Cardio - Path Flashcards

1
Q

polyarteritis nodosa (autoimmune) causes what kind of vasculitis

A

fibrinoid necrosis, segmental, transmural

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2
Q

3 causes of amyloidosis vasculitis

A

1) plasma cell dyscrasia
2) chronic systemic inflammation – RA
3) genetic - Transthyretin

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3
Q

what do injured endothelial cells secrete during the first step of atherosclerosis?

A

IL-1, TNFalpha (the pro-inflammatory cytokines)

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4
Q

What do injured endothelial cells have less of? (protein things)

A

decreased superoxide dismutase, less vasodilator and antithrombotic NO and prostacyclin

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5
Q

what drug protects against inflammation? specifically anti-interleukin-1beta?

A

canakinumab

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6
Q

what two things have been found to activate the inflammasome?

A

cholesterol crystals and free fatty acids

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7
Q

triggering the inflammasome results in activaiton of what enzyme

A

caspase-1

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8
Q

inflammasome –> caspase-1 –> (? inflammatory cytokine)

A

IL-1

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9
Q

why is neovascularization of atherosclerotic plaques important?

A

abnormal, irregular, small blood vessels - prone to rupture

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10
Q

what drug can be given to help reduce CV events in pts with atherosclerosis? (think anti-gout drug, b/c of similar mechanisms of urate crystals and cholesterol crystals)

A

colchicine –> improves CRP

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11
Q

effects of statins on atherosclerosis

A

1) decrease lipid content of plaques
2) decrease macrophage activity (inflammation) in plaques
3) increase stabilizing fibrous content of plaques

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12
Q

what percentage of ACD events in the LAD?

A

one-half

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13
Q

what percentage of ACD events are in the RCA?

A

one-third

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14
Q

what percentage of ACD events are in the LCX

A

one-sixth

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15
Q

a thrombus overlying an atherosclerotic plaque is result of superficial erosion - who is more common in?

A

women

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16
Q

what is thought to cause superficial erosion? what causes this?

A

apoptosis of endothelial cells –> due to oxidative stress and hypochlorous acid

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17
Q

why is methotrexate helpful in preventing atherosclerotic CV events?

A

cell proliferation of fibroblasts, SM cells, endothelial cells, and lymphocytes plays a role in atherosclerosis

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18
Q

what are common causes of coronary vasospasm?

A

stimulant abuse –> amphetamines, nose candy

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19
Q

atheroembolism is associated with what? (a histo feature)

A

eosinophilia

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20
Q

what is etiology of superficial erosion leading to thrombus formation?

A

erosion unamasks pro-coagulant stuff –> tissue factor released from apoptosed endothelial cells, or collagen

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21
Q

combination of abundant basophilic debris (nuclear dust) + geographic pattern necrosis

A

“pathergic necrosis”

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22
Q

pathergic necrosis - what disease?

A

granulomatosis with polyangiitis (Wegener’s)

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23
Q

contraction band necrosis

A

1) when the MI is caused by coronary vasospasm (cocaine, meth, epi - pheochromocytoma)
2) reperfusion

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24
Q

Trousseau syndrome

A

venous thrombi may result from elaboration of procoagulant factors from malignant tumors –> hypercoagulable state –> thromboses in different vascular beds at different times (migratory thrombophlebitis)

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25
Sturge Weber Syndrome
(encephalotrigeminal angiomatosis) - congenital disorder, facial port wine nevi, ipsilateral venous angiomas in (something), mental retardation, seizures, hemiplegia, radiopacities of the skull
26
SVC syndrome
neoplasms that compress or invade the SVC (bronchogenic carcinoma or mediastinal lymphoma) - the resulting obstruction --> marked dilation of veins of the nead, neck, and arms associated w/ cyanosis
27
Osler-Weber-Rendu disease
hereditary hemorrhagic telangiectasia --> autosomal dominant --> mutations in genes that encode components of TGF-beta signaling pathway in endothelial cells - telangiectasias present at birth - widely distributed - shit can spontaneously rupture, causing epistaxis (nosebleed), GI bleeding, or hematuria
28
IVC syndrome
neoplasms that compress or invade the IVC or by thrombus --> neoplasms -
29
what neoplasma (associated w/ IVC syndrome) - tend to grow within veins
hepatocellular carcinoma and renal cell carcinoma
30
what happens when you occlude the IVC
marked lower extremity edema, distention of superficial collaterla veins of lower abdomen
31
causes of portal vein HTN
liver cirrhosis --> less frequently, portal vein obstruction or hepatic vein thrombosis
32
results of portal vein HTN
opening of porto-systemic shunts - increased blood flow into veins at gastro-esophageal junction = esophageal varices, rectum = hemorrhoids, and periumbilical veins of abdominal wall = caput medusae
33
what is the most impt result of portal vein HTN
esophageal varices - prone to rupture, can lead to massive upper GI hemorrhage
34
Kaposi Sarcoma caused by HHV-8--> what induces VEGF
virally encoded G protein induces VEGF
35
HHV-8 - what drives proliferation
viral homologue of cyclin D,
36
what is something else that KSHV / HHV-8 has that helps mess w/ normal proliferation
virally encoded proteins that inhibit p53
37
AIDS patient w/ KS, what is good tx
HIV antiretroviral therapy
38
KS associated w/ immunosuppression - good tx?
withdraw the immunosuppression
39
8 risk factors of venous stasis dermatitis
1) age 2) female sex 3) obesity 4) DVT 5) standing occupation 6) fam hx of venous disease 7) heart failure 8) HTN
40
how to differentiate arterial vs venous in lower extremity ulcer (factors pointing towards venous)
1) medial ankle location 2) surrounding area of hemosiderin deposition 3) fibrosis around ulcer 4) granulation tissue in base
41
DVT - calf measurements
asymmetry over 2 cm = positive screening test
42
what is negative predictive value of negative D-dimer
99%
43
what about the Sn and Sp of D-dimer
good Sn, poor Sp
44
in addition to prolonged immobilization, what is risk for DVT (5)
1) postoperative state 2) CHF 3) pregnancy 4) oral contraceptive use 5) obesity
45
EKG w/ no p waves - most likely scenario
ventricular tachycardia (but could be a fib as well technically)
46
syncope likely to be caused by what abnormality in heart rate
sinus bradycardia
47
normal vector of the heart
R --> L top --> bottom anterior --> posterior
48
inferior leads
II, III, AvF
49
anterior leads
v leads
50
what is the number 1 cause of stroke
atrial fibrillation
51
primary cause of sudden cardiac death (SCD)
ventricular tach
52
tx for ventricular tach
AED or ICD
53
where do you put ICD
tip of RV
54
key word/phrase for complete heart block
atrio-ventricular dissociation
55
tx for heart block
pacemaker
56
the 2 determinants of myocardial O2 demand
1) HR | 2) systolic BP
57
what is the pathophysiology of MI and the findings on EKG
1) abrupt occlusion of coronary artery leading to muscle DYING 2) ST elevation (STEMI)
58
tx for bradycardia (after you have taken away Beta blockers and thyroid looks nml, but still bradycardic)
pacemaker
59
how long should QT interval be
less than 1/2 the RR interval
60
most common cause of long QT
certain drugs
61
complications of long QT
fatal arrhythmias
62
what is another example of dissociation (besides heart block - which is the most common form of dissociation)
ventricular tachycardia
63
what features present w/ hypertrophic cardiomyopathy cause it to be hypertrophic obstructive cardiomyopathy
subaortic stenosis and obstruction
64
histologic finding of hypertrophic cardiomyopathy
myocyte disarray
65
key clinical finding of hypertrophic cardiomyopathy
syncope after exercise
66
dx of hypertrophic cardiomyopathy (pt comes in w/ hx of syncope after exertion, what do you do)
get an echo
67
what is inheritance of HCM
autosomal dominant - test first degree relatives
68
what is the defect in HCM?
beta-myosin heavy chain - this is why it is auto dominant - you can't have only one good copy of the gene and be aight
69
how do you qunatify LVH? where do you measure
measure posterior wall, cut off is 1.5 cm
70
classic clinical triad for aortic stenosis
dyspnea, angina, SCD
71
gross anatomical features of rheumatic valvulitis
fibrous adhesions extending from commisures, closing valve partially, no calcifications
72
aortic stenosis due to rheumatic disease - what else common along with it
mitral stenosis 95% of the time
73
HTN causes what in the arteries
thickening of wall --> increased SM cells and fibrous tissue
74
finding of small arteries (can be pulmonary) associated w/ HTN
onion skinning
75
most common cause of cor pulmonale (50% in the state of TN)
COPD
76
second most common cause of cor pulmonale
old organized pulmonary thromboembolus - chronic PE w/ numerous small (individually asymptomatic) PE
77
micro pathology (morphology) or a subacute organizing PE
residual condensed fibrin, fibroblasts, myxoid ground substance and hemosiderin
78
a third, common cause of pulmonary HTN leading to cor pulmonale
IV drug abuse - leads to accumulation of foreign bodies - elicits a foreign body giant cell reaction
79
how do you measure preload?
pulmonary artery catheter --> somehow getting catheter into LV to measure pressure there
80
what are 2 major determinants of afterload?
1) SBP | 2) dimensions of LV
81
define heart failure
a syndrome of dysfunction of myocardial contractility, where heart cannot generate enough flow to meet the metabolic needs of the body
82
Dx of heart failure --> we talked about 4 things
1) PMI - displaced down and to the left 2) PMI - larger than the size of a dime 3) S3 gallop, auscultate w/ bell, goes away if you pres down 4) JVD - jugular distended above level of clavicle w/ pt supine
83
EF
SV/EDV
84
what does EF not tell us (4 things)
1) CO 2) renal blood flow 3) RAAS 4) salt and H2O retention
85
how much of CO goes to nephron
20%
86
when does kidney turn on RAAS?
if it gets less than 20% of CO
87
what other factors turn on the RAAS?
- standing up | - heat
88
RAAS upregulates renin, which upregulates Ang II --> what are the 2 effects of Ang II?
1) vasoconstrictor --> inc afterload | 2) promote secretion of aldosterone
89
what does aldosterone do
promotes retention of salt and water
90
ascites/anasarca - how much fluid has accumulated
30 L
91
put on diuresis, how much do you diurse per day
1 L
92
4 hypertrophic heart diseases
1) hypertensive 2) hypertrophic cardiomyopathy 3) aortic stenosis 4) cor pulmonale
93
hypertrophic cardiomyocytes - nuclei appearance
boxcars
94
hypertrophic heart disease - progressively develop what driven by what
myocardial fibrosis, driven by TGF-beta
95
what group of pts are very prone to getting hypertensive heart disease
chronic renal failure pts
96
the histologic organization of myocardial fibrosis in hypertensive heart disease is what
interstitial
97
HCM w/ IVS hypertrophy is accompanied by systolic anterior motion of the mitral valve - what is the significance
can cause LVOT obstruction and mitral regurgitation
98
what is the result of this systolic anterior motion of the mitral valve and hitting against the IVS
fibrous thickening of the mitral valve and mirror image patch of fibrosis on the subaortic upper septum
99
what is a tx (other than open heart surgery) for getting rid of the obstructing upper IVS
inject a poison into a septal coronary artery and infarct the inner part of the hypertrophied upper septum - use alcohol (EtOH)
100
what is a consequence of the fibrosis associated with hypertrophic cardiomyopathy?
provide a anatomic substrate for the development of reentrant ventricular tachycardia
101
aortic stenosis due to rheumatic valvultits, what happens to the valve leaflets?
inflammation, fibrosis, and fusion start at the commissue, and moves inward
102
what is a commissure?
heart valve commissure is where the valve opening meets the valve annulus
103
calcific bicuspid aortic valve - what is the epidemiology
male, probably in 40s, probably presented w/ sudden death
104
besides surgery to replace a stenotic aortic valve, what else can you do
stent
105
what is the numerical relationship of the thickness of the right ventricular wall compared to the left ventricular wall -
thickness of RV wall is less than 1/3 of the LV wall --> constant for normal sized heart or hypertrophied heart
106
what determines SV (2)
1) preload, | 2) contractility
107
what determines HR (2)
1) ANS, | 2) conduction system
108
2 things determine TPR
1) neurohumoral factors --> RAAS, etc | 2) local autoregulation - pH, hypoxia, kinins, PGs,
109
according to JNC8, what is the cutoff line for pts 60 or older for htn tx
150/90
110
for everyone less than 60, what is the cutoff to start treating for htn
140/90
111
what is the cardiac output like for pts w/ uncomplicated HTN
nml CO
112
causes of essential HTN
1) gain of function of pathways that promote vasoconstriction and renal sodium retention 2) loss of function of pathways that promote vasodilation and renal sodium excretion
113
what percentage of HTN is due to secondary causes (any HTN other than essential)
5%
114
what is the clinical significance of HTN (nace)
it is the most common preventable cause of death in developed countries
115
what is the upper limit of normal for pulmonary capillary pressure
10 mm Hg
116
at what level of pulmonary cap pressure will you have interstitial pulmonary edema
20 mm Hg
117
pulmonary capillary pressure - alveolar pulmonary edema
25 mm Hg
118
other causes of pulmonary edema - septic shock, what will the pulmonary capillary pressure be?
normal
119
hemorrhagic shock - pulmonary edema - pulmonary cap pressure?
low
120
does heart failure ever lead to a pro-inflammatory cytokine profile?
yes - TNF, IL-1, IL-6
121
what is a surgical emergency regarding the aortic valve
severe acute uncompensated aortic regurgitation
122
what is the synthetic, recombinant BNP
Nesiritide
123
BNP is an excellent blood test for heart failure
just know it
124
what is impt about diastolic heart murmurs
there are no innocent diastolic murmurs
125
arrhythmia defined by a RyR defect
familial catecholaminergic polymorphic ventricular tach
126
what is the epidemiology of familial cathecholaminergic polymorphic ventricular tach
mostly children | vent tach/fib during emotional stress
127
epidemiology of Brugada
young asian males
128
what is Brugada
group of channelopathies causing shortened cardiac myocyte APs and risk of vent tach and SCD
129
what leads do you look for the "coved type" ST elevations of Brugada
V1-V3
130
classical clinical presentation of congenital long QT syndrome
young person, exercise related SCD
131
pathophys of Long QT
phase 2 early after depolarization - LV
132
pathophys of Brugada
phase 2 reentry - RV
133
pathophys of catecholaminergic polymorphic VT
phase 4 delayed after depolarization - LV
134
what buzzword association for Long QT
Torsades
135
what is RV cardiomyopathy
disease due to genes encoding desmosomal proteins
136
what does RV cardiomyopathy cause
reentrant ventricular tach originating from RV - related to abnormalities in myocyte adhesion - desmosomal proteins
137
what is treatment of channelopathies
ICD
138
which channelopathy can you use Beta blockers for?
familial catecholaminergic polymorphic ventricular tach
139
type of cardiomyopathy that presents with arrhythmias
arrhythmogenic RV cardiomyopathy
140
histologic features of arrhythmogenic RV cardiomyopathy
extensive replacement of myocytes by adipocytes and fibrous tissue
141
asteroid body
sarcoidosis
142
prototype restrictive cardiomyopathy
amyloidosis
143
what is most common cause of myocarditis
viral infections - coxsackievirus
144
what else can cause myocarditis
lyme disease
145
drugs cause what type of myocarditis and what is a histologic feature
hypersensitivity myocarditis - eosinophils
146
Hx - reticulonodular interstitial lung disease, bilateral hilar lymphadenopathy
sarcoidosis
147
pathology of sarcoidosis
noncaseating granulomas in lungs, liver, lymph nodes, spleen, bone marrow, skin, eyes, heart
148
what does sarcoidosis favor in the heart
favors base of heart, commonly involves conducting system
149
spider cell
rhabdomyoma
150
pre-req for giant cell arteritis
calcification of internal elastic lamina and tunica media
151
what cells initiate immune response of giant cell art
dendritic cells
152
what mediates the activation of dendritic cells in giant cell art
ligation of their TLRs | mostly TLR-4
153
what do the dendritic cells produce (giant cell art)
IL-18, IL-12
154
what do dendritic cells upregulate (giant cell art)
IFN-gamma
155
the progression of the immune response in giant cell art depends on what
TH1 and TH17 CD4 T cells
156
what is the dominant cell type in the intramural lesions of giant cell arteritis
TH1
157
giant cell art - what is implicated in the response that leads to lumen stenosis
VEGF and PDGF
158
what cell type is elevated in untreated pts of giant cell arteritis in peripheral blood
Th17 cells
159
what is the tx for giant cell arteritis and what effect does it have on one of the cell types implicated
prednisone - almost complete reduction of Th17 cells - suppression of IL-1, IL-6, IL-17 axis
160
what plays a primary role in the internal elastic lamina degradation characteristic of giant cell art
MMP-2, MMP-9 - released by macrophages
161
what is the word for vacuolated cytoplasm of myocytes
myocytolysis
162
histologic appearance of MI 4 hours old
wavy myocytes
163
MI - when is coagulation necrosis visible
4-12 hrs
164
MI - neutrophilic infiltration
12-24 hrs
165
reperfusion effects of MI - contraction band necrosis
more contraction band necrosis
166
reperfusion effects MI - effect on neutrophils
fewer neutrophils
167
reperfusion effects MI - macrophages
more macrophages
168
nichols question that mentions irregular rhythm - what type of arrhythmia first
a fib
169
what is a common cause of a fib
heart failure
170
see a high level of BNP - first thought
heart failure
171
if you see a stroke from an MI - what time frame
7 days - embolus from mural thrombus
172
what other cell type can be present in an infarct around 6 days
fibroblasts
173
what is time frame for rupture of a MI
5 days
174
color of acute MI
light brown to tan
175
color of subacute MI
yellow
176
when do you expect to see granulation tissue with an MI
3-14 days
177
what is essential for making diagnosis of infective endocarditis
blood cultures
178
what is the most common cause overall of infective endocarditis
staph aureus
179
what causes mitral regurg from valve prolapse to go into remission
pregnancy - increase in blood volume causes LV to dilate
180
presentation of long QT
childhood - syncope or SCD -
181
"trigger" for long QT
exercise
182
epsilon wave
ARVC
183
disease of north Italy
ARVC
184
"trigger" for ARVC
exercise
185
channel involved in Brugada
sodium
186
"trigger" for catecholaminergic polymorphic vent tach
exercise or emotional stress - increased levels of catecholamines
187
Virchow's Triad
1) endothelial injury 2) abnormal blood flow 3) hypercoagulability - can be congenital
188
most likely underlying cause of mitral regurg
mitral valve prolapse
189
what do we call emboli from infective endocarditis
septic emboli
190
sites of septic embolization - common one we talked about
spleen
191
what do septic emboli cause when they get to their final destination
infection, abscess - needs drainage
192
what is clinical sign of septic emboli that caused abscess
recurrent fever
193
causes and manifestations of carcinoid heart disease
1) bioactive compounds such as serotonin released by carcinoid tumors 2) flushing, diarrhea, dermatitis, bronchoconstriction
194
what is normally affected in carcinoid heart disease?
endocardium and valves of Rt heart
195
gross pathology of carcinoid heart disease
distinctive glistening white intimal plaquelike thickenings
196
histologic features of carcinoid heart disease
SM cells and sparse collagen fibers - embedded in acid mucopolysaccharide-rich matrix
197
see many tiny little vegetations on a heart valve
Rheumatic Heart Disease - in the acute phase does have vegetations
198
what is the pattern of fibrosis in chronic rheumatic valve disease
starts at commissures, comes into the middle
199
Anytime there is a hole in the heart/ valve - not due to a projectile, or congenital - what is the cause
infective endocarditis
200
A pt w/ hypercoagulable state throws a DVT to their lungs and turns blue. How do you explain this?
If they had a probe patent foramen ovale --> cause Eisenmenger syndrome and push blood the other way and cause cyanosis
201
4 things, quick, to remember about MVP
1) Common 2) benign 3) midsystolic click 4) +/- regurgitation
202
3 things, quick, to remember Marantic Endocarditis
1) Common 2) Thrombi on valves 3) Precursor to infective endocarditis
203
3 things about Libman-Sacks Endocarditis
1) part of SLE 2) most common in young black females 3) rarely embolizes
204
4 things about infective endocarditis
1) uncommon 2) fatal if missed 3) heart murmurs 4) blood cultures
205
4 things for calcific aortic stenosis
1) common 2) male 3) systolic ejection murmur 4) onset of symptoms = time for valve replacement
206
What kind of septal defect can occur w/ transposition of great vessels?
VSD
207
what kind of septal defect will not ocur w/ TGV
ASD
208
What "defects" would help keep a pt alive in the case of TGV
VSD or PDA
209
What, besides eating a hole in the valve, is a complication of infective endocarditis that can lead to problems - 3rd degree heart block and cardiac arrest
rupture a hole in the IVS
210
when and how does the acute phase of rehumatic mitral valve disease present
acutely - age 10
211
chronic mitral valve disease
20 yrs after the acute rheumatic fever (so 30 yo) --> mitral stenosis, females, diastolic murmur
212
signs of heart failure --> dyspnea, ankle edema, S3, bibasilar pulmonary crackles --> what is potential pathophys of this?
Large acute MI --> heart failure --> inc LVEDV, inc LV dilation --> mitral regurgitation
213
pericardial effusions --> 1) appearance of serous pericarditis fluid 2) common causes
1) tan, looks like serum | 2) CHF, lymphatic obstruction, hypoalbuminemia
214
for serous pericarditis as a result of lymphatic obstruction by tumor - mets - most likely site of primary tumor
lung, breast, skin (melanoma)
215
shaggy pericarditis --> fibrinous --> most common causes
viral myopericarditis, uremia, acute MI, metastatic malignancy, autoimmune (SLE)
216
when is the maximal neutro infiltration seen in acute MI
2 days
217
subacute MI --> 1) what will you see 2) time frame
1) gray/tan w/ red rim of granulation tissue | 2) 2 weeks --> sometime during the 2nd week
218
what is the color progression of an MI
nml red/brown --> lighter brown --> tan --> yellow --> rim of red granulation tissue --> red moves in on yellow --> pink --> white
219
most common fatal sequence of complications of atherosclerosis
hemorrhage into a thin capped (vulneralbe) plaque --> rupture --> thrombus