left arm or jaw pain, diaphoresis, n/v, SOB, fatigue

75
Q

MI: 0-4 hrs

A

Minimal/ no change (coagulative necrosis only seen after 4 hrs)

76
Q

MI: 4-24 hrs

A

Coagulative necrosis- necrotic cell content released into blood
Neutrophils recruited

Potential for reperfusion injury (due to free radicals)

Complication: Ventricular arrythmia (spec. V-fib), HF, cardiogenic shock- (cold, clammy, decreased CO)

77
Q

MI: 1-3 days

A

Extensive coagulative necrosis + more neutrophils

Complication: fibrinous pericarditis

78
Q

MI: 3-14 days

A

3-10 days: Macrophages
10+ days: Granulation tissue

Complications: RUPTURE (S&S: hypotension, shock)
Free wall rupture –> tamponade
Papillary muscle rupture –> mitral regurg
Intraventricular septal rupture
LV pseudoaneurysm

79
Q

MI: 2 wks to months

A

Scar formed (complete)- made up of Type I collagen

Complications: 
Dressler syndrome (autoimmune- leads to fibrinous pericarditis)
HF, arrhythmias, true ventricular aneurysm

Cardiology (3 decks)

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