Cardiovascular- Pathology Flashcards
1
Q
Describe how a right-left shunt might appear clinically
A
there is early cynaosis (aka ‘blue babies”) often seen/diagnosed at birth and usually requiring intervention
2
Q
What are the five things that normally cause right-left shunts?
A
5T’s
Truncus arteriosus (1 vessel)
Transposition of the GVs (2 switched vessels)
Tricuspid atresia (Tri= 3)
Tetralogy of Fallot (tetra= 4)
TAPVR (5 letters)
3
Q
Describe persistent truncus arteriosus
A
this occurs when the truncus arteriosis fails to divide into the pulmonary trunk and aorta ***due to lack of aorticopulmonary septum formation**
4
Q
Most pts with persistent truncus arteriosus also have _____
A
a VSD
5
Q
Transposition of the GVs is not compatible with life unless accompanied by what?
A
a shunt like a VSD, PDA, or a patent foramen ovale
6
Q
What causes transpositon of the GVs?
A
failure of the aorticopulmonary septum to spiral
7
Q
What are the 4 main parts of Tetralogy of fallot?
A
a VSD, a hole between the two ventricles
- pulmonary stenosis
- right ventricular hypertrophy
- an overriding aorta, which allows blood from both ventricles to enter the aorta
8
Q
What does this show?
A
the classic ‘boot-shaped heart’ on CXR as seen in tetralogy of Fallot due to right heart hypertrophy
9
Q
What is the most common cause of early childhood cyanosis?
A
TOF
10
Q
What are the risk factors for TOF?
A
Risk factors include a mother who uses alcohol, has diabetes, is over the age of 40, or gets rubella during pregnancy. It may also be associated with Down syndrome
11
Q
What occurs with total anomalous pulmonary venous return (TAPVR)?
A
pulmonary veins drain into the RIGHT heart instead of the left
12
Q
Late cyanosis is associated more with left-right shunts. What are some common LTR shunts?
A
- VSD (most common)
- ASD
- PDA
13
Q
What is the most common congenital cardiac defect?
A
VSD
14
Q
What is the prognosis of a VSD?
A
most spontaneously resolve
15
Q
How do heart sounds with an ASD?
A
there is a loud S1 with a wide, fixed split S2
16
Q
How does a patent PDA present?
A
late onset lower extremity cyanosis (aka ‘differential’ cyanosis) and a continuous machine-like murmur
17
Q
What can be used to close a patent PDA? Keep it open (as in the case of transposition of the GVs)?
A
Close- Indomethacin
KEEp open- PGEs 1 and 2
18
Q
What is Eisenmenger syndrome?
A
An uncorrected LTR shunt will cause increased pulmonary blood flow leading to PAH and subsequently RVH causing the shunt to switch to the right to left shunt and causing late cyanosis
19
Q
How does corarctation of the aorta appear clinically?
A
HTN in the upper extremities and weak,delayed pulses in the lower extremities (brachial-femoral delay). With age, collateral aa. erode the ribs giving them a notched appearance on CXR
20
Q
What congenital defects can be caused by alcohol exposure in utero?
A
VSD, PDA, ASD (all LTRs)
TOF
21
Q
What congenital defects can be caused by congenital rubella?
A
PDA, pulmonary a. stenosis
22
Q
What congenital defects can be caused by down syndrome?
A
AV septal defects (endocardial cushion defects), VSD, ASD
23
Q
What congenital defects can be caused by having a diabetic mother?
A
transposition of the GVs
24
Q
What congenital defects can be caused by Marfan Syndrome?
A
MVP, thoracic aortic aneurysm and dissection, aortic regurg
25
What congenital defects can be caused by prenatal lithium exposure?
Ebstein anomaly
26
What congenital defects can be caused by Turner Syndrome?
Bicuspid aortic valve, coarctation of the aorta
27
What congenital defects can be caused by Williams Syndrome?
supravalvular aortic stenosis
28
What congenital defects can be caused by 2q11 Syndromes?
truncus arteriosus, TOF
29
What is HTN defined as?
Persistent systolic BP 140+ and/**OR** diastolic BP 90+
30
What is 'hypertensive urgency'?
severe (180+/120+) HTN without acute end-organ damage
31
What is 'hypertensive emergency'?
severe HTN with evidence of acute end-organ damage (e.g. encephalopathy, stroke, retinal dmaage, MI, HF, kidney damage, etc.)
32
What is this?
Hypertensive nephropathy
33
While the vast majority of HTN pts are primary, other things such as fibromuscular dysplasia can cause it. Describe this
a non-atherosclerotic, non-inflammatory disease of the blood vessels that causes abnormal growth within the wall of an artery. FMD has been found in nearly every arterial bed in the body. However, the most common arteries affected are the renal and carotid arteries
Below: classic **'beads on a string'** appearance of the renal a.
34
What are some superficial signs of hyperlipidemia?
- xanthomas
- tendinous xanthomas
- corneal acrus
35
What is xanthelasma?
xanthomas, or plaques/nodules of lipid-laden histiocytes, deposited periocularly
36
What is this?
corneal arcus, as seen in hyperlipidemia
37
What is arteriosclerosis?
HARDENING of the arteries, with arterial wall thickening and loss of elasticity
38
What are the two main types of arteriosclerosis?
- hyaline
- hyperplastic (onion-skin appearance)
39
What is Monckeberg (medial calcific sclerosis) arteriosclerosis?
uncommon type of arteriosclerosis affecting medium-sized aa. and marked by **calcification of the elastic lamina of aa.**
40
What is atherosclerosis?
a form of arteriosclerosis affecting elastic aa. and large- and medium-sized muscular aa. caused by buildup of cholesterol plaques
41
How does atherosclerosis occur?
endothelial cell dysfunction caused by inflammation/etc. causes macrophage and LDL accumulation leading to the formation of foam cells, subsequent fatty streaks, and smooth muscle cell migration and ECM deposition
42
Where is atherosclerosis most common?
abdominal aorta \> coronary a. \> popliteal a. \> carotids
43
What are the two types of aortic dissection?
Stanford Type A: in the ascending aorta; tx is surgery
Stanford Type B: in the descending aorta/aortic arch; tx is B blockers, then vasodilators
44
What causes angina?
chest pain due to an ischemic myocardium (no myocyte necrosis)
45
What are the main causes of angina?
- Stable
- Variant (Prinzmetal)
- Unstable
46
Describe stable angina
This usually occurs secondary to atherosclerosis with exerteional chest pain resolving with rest or nitroglycerin
47
How might angina appear on an ECG?
ST depression
48
Describe variant angina
this occurs at rest 2ndary to coronary a. spasm with transient ST ELEVATION on ECG. Triggers include tobacco, cocaine, and triptans
49
Describe unstable angina
there is usually thrombosis with incomplete coronary a. occlusion +/- ST depression and/or T wave inversion on ECG but no cardiac biomarker elevation
50
What is coronary steal syndrome?
a phenomenon where an alteration of circulation patterns lead to a reduction in the blood directed to the coronary circulation. It is caused when there is narrowing of the coronary arteries and a coronary vasodilator is used – "stealing" blood away from those parts of the heart. This happens as a result of the narrowed coronary arteries being always maximally dilated to compensate for the decreased upstream blood supply. Thus, dilating the resistance vessels in the coronary circulation causes blood to be shunted away from the coronary vessels supplying the ischemic zones, creating more ischemia.
51
MI is most often caused by what?
thrombosis of ruptured atherosclerotic plaque
52
What is the difference between a STEMI and NSTEMI?
STEMI- if transmural, ECG may show ST elevation
if subendocardial, ECG may show ST depression (NSTEMI)
53
What are the most commonly occluded vessels resulting in MI?
LAD \> RCA \> circumflex
54
What is the gold standard of MI diagnosis in the first 6 hrs?
ECG
55
How does cardiac troponin I respond to MI?
It rises after 4 hrs and is elevated for 7-10 days (specific to MI)
56
How does CK-MB respond to MI?
it rises after 6-12 hrs and is predominantly found in the myocardium but can also be released from skeetal muscle. Levels typically return to normal within 48 hrs (good for evaluating subsequent infarcts)
57
How does an ECG respond to an MI?
It can include ST elevation (STEMI, transmural infarct), ST depression (NSTEMI, subendocardial infarct), hyperacute ('peaked) T waves, T-wave inversion, and pathologic Q waves
58
Describe the findings of a transmural infarct
- elevated necrosis
- ST elevation
59
MI of which artery would present with ST elevations or Q waves in leads V1-V2?
Anteroseptal (LAD)
60
MI of which artery would present with ST elevations or Q waves in leads V3-V4?
Anteroapical (distal LAD)
61
MI of which artery would present with ST elevations or Q waves in leads V5-V6?
Anterolateral (LAD or LCX)
62
MI of which artery would present with ST elevations or Q waves in leads I or aVL?
LCX
63
MI of which artery would present with ST elevations or Q waves in leads II, III, and aVF?
InFerior (RCA)
64
When is cardiac arrhythmia one of the most common causes of death following MI?
first few days
65
When is ventricular free wall rupture one of the most common causes of death following MI?
3-14 days post-MI
66
When is ventricular aneursym one of the most common causes of death following MI?
2 weeks- several months post MI
67
When is postinfarct fibrinous pericarditis common following MI?
1-3 days- resulting in a friction rub
68
What causes Dressler Syndrome?
It is believed to result from an autoimmune inflammatory reaction to myocardial neo-antigens formed as a result of the MI. A similar pericarditis can be associated with any pericardiotomy or trauma to the pericardium or heart surgery.
69
How does Dressler Syndrome present?
The disease consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), pericarditis (usually evidenced by a pericardial friction rub), and/or a pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction, but can also be delayed for a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade.[8] An elevated ESR is an objective, yet nonspecific, laboratory finding.
70
How is unstable angina/NSTEMI tx?
anticoagulation (e.g. heparin), antiplatelet therapy (e.g. aspirin + clopidogrel), B-blockers, ACEIs, stains
symptom control with nitroglycerin and morphine
71
How is STEMI tx?
same as unstable angina/NSTEMI + reperfusion therapy
72
What is the most common cardiomyopathy?
dilated cardiomyopathy
73
What are some causes of dilated cardiomyopathy?
- idiopathic/familial
- chronic **A**lcohol abuse
- wet **B**eriberi
- **C**oxsachie B vrus, chronic **C**ocaine use, or **C**hagas disease
- **D**oxorubicin
- hemochromatosis, sarcoidosis
74
What are the findings of dilated cardiomyopathy?
HF, S3, systolic regurgitant murmur, balloon heart on CXR
SYSTOLIC dysfunction
75
How is dilated cardiomyopathy tx?
Na+ restriction, ACEIs, BBs, diuretics, digoxin, ICD
heart transplant
76
What are the main causes of hypertrophic cardiomyopathy?
60-70% are familial, AD (commonly a B-myosin heavy-chain mutation)
-Friedreich ataxia
77
What are the findings of hypertrophic cardiomyopathy?
S4, systolic murmur, sudden death in young athletes common, mitral regurg
DIASTOLIC dysfunction
78
How is hypertrophic cardiomyopathy tx?
cessation of high-intensity athletics, BBs or non-dihydropyridine CCBs (e.g. verapamil)
ICD for high risk pts.
79
What are the main causes of restrictive/infiltrative cardiomyopathy?
- sarcoidosis, amyloidosis
- postradiation fibrosis
- endocardial fibroelastosis in children
- Loffler Syndrome
80
What is Loffler Syndrome?
a disease in which eosinophils accumulate in the lung in response to a parasitic infection.
Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection
81
What are the clinical signs of left heart failure?
82
Pathogenesis of left heart failure and edema
decreased LV function causes pulmonary venous congestion leading to pulmonary edema and decreased CO leading to increased renin activity, Na+/H2O reabsorption, and sympathetic activity all increasing preload and venous pressure contributing to peripheral edema
83
What are the findings of right heart failure (most commonly due to left heart failure)?
-hepatomegaly (nutmeg liver), JVD, and peripheral edema
84
What are the main types of shock?
- hypovolemic
- cardiogenic
- obstructive
- distributive
85
What are the main causes of hypovolemic shock?
-hemorrhage, dehydration, burns (all leaving the skin cold and clammy)
86
How are preload, CO, and afterload affected by hypovolemic shock?
preload- very decreased
CO- decreased
afterload- increased
87
What is the tx of hypovolemic shock?
IV fluids
88
What are some causes of cardiogenic shock?
- acute MI, HF
- valvular dysfunction
- arrhythmia
(all leaving the skin cold and clammy)
89
What are some causes of obstructive shock?
PE, cardiac tamponade (skin cold and clammy)
90
How are preload, CO, and afterload affected by cardiogenic and obstructive shock?
preload- increased
CO- very decreased
afterload- increased
91
How is cardiogenic shock tx?
inotropes and diuresis
92
What are some causes of distributive shock?
-sepsis, CNS injury, and anaphylaxis (leaving the skin warm and dry)
93
How are preload, CO, and afterload affected by cardiogenic and obstructive shock?
preload- decreased
CO- increased
afterload- very decreased
94
What are the symptoms of bacterial endocarditis?
Bacteria **FROM JANE**
**F**ever
**R**oth Spots
**O**sler Nodes
**M**urmur
**J**aneway lesions
**A**nemia
**N**ail-bed ('splinter') hemorrhage
**E**mboli
95
96
What is the difference between Osler nodes and Janeway lesions?
Osler nodes are tender raised lesions on the finger or toe pads
Janway lesions are small, painless, lesions on the palm or soles
97
T or F. Multiple blood cultures are needed for diagnosis of bacterial endocarditis
T.
98
What is the major cause of acute bacterial endocarditis?
s. aureus
99
What is the major cause of subacute bacterial endocarditis?
viridans streptococci (low virulence so valves are usually damaged)
100
What is a common cause of bacterial endocarditis in colon cancer?
S. bovis
101
What is a common cause of bacterial endocarditis in prosthetic valves?
S. epidermidis
102
What is the most common valve for bacterial endocarditis?
mitral (Tricuspid with IVDU)
103
Culture negative bacterial endocarditis is most likely due to what?
Coxiella burnetii, Bartonella spp.
HACEK (haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
104
What causes Rheumatic fever?
group A B-hemolytic strep
105
How does rheumatic fever present?
The disease typically develops two to four weeks after a throat infection. Symptoms include: fever, **migratory polyarthritis**, **sydenham chorea**, and occasionally a characteristic non-itchy rash known as **erythema marginatum**. The heart is involved in about half of cases. Damage to the heart valves usually occurs only after multiple attacks but may occasionally occur after a single case of RF. The damaged valves may result in heart failure and also increase the risk of atrial fibrillation and infection of the valves
106
What are the Jones criteria of Rheumatic fever?
- Joint (migratory polyartritis)
- Carditis
- Nodules in skin (subQ)
- Erythema marginatum
- Sydenham chorea
107
Erythem marginatum in RF
108
The _____ valve is most commonly affected in rheumatic fever
mitral
109
What is this?
Aschoff body as seen in RF
110
Seen in RF
111
Rheumatic fever is caused by molecular mimicry to the GAS ____ protein
M
112
How does acute pericarditis present?
sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Presents with friction rub
113
What are some common causes of pericarditis?
- idiopathic
- infection (e.g.Coxsachivirus)
- autoimmune (e.g. SLE, rheuamtoid arthritis)
- uremia
STEMI or Dressler syndrome
114
Cardiac tamponade is marked by the ____ triad, consisting of:
Beck triad: hypotension, distended neck veins, and distant heart sounds
as well as tachcyardia and pulsus paradoxus
115
What is pulsus paradoxus?
a decreased in the amplitude of the systolic BP by 10+ mmHg during inspiration
116
When else is pulsus paradoxus seen?
-asthma
obstructive sleep apnea
- percarditis
- croup
117
Describe syhpillis related heart disease
Involvement of the vasa vasorum of the aorta resulting in a characteristic "tree-bark" appearance
118
What is the most common cardiac tumor?
METs
119
What is the most common primary cardiac tumor in adults?
myxomas
120
Where do most myxomas occur?
in the left atria, commonly described as a 'ball valve" obstruction
121
What is the most common primary tumor in children?
rhabdomyomas, associated with tuberous sclerosis
122
What is a Kussmaul sign?
Increase in JVP on inspiration instead of the normal decrease
123
What are some common vascular tumors?
- Angiosarcoma
- bacillary angiomatosis
- cherry hemangiomas
- cystic hygromas
- glomus tumors
- Kaposi sarcoma
- Pyogenic granulomas
- Strawberry hemangiomas
124
Describe angiosarcomas
rare blood vessel tumors typically occurring in the head, neck, and breast areas usually in elderly, on sun-exposed areas
associated with radiation therapy and chronic postmastectomy lymphedema
125
Hepatic angiosarcomas are associated with what?
vinyl chloride and arsenic exposure
126
What is this?
Bacillary angiomatosis, a benign capillary skin lesion found in AIDS pts.
127
What causes Bacillary angiomatosis?
Bartonella henselae (neutrophilic infiltrate distinguishes from Kaposi sarcoma)
128
What is this?
Cherry hemangioma, a benign capillary hemangioma of the elderly that does not regress
129
What is this?
**Cystic hygroma**, a cavernous lymphangioma of the neck seen in **Turner Syndrome**
130
What is this?
A glomus tumor
131
What causes a glomus tumor?
modified smooth muscle cells of the thermoregulatory glomus body
132
Describe Raynaud Phenomenon
Decreased blood flow to the skin due to arteriolar vasospasm in response to cold or stress
133
How do you tx Raynaud Syndrome?
CCBs
134
What are the large vessel vasculites?
- Temporal (giant cell) arteritis
- Takayasu arteritis
135
Describe temporal arteritis
This is a disease mostly affecting elderly females and presenting as a unilaterla HA and jaw claudication that may lead to ophthalmic a. occlusion and blindness
136
How is temporal arteritis tx?
high-dose steroids to prevent blindness
137
How does Takayasu arteritis present?
usually in Asian females under 40 yo with granulomatous thickening of the aortic arch described as 'pulseless disease' (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules
138
What are the medium-vessel vasculites?
- Polyarteritis nodosa
- Kawasaki disease
- Buerger disease (thromboangiitis obliterans)
139
Describe polyarteritis nodosa
vasculitis of the renal and visceral aa. (NOT pulmonary arteries) of *_young adults_* without ANCA association but with a high correlation of **Hep B** seropositivitiy
140
How does polyarteritis nodosa present?
constitutional symptoms of fever, weight loss, malaise
GI disturbances
HTN, neurologic dysfunction, renal damage
141
What causes polyarteritis nodosa?
deposits containing HBsAg-HBsAb complexes in affected vessels, indicating an immune complex–mediated etiology in that subset.
142
Diagnosis criteria for polyarteritis nodosa
A patient is said to have polyarteritis nodosa if he or she has three of the 10 signs known as the 1990 American College of Rheumatology (ACR) criteria:
Weight loss greater than/equal to 4.5 kg
Livedo reticularis (a mottled purplish skin discoloration over the extremities or torso)
Testicular pain or tenderness (occasionally, a site biopsied for diagnosis)
Muscle pain, weakness, or leg tenderness
Nerve disease (either single or multiple)
Diastolic blood pressure greater than 90 mmHg (high blood pressure)
Elevated kidney blood tests (BUN greater than 40 mg/dl or creatinine greater than 1.5 mg/dl)
Hepatitis B or hepatitis C virus tests positive (for surface antigen or antibody)
Arteriogram (angiogram) showing the arteries that are dilated (aneurysms) or constricted by the blood vessel inflammation
Biopsy of tissue showing the arteritis (typically inflamed arteries):[9] The sural nerve is a frequent location for the biopsy.
143
How is PAN tx?
corticosteroids and cyclophosphamide
144
Describe Kawasaki Disease
this is a medium vessel vasculitis of asian children (under 4 yo) that can lead to coronary a. aneurysm
145
What are the symptoms of Kawasaki Disease?
CRASH and burn
**C**onjunctival infection
**R**ash
**A**denopathy (cervical)
**S**trawberry tongue
**H**and-foot changes (edema, erythema)
fever
146
What is this?
Strawberry tongue seen in Kawasaki disease
147
How is Kawasaki disease tx?
IV immunoglobin and ***ASPIRIN*** (ONLY time in children)
148
Describe Buerger Disease
Buerger's disease (thromboangiitis obliterans) is a rare disease of the arteries and veins in the arms and legs. In Buerger's disease, your blood vessels become inflamed, swell and can become blocked with blood clots (thrombi).
This eventually damages or destroys skin tissues and may lead to **infection and gangrene.** Buerger's disease usually first shows in your hands and feet and may eventually affect larger areas of your arms and legs.
**Virtually everyone diagnosed with Buerger's disease smokes cigarettes or uses other forms of tobacco, such as chewing tobacco**. Quitting all forms of tobacco is the only way to stop Buerger's disease. For those who don't quit, amputation of all or part of a limb is sometimes necessary.
149
What are the main small-vessel vasculites?
- Granulomatosis with polyangiitis (Wegener)
- Microscopic Polyangiitis
- Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
- Henoch-Schonlein purpura
-
150
Describe Wegeners
This is a small vessel vasculitis affecting the lungs and the kidneys associated with deposition of **PR3('c')-ANCA** immune complexes
151
How does Wegeners affect the URT?
can cause perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
152
How does Wegeners affect the LRT?
hemoptysis, cough, dyspnea
153
How does Wegeners affect the kidneys?
hematuria, red cell casts
154
What is the triad of histo findings with Wegener's?
- focal necrotizing vasculitis
- necrotizing granulomas in the lung and upper airway
- necrotizing glomerulonephritis
155
How is Wegener tx?
-cyclophosphamide and corticosteroids
156
Describe microscopic polyangiitis
necrotizing vasculitis commonly affecting the lungs, kidneys, and skin with **pauci-immune glomerulonephritis and palpable purpura**
Presents similar to Wegeners but without nasopharyngeal involvement or granulomas
157
microscopic polyangiitis is associated with \_\_\_-ANCA
MPO ('p') (anti-myeloperoxidase)
