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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
Coarctation of aorta
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
26
Coarctation of aorta- S&S
Difference in pressure between upper and lower extremities HTN in upper extremities Weak femoral/ lower extremity pulses
27
Coarctation of aorta- complications
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
28
Cardiac defects associated with alcohol
All L--> R shunts (VSD, ASD, PDA) + Tetralogy of Fallot
29
Cardiac defects associated with congenital rubella
PDA, pulmonary artery stenosis, septal defects
30
Cardiac defects associated with Down Syndrome
VSD, ASD, AV septal defects (endocardial cushion defects)
31
Cardiac defects associated with diabetic mother
Transposition of great vessels
32
Cardiac defects associated with Marfan
MVP, thoracic aortic aneurysm and dissection, aortic regurg
33
Cardiac defects associated with lithium in utero
Ebstein anomaly (tricuspid moved down in RV)
34
Cardiac defects associated with Turner
Coarctation of aorta, bicuspid aortic valve
35
Cardiac defects associated with Williams
Supravalvular aortic stenosis
36
Cardiac defects associated with 22q11 syndromes
Truncus arteriosus, Tetralogy of Fallot
37
Quick aside: what are the ToRCHES infections
``` Toxoplasmosis Rubella Cytomegalovirus Herpes Simplex (HSV)/ HIV Syphillis Plus there are some others like Listeria, etc. ```
38
Hypertension- definition (Sys/Dias pressures)
Systolic > 140 | Diastolic > 90
39
HTN- RFs
Age, obesity, diabetes, physical inactivity, salt intake, alcohol, FH AA > Caucasian > Asian
40
HTN- Features
90%- primary (essential) and related to increased CO 10%- renovascular (e.g. fibrovascular dysplasia- string of beads; seen in younger women), hyperaldo
41
Hypertensive urgency defn
Severe HTN; high BP, but no end-organ damage Sys > 180mmHg Dias > 120mmHg
42
Hypertensive emergency defn
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
Hypertensive emergency tx
Sodium nitroprusside (vasodilator)
44
HTN predisposes to:
CAD, LVH, HF, AF, aortic dissection and aneurysm (vs. just aneurysm for atherosclerosis), CKD, retinopathy
45
Hyperlipidemia- xanthomas
plaques or nodules composed of lipid-laden histiocytes in skin (e.g. eyelids)
46
Hyperlipidemia- tendinous xanthoma
Lipid deposits in tendon (especially Achilles- seen in familial hypercholesterolemia- w/ defective LDL receptor)
47
Corneal arcus
Lipid deposits in cornea Seen in elderly, but can also be seen with familial hypercholesterolemia
48
Arteriosclerosis- defn
Hardening of the arteries Arterial wall thickening and loss of elasticity
49
Arteriolosclerosis- defn (hyaline vs. hyperplastic)
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
Monckeberg sclerosis (medial calcific sclerosis)
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
Atherosclerosis- defn
Disease of elastic arteries and large and medium-sized muscular arteries A form of arteriosclerosis- caused by buildup of cholesterol plaques
52
Atherosclerosis- most common locations
Abdominal aorta > Coronary a. > Popliteal a. > Carotid a.
53
Atherosclerosis- characteristics
Eccentric intimal thickening with fibrous cap, smooth muscle proliferation, macrophage/ foam cell infiltrate, lipid-filled core
54
Atherosclerosis- S&S
Angina, claudication, arterial ulcers (e.g. ulcers on toes), renal artery stenosis
55
Atherosclerosis- RFs (modifiable and non-modifiable)
Modifiable: smoking, HTN, hyperlipidemia, diabetes Non-modifiable: age, gender (men and post-menopausal women), FH
56
Atherosclerosis- progression
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
Atherosclerosis- complications
Aneurysms- (not dissections- this is bigger risk with HTN), ischemia, infarct, nephropathy (renal artery stenosis), peripheral vascular disease, thrombus, emboli
58
Aneurysm- defn
Localized pathologic dilatation of all three layers of the arterial wall (intima, media, and adventitia)
59
Aortic dissection vs. aneurysm- S&S
Aneurysm: back/ abdominal pain, palpable pulsatile abdominal mass, bruit Dissection: chest pain, pain RADIATING to back, unequal BP between arms
60
Aneurysm- RF
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
Traumatic aortic rupture
Due to trauma/ deceleration injury Most often affects aortic isthmus (proximal descending artery, distal to the left subclavian-- where ligamentum afteriosum resides)
62
Aortic dissection- defn
Longitudinal intimal tear forming false lumen (between intima and media) CXR: shows mediastinal widening
63
Aortic dissection- RF
Same as thoracic aneurysm RF: HTN, bicuspid aortic valve, connective tissue disease (e.g. Marfan)
64
Aortic dissection- Stanford type A (proximal)
Proximal-- involves Ascending aorta; may result in aortic regurg or cardiac tamponade Tx: surgery
65
Aortic dissection- Stanford type B (distal)
Distal-- involves Descending aorta (no ascending aorta involvement); generally near subclavian artery Tx: beta blockers and vasodilators
66
Ischemic heart disease manifestations (5)
``` Angina Coronary steal syndrome Sudden cardiac death Chronic ischemic heart disease Myocardial infarction ```
67
Angina (3 subtypes)
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
Coronary steal syndrome
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
Sudden cardiac death
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
Chronic ischemia heart disease
progressive HF over many years due to chronic ischemic myocardial damage
71
Myocardial infarction- STEMI vs. NSTEMI
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
Hibernating myocardium
Decreased blood flow at rest causes dysfunction of heart (e.g. LV)--> partially or completely reversible with coronary revascularization
73
MI- vessels most commonly affected
LAD (anterior LV) > RCA (anterior RA and RV) > circumflex (lateral and posterior LV)
74
MI- S&S
Angina, left arm or jaw pain, diaphoresis, n/v, SOB, fatigue
75
MI: 0-4 hrs
Minimal/ no change (coagulative necrosis only seen after 4 hrs)
76
MI: 4-24 hrs
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
MI: 1-3 days
Extensive coagulative necrosis + more neutrophils Complication: fibrinous pericarditis
78
MI: 3-14 days
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
MI: 2 wks to months
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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