Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

First Aid > cardio first aid > Flashcards

cardio first aid Flashcards

1
Q

umbilical vein

A

ligamentum teres hepatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

umbilic arteries

A

medial umbilical ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ductus arteriosus

A

ligamentum arteriosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ductus venosus

A

ligamentum venosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

foramen ovale

A

fossa ovalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

allantois

A

urachus-median umbilical ligamnt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

notochord

A

nucleus pulposus of intervertebral disc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where do you see increased pulse pressure?

A

hyperthyroidism, AR, arteriosclerosis, obstructive sleep apnea, increased sympathetic tone, exercise (transient)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

where do you see decreased pulse pressure?

A

AS, cardiogenic shock, cardiac tamponade, advanced heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

contractility increases with

A

catecholamines
increased intracellular Ca2+
decreased extracellular Na+
digitalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

contractility decreases with

A 
beta1 blockade
heart failure with systolic dysfunction
acidosis
hypoxia and hypercapnea
non-dihydropyridine ca2+ channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

SV inreases with

A

anxiety
exercise
pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

myocardial oxygen demand increases with

A

afterload
contractility
HR
ventricular diameter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

venodilators effect what cardiac output variable?

A

decrease preload (nitroglycerin is an example)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

vasodilators effect what cardiac output variable?

A

decrease afterload (eg. Hydralazine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ACE inhibiors and ARBs effect what cardiac output variable?

A

decrease preload and afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is ejection fraction effected by heart failure

A

decreased in systolic heart failure but normal in diastolic heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what increases venous return

A

fluid infusion

sympathetic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what decreases venous return

A

acute hemorrhage

spinal anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what increases TPR?

A

vasopressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what decreases TPR?

A

exercise, AV shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

S1

A

MV and TV closure

loudest at mitral area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

S2

A

AV and PV closure

loudest at left sternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

S3

A

early diastole during rapid ventricular illing

patho: MR, CHF, dilated ventricles
normal: children, pregnant women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

S4

A

late diastole
high atrial pressure
patho: ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

a wave

A

atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

c wave

A

RV contraction, closed TV bulging into atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

x descent

A

atrial relaxation and downward displacement ofclosed tricuspid valve during ventricular contraction
absent in tricuspid regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

v wave

A

increased right atrial pressure dur to filling against closed tricuspid valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

y descent

A

blood flow from RA to RV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

aortic area sounds

A

systolic murmur
aortic stenosis
flow murmur
aortic valve sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

pulmonic area sounds

A

systolic ejection murmur
pulmonic stenosis
flow murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what causes normal splitting?

A

inspiration causes a drop in intrathoracic pressure causing increased venous return to the RV which increases the RV stroke volume. Ejection time of the RV increases leading to delayed closure of the pulmonic valve. There is decreased pulmonary impedence meaning that there is increased capacity of the pulmonary circulations allowing for the delayed closure of the pulmonic valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

when do you see wide splitting

A

pulmonic stenosis and RBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

when do you see fixed splitting

A

ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

when do you see paradoxical splitting

A

delayed LV emptying like in AS and LBBB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

left sternal border sounds

A

diastolic murmurs: aortic regurgitation and pulmonic regurgitation
systolic murmurs: hypertrophic cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

tricuspid area sounds

A

pansystolic murmur: tricuspid regurgitation, VSD

diastolic murmur: tricuspid stenosis, ASD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

mitral area sounds

A

systolic: mitral regurgitation
diastolic: mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

how does inspiration effect heart sounds/

A

increase intensity of right heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how does hand grip effect heart sounds

A

increasing systemic vascular resistance causes increased intensity of MR, AR, VSD
decreased intensity of AS, hypertrophic cardiomyopathy murmurs
MVP: has increased intensity and later onset of click/murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how does valsalva and standing affect heart sounds?

A

valsalva then standing decreases venous return
it decreases intensity of most murmurs including AS
it increases intensity of hypertrophic cardiomyopathy murmur
MVP: decreased murmur intensity and earlier onset of click/murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how does rapid squatting effect heart sounds?

A

it causes increased venous return and increased preload. The afterload also increases with prolonged squatting
this causes a decreased intensity of hypertrophic cardiomyopathy murmurs
increased intensity of AS murmurs
MVP: increased murmur intensity and later onset of click/murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what are the systolic heart sounds?

A

AS, PS, MR, TR, VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what are the diastolic heart sounds?

A

AR, PR, MS, TS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

speed of conduction of the cardiac cells

A

purkinge > atria > ventricles > AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

pacemaking capability of cardiac cells

A

SA > AV > bundle of his > purkinge/ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what causes torsades de points

A

drugs, decreased K+, decreased Mg2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

how do you treat torsades de pointes

A

magnesium sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what meds prolong QT?

A 
sotalol
risperidone
macrolodes
chloroquine
preotease inhibitors
quinidine
thiazide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is romano ward syndrome

A

AD
congenital long QT syndrome
purely cardiac phenotype

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is jervell and lange-nielsen syndrome?

A

AR
congenital long QT syndrome
also sensorineural deafness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what is Wolff-Parkinson white syndrome?

A

ventricular pre-excitation
abnormal fast accessory conduction pathway from atria to ventricle that bypasses the rate slowing AB node
ventricles partially depolarize earier
delta wave appearance with shortened PR on ECG
leads to reentry circuit –> supraventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is ANP

A

released from atrial myocytes in response to increased blood volumeand atrial pressure. It causes vasodilation and decreased Na reabsorption at the renal collecting tubule. It constricts efferent renal arterioles and dilates afferent arterioles via cGMP promoting diuresis and leading to aldosterone escape mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is BNP

A

released from ventricular myocytes in response to increased tension. Has longer half life than ANP, used for diagnosing heart failure
recombinant form: nesirtide is used for treatment of heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what do the receptors on the aortic arch respond to and how is the information transmitted?

A

only increased BP

via the vagus to solitary nucleus in medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what do the receptors on the carotid sinus respond to and how is the information transmitted?

A

both increased and decreased BP

via the glossopharyngeal to solitary nucleus of medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

describe the baroreceptor response to hypotension

A

the decreased arterial pressure leades to decreased stretch and decreased afferent baroreceptor firing.
This leads to increased efferent sympathetic firing and decreased efferent parasympathetic stimulation leading to vasoconstriction increased HR, increased contractility, and increased BP. this response is important in severe hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is carotid massage?

A

it is the increased pressure on the carotid sinus that leads to increased stretch, increased afferent baroreceptor firing and then to increased AV node regractory period which decreases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what is the cushing reaction?

A

it is the triad of hypertension, bradycardia, and respiratory depression
the increased intracranial pressure causes constriction of the arterioles and leads to cerebral ischemia and reflex sympathetic and increase in perfusion pressure. There is increased stretch and reflex baroreceptor induced bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what stimulates the chemoreceptors in the carotid and aortic bodies?

A

decreased PO2
increased PCO2
decreased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what stimulates the central chemoreceptors

A

pH and PCO2 changes of the brain interstitial fluid. These are influenced by arterial CO2 and do not directly respond to PO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what does PCWP approximate?

A

left atrial pressure

measured with pulmonary artery catheter (Swan-Ganz)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

autoregulation of the heart

A

local metabolites, CO2, adenosine, NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

autoregulation of the brain

A

local metabolites, CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

autoregulation of the kidneys

A

myogenic and tubuloglomerular feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

autoregulation of the lungs

A

hypoxia induced vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

autoregulation of the skeletal muscle

A

local metabolites, lactate, adenosine, K+, H+, CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

autoregulation of the skin

A

sympathetic stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what causes edema?

A

increased capillary pressure (heart failure)
decreased plasma proteins (nephrotic syndrome, liver failure)
increased capillary permeability (toxins, infections, burns),
increased interstitial fluid colloid osmotic pressure (lymphatic blockage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what are the causes of right to left shunting

A 
truncus arteriosus
transposition of the great vessels
tricuspid atresia
tetralogy of fallot
total anomalous pulmonary venous return
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

how do you treat right to left shunts

A

surgical or maintenance of PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

persistent truncus arteriosus

A

fulture of TA division

accompanied by VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

D-transposition of great vessels

A

separation of the systemic and pulmonary circulations
not compatible with life
failure of AP septum spiral
needs surgery and presence of shunting to allow blood mixing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

tricuspid atresia

A

absence of tricuspid valve and hypoplstic RV

requires ASD and VSD for viability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

tetralogy of fallot

A

anterosuperior displacement of the infundibular septum

  1. pulmonary infundibular stenosis
  2. RVH
  3. overriding aorta
  4. VSD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

how does squatting improve cyanosis in tet.

A

increased SVR leads to decreased right to left shunting and improves cyanosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

what is the treatment for tet

A

surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what do you see on CXR in tet

A

boot shaped heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

total anomalous pulmonary venous return

A

pulmonary veins drain into right heart circulation

associated with ASD and sometimes PDA to allow right to left shunting to maintin CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the causes of left to right shunting?

A

VSD, ASD, PDA, eisenmenger syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

VSD

A

asymptomatic usually , may self resolve

larger lesions may lead to LV overload and heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

ASD

A

loud S1 and wide fixed split of S2
septum secundum defect
symptoms: none to heart failure
different than patent foramen ovale because septa are missing tissue rather than unfused

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

PDA

A

fetally: right to left
with decreased lung resistance the shunt becomes left to right
can lead to RVH, LVH or heart failure
machine like murmur - continuous
maintained patency with PGE and low O2 tension
can result in cyanosis in the lower extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what opens and closes PDA?

A

indomethacin closes, PGE opens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

eisenmenger syndrom

A

uncorrected LtoR shunting leads to increased pulmonary blood flow and pathologic remodeling of vasculature leading to pulmonary arteriolar hypertension
RVH occurs to compensate the the shunt bcomes right to left
causes late cyanosis, clubbing and polycythemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

coartation of the aorta associations

A

bicuspid aortic valve and other heart defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is the infantile type of coarctation of the aorta

A

aorta narrowing is proximal to insertion of the ductus arteriosus
associated with turner syndrome
closure of ductus arteriosus (can reverse with PGE2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is the adult type of coarctation of the aorta

A

aorta narrowing is distal to ligamentum arteriosum
associated with notching of the ribs (collageral circulation), HTN in the upper extremities and weak, delayed pulses in the lower extremities

90
Q

22q11 syndromes

A

truncus arteriosus, tetralogy of Fallot

91
Q

down syndrome

A

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

92
Q

congenital rubella

A

septal defects, PDA, pulmonary artery stenosis

93
Q

turner syndrome

A

bicuspid aortic vavlve, coarctation of the aorta (preductal)

94
Q

marfan syndrome

A

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation

95
Q

infant of diabetic mother

A

transposition of great vessels

96
Q

xanthomas

A

plaques or nodules composed of lipid laden histiocytes in the skin - eyelids

97
Q

tendinous xanthoma

A

lipid deposits in tendon (esp achilles)

98
Q

corneal arcus

A

lipid deposits in cornea, early in life wit hypercholesterolemia, or in elderly

99
Q

monckeberg

A 
medial calcific sclerosis
calcification in the media of the arteries, radial and ulnar,
benign
pipestem areteries on x ray
does not obstruct blood flow
intima not involved
100
Q

arteriolosclerosis

A

common
two types: hyaline (thickening of the small arteries in essential HTN or DM) and hyperplastic (“onion skinning” in severe HTN)

101
Q

what are the types of arteriosclerosis

A

monckeberg and arteriolosclerosis

102
Q

describe the progression of atherosclerosis

A

endothelial dysfunction leads to macrophafe and LDL accumulation. Foam cell formation –> fatty streaks –> smooth muscle cell migration + proliferation + ECM deposition –> fibrous plaques –> complex atheromas

103
Q

common locations of atherosclerosis

A

abdominal aorta> coronary artery > popliteal artery > carotid artery

104
Q

difference in abdominal and thoracic aortic aneurysm presentations

A

abdominal is associated with atherosclerosis and more often in HTN males smokers > 50yrs
thoracic: cystic medial degeneration due to HTN in older patients, Marfans, tertiary syphillis

105
Q

what is aortic dissection

A

longitudinal intraluminal tear forming a false lumen that can be limited to ascending or propogate to descending aorta

106
Q

what are aortic dissections asscoatied with

A

HTN, bicuspid aortic valve, inherited connective tissue disorders (marfans)

107
Q

how does aortic dissection present

A

tearing chest pain of sudden onset radiating to the back
possible unequal BP in arms
mediastinal widening on CXR
can lead to pericardial tamponade, aortic rupture, death

108
Q

what is angina

A

chest pain from ischemic myocardium secondary to coronary artery narrowing or spasm
no myocardia necrosis

109
Q

what is stable angina

A

exertional chest pain
often secondary to atherosclerosis
ECG: ST depression
resolves with rest

110
Q

what is variant or prinzmetal angina?

A

occurs at rest secondary to coronary artery spasm
ECG: transient ST elevation
triggers: tobacco, cocaine, triptans
tx: Ca2+ channel blockers, nitrates, smoking cessation

111
Q

what is unstable/crescendo angina?

A

thrombosis with incomplete coronary artery occlusion

ECG: ST depression

112
Q

coronary steal syndrome

A

distal to coronary stenosis
maximally dilated vessels
vasodilators (dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas. This leads to decreased flow and ischemia in the post stenotic region
used in pharmacologic stress tests

113
Q

MI

A

acute thrombosis due t coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis

114
Q

SCD

A

within 1 hour of symptoms, lethal arrhythmias, CAD, cardiomyopathy, hereditary ion channelopathies (long QT)

115
Q

chronic ischemic heart disease

A

progressive onset of CHF over many years due to chronic ischemic myocardial damage

116
Q

commonly occluded coronary arteries

A

LAD > RCA > circumflex

117
Q

symptoms of MI

A

diaphoresis, nausea, comiting, severe retrosternal pain, pain in left arm and jaw, shortness of breath, fatigue

118
Q

What do you see on ECG in Mis

A

ST elevations if transmural
ST depression if subendocardial
pathologic Q waves if evolving or old transmural infarcts

119
Q

what are the biomarkers that you use in MI evaluation

A

cardiac troponin I rises after 4 hours and is increased for 7 to 10 days, more specific than other protein markers
CK-MB is good for reinfarction diagnosis because it returns to normal after 48 hours. Also released from skeletal muscle

120
Q

where do you see q waves if the infarct is in the anterior wall (LAD)?

A

V1-V4

121
Q

where do you see q waves if the infarct is in the anteroseptal (LAD)?

A

V1-V2

122
Q

where do you see q waves if the infarct is in the anterolateral (LAD or LCX)?

A

V4-V6

123
Q

where do you see q waves if the infarct is in the lateral wall (LCX)?

A

I, aVL

124
Q

where do you see q waves if the infarct is in the inferior wall (RCA)?

A

II, III, aVF

125
Q

when is the greatest risk of having a ventricular free wall rupture?

A

6-14 days postinfarct

126
Q

when is the greatest risk of having ventricular pseudoaneurysm formation?

A

1 week post MI

127
Q

what do you see with ventricular pseudoaneurysm formation?

A

decreased CO, risk of arrhythmia, embolus from mural thrombus

128
Q

when is the greatest risk of having postinfarction fibrinous pericarditis?

A

1 to 3 days post-MI

129
Q

what is dressler syndrome?

A

autoimmune thing that results in fibrinous pericarditis several weeks post-MI

130
Q

what are the types of cardiomyopathies?

A

dilated cardiomyopathy
hypertrophic cardiomyopathy
restrictive/infiltrative cardiomyopathy

131
Q

causes of dilated cardiomyopathy

A 
idiopathic
congenital
alcohol abuse,
wet Beri beri
Coxsackie B
chronic cocaine
chagas
doxorubicin toxicity
hemochromatosis
peripartum cardiomyopathy
132
Q

dilated cardiomyopathy findings

A

heart failure
S3
dilated heart on echo
balloon appearance of heart on CXR

133
Q

treatment of dilated cardiomyopathy

A 
Na+ restriction
ACE inhibitors
beta blockers
diuretics
digoxin
ICD
heart transplant
134
Q

causes of hypertrophic cardiomyopathy

A

familial (AD), sometimes friedreich ataxia

athletes

135
Q

hypertrophic cardiomyopathy findings

A

S4

systolic murmur

136
Q

treatment of hypertrophic cardiomyopathy

A

cessation of high intensity athletics
beta-blockers or non-dihydropyridine calcium channel blockers (verapamil)
ICD

137
Q

causes of restrictive/infiltrative cardiomyopathy

A 
sarcoidosis
amyloidosis
postradiation fibrosis
endocardial fibroelastosis
loffler syndrome
hemochromatosis
138
Q

what is loffler syndrome

A

endomyocardial fibrosis with prominent eosinophillic infiltrate

139
Q

what is CHF

A

cardiac pump dysfunction
symptoms: dyspnea, orthopnea, fatigue, rales, JVD, pitting edema
right heart failure often with left heart failure

140
Q

systolic dysfunction CHF

A

low EF, poor contractility, secondary to ischemic heart disease or DCM

141
Q

diastolic dysfunction

A

normal EF and contractility, impaired relaxation, decreased compliance

142
Q

isolated right heart failure is usually due to?

A

cor pulmonale

143
Q

what drugs are used in CHF?

A

ACE inhibitors, beta blockers (except acute decompensated), Ang II receptor blockers, spiranolactone
thiazide or loop diuretics for symptomatic relief
hydralazine and nitrate therapy for symptoms and increased mortality

144
Q

what causes cardiac dilation

A

greater ventricular EDV

145
Q

what causes dyspnea on exertion?

A

failure of CO to increase during exercise

146
Q

what are symptoms of left heart failure

A

pulmonary edema
orthopnea
PND

147
Q

pulmonary edema

A

increased pulmonary venous pressure leads to pulmonary venous distention and trsudation of fluid
presence of hemosiderin-laden macrophages in the lungs

148
Q

orthopnea

A

shortness of breath when supine becaouse of increased venous return from redistribution of blood exacerbating pulmonary vascular congestion

149
Q

PND

A

breathless awakening from sleep: increased venous return from redistribution of blood, reabsorption of edema

150
Q

what are symptoms of right heart failure

A

hepatomegaly
peripheral edema
JVD

151
Q

symptoms of bacterial endocarditis

A 
fever
new murmur
roth spots (round white spots on retina surrounded by hemorrhage)
osler nodes
janeway lesions
anemia
splinter hemorrhages
152
Q

cause of acute endocarditis

A

s. aureus (leads to large vegetations on previously normal valves)
rapid onset

153
Q

cause of subacute endocarditis

A

ciridans streptococci
smaller vegetations on congenitally abnormal or diseased valves
gradual onset
sequela of dental procedures

154
Q

cause of culture negative bacterial endocarditis

A

coxiella burnetti and bartonella

155
Q

non bacterial causes of endocarditis

A 
malignancy
hypercoagulable state
lupus
s. bovis in colon cancer
s.epidermidis on prosthetic valves
156
Q

what valve is most commonly effectd in bacterial endocarditis?

A

mitral

157
Q

what causes tricuspid valve endocarditis?

A

IV drug abuse, s. aureus, pseudomonas, candida

158
Q

what are complications of bacterial endocarditis

A

chordae rupture
glomerulonephritis
supporative pericarditis
emboli

159
Q

what causes rheumatic fever

A

s.pyogenes

160
Q

what valves are effects in rheumatic fever?

A

mitral > aortic&raquo_space; tricuspid

161
Q

what are the early and late lesions associated with rheumatic fever?

A

early: MR, late: mitral stenosis

162
Q

what histological and clinical features are present in rheumatic fever?

A 
aschoff bodies (granulomas with giant cells)
anitschkow cells (enlarged macrophages with ovoid wavy, rod like nucleus)
increased ASO titers
163
Q

what type of immune mediated hypersensitivity is rheumatic fever?

A

II, antibodies to M protein cross react with self antigens

164
Q

how does acute pericarditis present?

A

sharp pain aggravated ith inspiration and relieved with sitting up and leaning forward
friction rub
ECG: widespread ST segment elevation and/or PR depression

165
Q

fibrinous acute pericarditis

A

causes: dressler syndrome, uremia, radiation

presents with loud friction rub

166
Q

serous acute pericarditis

A

viral pericarditis, noninfectious inflammatory diseases (rheumatoid arthritis, SLE)

167
Q

suppurative/purulent

A

caused by bacterial infections (pneumococcus, streptococcus)

168
Q

cardiac tamponade

A

compression of heart by fluid in the pericardium that leads to decreased CO
equilibration of diastolic pressures in all 4 chambers

169
Q

hat are findings associated with cardiac tamponade

A

beck triad
increased heart rate
pulsus paradoxus
kussmaul sign

170
Q

what is the beck triad

A

hypoTN
distended neck veins
distant heart sounds

171
Q

what is seen on ECG with cardiac tamponade?

A

low-voltage QRS and electrical alternans (due to “swinging” movement of heart in large effusion)

172
Q

pulsus paradoxus

A

decreased amplitude of systolic blood pressure by > 10 mmHg during inspiration
seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup

173
Q

syphillitic heart disease

A

tertiary syphillis disrupts vaso vasorum of aorta –> atrophy of the vessel wall and dilation of the aorta and valve ring
calcification of the aortic root and ascending aortic arch
tree bark aorta

174
Q

what is the most common heart tumor?

A

metastasis (from melanoma, lymphoma)

175
Q

myxsomas

A

most common primary cardiac tumor in adults
mostly in the atria (left)
ball valve obstruction
associated with multiple syncopal episodes

176
Q

rhabdomyomas

A

most frequent primary cardiac tumor in children

associated ith tuborous sclerosis

177
Q

kussmaul sign

A

increasee in jvp on inspiration instead of the normal decrease
the negative intrathoracic pressure from inspiration ins not transmitted to the heart so there is impaired filling of the right ventricle. Blood backs up into the vena cava and causes JVD

178
Q

when do you see kussmaul sign

A

constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors

179
Q

what is raynaud’s phenomenon?

A

decreased blood flow to the skin (fingers and toes usuually) due to arteriolar vasospasm in response to cold temperature or emotional stress
disease if primary idiopathic
syndrome if caused by disease process

180
Q

what are causes of raynaud’s syndrome?

A

mixed connective tissue disease
SLE
CREST

181
Q

strawberry hemangioma

A

benign capillary hemangioma of infancy
first few weeks
grows rapidly and regresses spontaneously at 5-8

182
Q

cherry hemangioma

A

benign capillary hemangioma of the elderly

does not regress

183
Q

pyogenic granuloma

A

polypoid capillary hemacioma that an ulcerate and bleed

associated with trauma and pregnancy

184
Q

cyctic hygroma

A

cavernous lymphangioma of the neck

associated with turner syndrome

185
Q

glomus tumor

A

benign painful red-blue tumor under fingernails

arises from modified smooth muscle cells of the glomus body

186
Q

bacillary angiomatosis

A

benign capillary skin papules found in AIDS patients
caused by bartonella henselae
mistake for kaposi

187
Q

angiosarcoma

A

rare blood vessel malignancy occurring in head neck and breast areas
usually in elderly on sun-exposed areas
associated with radiation therapy and arsenic exposure
very aggressive and difficult to resect due to delay in diagnosis

188
Q

lymphangiosarcoma

A

lymphatic malignancy associated with persistent lymphedema (post-radical mastectomy

189
Q

kaposi sarcoma

A

endothelial malignancy
commonly effects skin, mouth, GI tract, respiratory tract
associated with HHV8 and HIV
mistake for bacillary angiomatosis

190
Q

what are the large vessel vasculitis

A

temporal (giant cell) arteritis

takayasu arteritis

191
Q

what are the medium vessel vasculitis

A 
polyarteritis nodosa
kawasaki disease
buerger disease (thromboangiitis obliterans)
192
Q

what are the small vessel vasculitis?

A

granulomatosis with polyangiitis (wegener’s)
microscopic polyangitis
churg-strauss syndrome
henoch-schonlein purpura

193
Q

epidemiology of large vessel vasculitis

A

temporal - elderly females

takayasu - asian females <40

194
Q

temporal (giant cell) arteritis symptoms and associations

A

elderly females
unilateral headache, jaw claudication
irreversible blindness due to ophthalmic artery occlusion
associated with polymyalgia rheumatica

195
Q

what is the pathology of temporal arteritis

A

focal granulomatous inflammation with increased ESR

196
Q

what arteries are most commonly affected in temporal arteritis

A

branches of the carotid

197
Q

how do you treat temporal arteritis

A

high dose corticosteroids prior to temporal artery biopsy to prevent vision loss

198
Q

takayasu’s arteritis symptoms

A 
pulseless disease (weak upper extremity pulses)
fever
night sweats
arthritis
myalgias
skin nodules
ocular disturbances
199
Q

pathology of takayasu’s

A

granulomatous thickening and narrowing of the aortic arch and great vessels
increased ESR

200
Q

treatment of takayasu’s

A

corticosteroids

201
Q

epidemiology of medium vessel vasculitis

A

polyarteritis nodosa: young adults

kawasaki disease: asian children <40

202
Q

polyarteritis nodosa symptoms

A

fever, weightloss, malaise, headache
ab pain, melena
HTN, neuro dysfxn, cutaneous eruptions, renal damage
hep B seropositivity in 30%

203
Q

arteries effected in polyarteritis nodosa

A

renal and visceral vessels, not pulmonary arteries

204
Q

pathology of polyarteritis nodosa

A

immune complex mediated
transmural inflammation of the arterial wall w/ fibrinoid necrosis
innumerable microaneurysms and spasm on arteriogram

205
Q

treatment of polyarteritis nodosa

A

corticosteroids, cyclophosphamide

206
Q

symptoms of kawasaki disease

A 
fever
cervical lymphadenitis
conjunctival injection
strawberry tongue
hand-foot erythema
desquamating rash
possible coronary artery aneurysm thrombosis leading to MI and rupture
207
Q

treatment of kawasaki’s

A

IVIg, aspirin

208
Q

buerger disease symptoms

A

intermittent claudication may lead to gangrene, autoamputation of digitis, superficial nodular phlebitis
raynaud’s
(segmental thrombosing vasculitis)

209
Q

treatment of buerger’s

A

smoking cessation

210
Q

symptoms of granulomatosis with polyangiitis

A

upper respiratory tract: perforation of nasal septum, chronic sinusits, otitis media, mastoiditis
lower respiratory tract: hemoptysis, cough, dyspnea
renal: hematuria, red cell casts

211
Q

what is the triad that is associated with granulomatosis with polyangiitis

A

focal necrotizing vasculitis
necrotizing granulomas in the lung and upper airway
necrotizing glomerulonephritis

212
Q

what are the ANCA associated vasculitis?

A

PR3-ANCA/c-ANCA (anti-proteinase 3): wegner’s

MPO-ANCA/ p-ANCA (anti-myeloperoxidase): microscopic polyangiitis and churg strauss

213
Q

what do you see on CXR in wegners

A

large nodular deposits

214
Q

how do you treat wegner’s

A

cyclophosphamide and corticosteroids

215
Q

microscopic polyangiitis symptoms

A

necrotizing vasculitis ommonly involving lung, kidneys and skin ith pauci-immune glomerulonephritis and palpable purpura
like wegners without nasopharyngeal involvement and no granulomas

216
Q

treatment of microscopy polyangiitis?

A

cyclophosphamide and corticosteroids

217
Q

symptoms of churg-strauss?

A

asthma, sinusitis, palpable purpura, peripheral neuropathy (wrist and foot drop)
can involve heart, GI, kidneys

218
Q

pathology of churg-strauss

A

granulomatous, necrotizing vasculitis with eosinophilia, increased IgE

219
Q

henoch-schonlein purpura presentation

A

follows URI
classic triad: skin (palpable purpura on buttocks and leg), arthralgias, and GI (abdominal pain, melena, multiple lesions of same age)

220
Q

cause of henoch-schonlein purpura?

A

vasculitis secondary to IgA complex deposition, associated with IgA nephropathy

First Aid (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions