Cardiovascular Flashcards
1
Q
Cardiovascular Pathology:
What patient populations are more affected by hypertension?
A
Blacks > Whites > Asian
2
Q
Cardiovascular Pathology:
What is the most common risk factor for Atrial fibrillation?
A
Hypertension
3
Q
Cardiovascular Pathology:
What is the correlation between blood pressure and Cardiovascular disease?
A
For every 20 mmHg increase in systolic or every 10 mmHg increase in diastolic, the risk for cardiovascular disease doubles.
4
Q
Cardiovascular Pharmacology:
What is the initial drug of choice for primary hypertension?
A
Thiazide diuretics
5
Q
Cardiovascular Pharmacology:
How do ACE inhibitors lower renal hypertension?
A
Decrease vasoconstriction of the efferent arteriole
6
Q
Cardiovascular Pharmacology:
How do you slow down the progression of Renal parenchymal disease?
A
ACE inhibitors
7
Q
Cardiovascular Pharmacology:
What drugs/ drug classes can cause drug induced HTN?
4 points
A
- oral contraceptives
- glucocorticoids
- Phenylephrine
- NSAIDs (preferentially constrict the afferent arteriole)
8
Q
Cardiovascular Pathology/ Endocrinology Pathology:
What is the triad to be aware of with a Pheochromocytoma?
A
- hypertension
- diaphoresis
- tachycardia
9
Q
Cardiovascular Pathology/ Endocrinology Pathology:
What is the triad to be aware of with Primary Aldosteronism (Conn Syndrome)?
A
Aldosterone producing tumor causing
- hypertension
- hypokalemia
- metabolic alkalosis
10
Q
Cardiovascular Pathology/ Endocrinology Pathology:
How can hyperthyroidism cause secondary HTN?
A
increase stimulation of beta-adrenergic receptors
11
Q
Cardiovascular Pathology/ Endocrinology Pathology:
How can Cushing syndrome cause secondary HTN?
A
Excess cortisol up regulates alpha 1 receptors on arterioles leading to increased sensitivity to NE and E
12
Q
Cardiovascular Pathology:
What must be present for an infant to have differential cyanosis in the setting of a Coarctation?
A
Patent ductus Arteriosus
13
Q
Cardiovascular Pathology:
What diagnosis can you make in a patient with ongoing drug resistant hypertension?
3 points
A
- Dx: Unilateral Renal Artery Stenosis
- Grossly the kidney appears shrunken
- Bx: showed crowding with tubulointerstitial atrophy, fibrosis, and focal inflammation
14
Q
Cardiovascular Pharmacology:
What is the best treatment for fibromuscular dysplasia?
A
Percutaneous transluminal angioplasty with or without stenting.
15
Q
Cardiovascular Pathology:
How can you distruingish primary hyperaldosteronism from conditions causing high renin?
A
Aldosterone to renin ratio (ARR)
ARR > 20:1 is suggestive of Primary hyperaldosteronism
16
Q
Cardiovascular Pathology:
How is malignant hypertension classified?
A
Severe, rapid increase in BP, usually >240/120 mmHg associated with end organ damage
17
Q
Cardiovascular Pathology:
Which metabolic syndromes increases the risk for CVD?
5 points
A
Insulin resistance, hypertension, abdominal obesity, dyslipidemia, and prothrombotic states
18
Q
Cardiovascular Pathology:
How many different types of arteriolosclerosis are there?
Name them
A
2; Hyaline arteriolosclerosis and Hyperplasticity’s arteriolosclerosis
19
Q
Cardiovascular Pathology:
Which type of arteriolosclerosis is associate with malignant hypertension?
A
Hyperplastic arteriolosclerosis ‘onion skinning” of the tunica intima
20
Q
Cardiovascular Pathology:
Describe Mönckeberg Arteriosclerosis:
4 points
A
- Benign calcification affecting the elastic lamina of the tunica Media, leading to stiffening WITHOUT obstruction.
- Affects medium sized arteries like the radial, ulnar, tibial, uterine, or femoral arteries in the elderly.
- Has a “pipestem appearance on X-ray.
- Risk factors include increase in age, DM, CKD, SLE, increase in vitamin D
21
Q
Cardiovascular Pathology:
List the arteries most often affected by atherosclerosis listed from most to least likely?
A
Abdominal aorta > coronary artery > popliteal artery > internal carotid artery > circle of willis
22
Q
Cardiovascular Pathology:
What are the non modifiable risk factors associated with Atherosclerosis?
4 points
A
Age, gender (men and postmenopausal women), homocystinuria, family history
23
Q
Cardiovascular Pathology:
Explain the 5 steps of the pathogenesis of Atherosclerosis:
A
- Endothelial cell injury causes monocyte emigration into intima
- Activated macrophages release cytokines causing smooth muscle cells to migrate into intima
- macrophages form foam cells into a fatty streak and a fibrous cap develops
- as intimal muscles cells become old and die, fibrous matrix degrades
- Fibrous cap (plaque) calcifies and ulcerates, causing vessel thrombosis
24
Q
Cardiovascular Pathology:
What is the most common cause of myocarditis in developed countries?
A
Viral infection:
- Coxsackie B virus
- Rubella virus
- Cytomegalovirus
25
Cardiovascular Pathology:
What is the most common cause of myocarditis worldwide?
Chagas disease
- Trypanosoma cruzi (protozoan parasite)
26
Cardiovascular Pathology:
Which bacteria are well known to cause myocarditis?
- staphylococcus aureus
- corynebacterium diphtheria
- haemophilus influenzae
27
Cardiovascular Pathology:
What are some causes of Myocarditis in patients with HIV?
- toxoplasmosis
- kaposi sarcoma metastases
28
Cardiovascular Pathology:
How does myocarditis present?
4 points
- symptoms of CHF: chest pain*, peripheral edema, dyspnea
- palpitations* from arrhythmias
- viral sequelae: fever, diarrhea, and fatigue
- PE: muffled S1 and S3 and/or mitral regurgitation murmur
29
Cardiovascular Pathology:
How can you diagnose myocarditis?
3 points
- ECG shows diffuse T wave inversions and ST segment elevations* (mimics an MI or pericarditis
- cardiac biopsy is the gold standard: shows edematous myocardial interstitial with lymphocytic infiltrate (neutrophilic or mononuclear)
- Creatine kinase-myocardial bound fractions (CK-MB) and troponin may be elevated
30
Cardiovascular Pathology:
What is right-sided endocarditis suggestive of?
IVDA
31
Cardiovascular Pathology:
What is the definition of Endocarditis?
Inflammation of the lining of the heart and heart valves
32
Cardiovascular Pathology:
Why is infective endocarditis so dangerous?
There is no blood supply to the heart valves so leukocytes cannot be recruited if bacteria attach.
33
Cardiovascular Pathology:
When can you suspect subacute infective endocarditis?
Hx of previously damaged or abnormally developed valve in the setting of oral surgery or poor dentition as is associated with Strep Viradins
34
Cardiovascular Pathology:
How does Infective endocarditis present?
5 points
- Janeway lesions: small, painless erythematous lesions on the palms and soles
- Osler nodes (painful raised lesions on the finger and toe pads
- splinter hemorrhages
- Roth spots (round white spots on the retina surrounded by hemorrhage)
- valvular involvement: (mitral > aortic > tricuspid)
35
Cardiovascular Pathology:
How would you diagnose infective endocarditis?
6 points
Duke criteria:
- positive serial blood cultures
- hx of infective endocarditis
- IVDA
- fever
- vascular or immune phenomena
- valvular lesions on echocardiography
36
Cardiovascular Pathology:
How would you treat infective endocarditis?
3 points
- Acute endocarditis empirical antibiotics: nafcillin and gentamicin for good coverage
Subacute endocarditis obtain blood cultures before abx:
- ampicillin + gentamicin for native valves
- vancomycin, gentamicin, and rifampin for prosthetic valves
37
Cardiovascular Pathology:
What bacteria is considered with endocarditis + prosthetic device?
Staphylococcus epidermidis
38
Cardiovascular Pathology:
What bacteria is considered with endocarditis + colon cancer?
Streptococcus bovis
39
Cardiovascular Pathology:
What bacteria is considered with endocarditis + dental procedure?
Streptococci viridans
40
Cardiovascular Pathology:
What bacteria is considered with endocarditis + GI surgery?
Enterococcus
41
Cardiovascular Pathology:
What species is considered with endocarditis + total parenteral nutrition?
Fungal
42
Cardiovascular Pathology:
What bacteria is considered with endocarditis + alcoholics or the homeless?
Bartonella henselae
43
Cardiovascular Pathology:
What bacteria is considered with endocarditis + fastidious and culture negative?
HACEK organisms:
- Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella
44
Cardiovascular Pathology:
How does Strep Viridans adhere to enamel and valves to cause endocarditis?
Converts glucose to dextrans
45
Cardiovascular Pathology:
How do Janeway lesions differ from Osler nodes?
Janeway lesions are caused by micro abscesses of the dermis surrounding septic emboli, whereas Osler nodes are caused by deposition of immune complexes
46
Cardiovascular Pathology:
What is the mnemonic for endocarditis?
FROM JANE
- fever
- roth spots
- Osler nodes
- murmur
- Janeway lesions
- anemia
- nailbed hemorrhage
- Emboli
47
Cardiovascular Pathology:
What are the complications of endocarditis?
4 points
- Septic emboli
- chordae rupture
- glomerulonephritis
- suppurative (pus) pericarditis
48
Cardiovascular Pathology:
Explain Marantic Endocarditis:
4 points
Nonbacterial endocarditis/ NBTE
- small, sterile fibrin vegetations deposit on the heart valves of pts with debilitating disease
- can occur as a paraneoplastic syndrome of mucin-secreting tumors (usually colon or pancreatic)
- platelets aggregate and become infected
- can occur with hyper coagulable state and lupus
49
Cardiovascular Pathology:
What is the complication of Marantic Endocarditis?
Sterile embolus leading to cerebral infarction
50
Cardiovascular Pathology:
Describe Libman-Sacks endocarditis:
Sequela of SLE where autoantibodies target and damage the heart valves. Steril vegetations (fibrin, neutrophils, lymphocytes, and histiocytes) form on both sides of the heart valve. Asymptomatic but can be detected via murmur on the mitral valve (holosystolic 'blowing' murmur)
51
Cardiovascular Pathology:
Why are carcinoid tumors related to cardiovascular pathology?
Increased serotonin leads to systemic vasodilation as well as thickening, contraction, and decreased mobility of right-sided heart valves. Results in reduced preload and end-diastolic volume. Includes tricuspid regurgitation and pulmonic stenosis.
Look for high-pitched holosystolic murmur at the left fourth intercostal space.
52
Cardiovascular Pathology:
Describe Rheumatic fever:
Multisystem involvement
- typically occurs after a pharyngeal infection with GAS (Beta hemolytic)
- symptoms referred to as JONES criteria
53
Cardiovascular Pathology:
Describe the Mneumonic to remember the symptoms for Rheumatic Fever:
JONES PEACE:
Major criteria:
- Joints: Migratory arthritis
- Carditis: now-Onset murmur
- Nodules, subcutaneous: extensor surfaces
- Erythema marginatum
- Sydenham chorea
Minor criteria:
- PR interval, prolonged
- ESR elevated
- Arthralgias
- CRP elevated
- Elevated temperature (fever)
54
Cardiovascular Pathology:
How can you show evidence of streptococcal infection:
- Antistreptolysin O titers (ASO)
- Positive throat culture for streptococci group A
55
Cardiovascular Pathology:
What is the most serious complication of rheumatic fever?
Acute Rheumatic Heart Disease, affecting all 3 layer of the heart.
Divided into Fibrinous pericarditis, Myocarditis, Endocarditis.
56
Cardiovascular Pathology:
How does Fibrinous pericarditis present?
Presents with chest pain and friction rub
57
Cardiovascular Pathology:
Describe what you would see in Myocarditis:
Collagen and fibrinoid material form nodule call Aschoff bodies and are surrounded by macrophages (Anitschkow cells), lymphocytes, plasma cells, and multinucleated giant cells (Aschoff cells)
58
Cardiovascular Pathology:
Describe Endocarditis as a complication of Rheumatic Fever:
Valves become inflamed and small verrucae (rubber fibrin vegetations) form along the line of closure. Valves thicken and calcify, leading to insufficiency or stenosis. Mitral and Aortic valve commonly affected because of high pressure gradient.
59
Cardiovascular Pathology:
What is the cause of death of acute rheumatic fever?
Myocarditis leading to cardiac failure
60
Cardiovascular Pathology:
What is Sydenham chorea?
Involuntary, purposeless contraction of the trunk muscles and extremeties
61
Cardiovascular Pharmacology:
What is the treatment for chronic rheumatic heart failure?
5 points
- high dose PCN for GAS
- symptomatic treatment
- Steroids and salicylates to reduce pain and inflammation
- Digitalis (digoxin) to reduce the symptoms of heart failure
- Haloperidol to treat Sydenham chorea if present
62
Cardiovascular Pathology:
What are the causes of Dilated Cardiomyopathy?
14 points
- acromegaly
- alcohol abuse
- wet beri beri (thiamine deficiency)
- coxsackie B virus myocarditis
- Chronic cocaine use
- Chagas disease
- doxorubicin toxicity
- hemochromatosis
- HIV
- hypothyroidism
- idiopathic
- Lyme disease
- peripartum cardiomyopathy
- sarcoidosis
63
Cardiovascular Pathology:
What are the complication of dilated cardiomyopathy?
5 points
- cardiac arrhythmias
- mural thrombi
- CHF
- bundle-branch blocks
- death
64
Cardiovascular Pathology:
How does dilated cardiomyopathy present?
9 points
Right or left heart failure
- decreased ejection fraction
- JVD
- edema
- orthopnea
- hepatomegaly
- cardiomegaly
- arrhythmias
- S3
- systolic regurgitant murmur
65
Cardiovascular Pathology:
How can you diagnose dilated cardiomyopathy?
3 points
- radiography showing an enlarged cardiac silhouette with pulmonary congestion
- Echocardiography showing dilated LV with decreased EF
- Lymphocytic infiltrate with myocyte necrosis if caused by coxsackie B virus myocarditis
66
Cardiovascular Pathology:
How is T Cruzi transmitted?
Bite of the reduviid bug
67
Cardiovascular Pathology:
What is the strategy to treat dilated cardiomyopathy?
Improve the symptoms of CHF
If EF < 35% despite therapy consider ICD placement to control arrhythmias or heart transplant
68
Cardiovascular Pathology:
What is the inheritance pattern and its defect in HCM?
Autosomal dominant mutation in the beta-myosin heavy-chain
69
Cardiovascular Pathology:
Explain the Venturi effect in HCM:
The anterior mitral leaflet blocking in the outflow tract due to increased blood flow velocity over the hypertrophied septum, which creates negative pressure.
70
Cardiovascular Pathology:
How do syncopal episodes during exercise occur during HCM?
The Venturi effect causing sub aortic obstruction to outflow
71
Cardiovascular Pathology:
How do young athletes die in the presence of HCM?
Ventricular arrhythmias
72
Cardiovascular Pathology:
How does hypertrophic cardiomyopathy present?
8 points
- syncope
- dyspnea
- chest pain brought on by exercise and relieved by rest
- PE may show S4 cardiac gallop (atrial kick into a noncompliant ventricle
- harsh systolic crescendo-decrescendo murmur at left-upper sternal border
- mitral valve regurgitation
- pulses bisferiens (a biphasic pulse), consisting of two strong systolic pulse peaks
73
Cardiovascular Pathology:
How would you diagnose HCM?
3 points
- imaging will show cardiomegaly and a dilated left atrium
- ECG will show LVH, MR, and diastolic dysfunction
- Biopsy shows myofibrillar disarray and fibrosis
74
Cardiovascular Pathology:
What is the treatment for HCM?
3 points
Goal to maintain ventricular filling in order to prevent obstruction
- Beta Blockers and CCBs to slow HR and increase diastolic filling time, and decrease myocardial O2 consumption
- Implantable cardioverter defibrillators ICDs for high risk pts to prevent sudden cardiac death
- avoid high intensity exercise
75
Cardiovascular Pathology:
What is Restrictive Cardiomyopathy?
Least common CM but is caused by diseases that infiltrate the myocardium to impede diastolic filling of the heart.
76
Cardiovascular Pathology:
What circumstances can cause Restrictive Cardiomyopathy?
8 points
- amyloidosis
- endocardial fibroelastosis ( endocardium of young children)
- glycogen storage disorders (Pompe disease)
- Hemochromatosis (dilated CM can also occur)
- inborn errors of metabolism (Gaucher and Fabry diseases)
- Löeffler syndrome (end-myocardial fibrosis with prominent eosinophilic infiltrate)
- postradiation fibrosis
- sarcoidosis
77
Cardiovascular Pathology:
How does Restrictive Cardiomyopathy present?
10 points
- arryhthmias from confiction defects
- ascites
- CHF
- Dyspnea
- exercise intolerance
- JVD
- peripheral edema
- pulsus paradocus (phenomenon where the systolic blood pressure drops significantly during inspiration)
- S4 gallop
- weakness
78
Cardiovascular Pathology:
How do you diagnose Restrictive CM?
2 points
- Imaging will show mild cardiomegaly
- In cases of amyloidosis, ECG shows low voltage despite thick myocardium
79
Cardiovascular Pathology:
What is the effects of the Valsalva maneuver or exercise on a murmur caused by Mitral Valve Prolapse and HCM?
Increases the intensity because of a decrease in end- diatonic volume. The decrease in volume leads to a decrease in chamber size and increase in obstruction.
80
Cardiovascular Pathology:
How is Primary amyloidosis diagnosed?
Apple-green birefringence on condo red
81
Cardiovascular Pathology:
How is an S3 heart sound caused?
Vibration and turbulence as blood fills a ventricle that already has excess fluid due to systolic dysfunction
82
Cardiovascular Pathology:
What is congestive heart failure?
Inability of the heart to generate sufficient cardiac output to meet the metabolic demands of the body
83
Cardiovascular Pathology:
How many types of left sided heart failure are there?
2 types; HFrEF, HFpEF
84
Cardiovascular Pathology:
How does Systolic Failure look on an ESPVR loop?
Downward + rightward
-> Decrease SV, decrease EF, increase LVEDP (preload)
Relates to decrease ability to eject blood
85
Cardiovascular Pathology:
How does diastolic failure look on an ESPVR loop?
Upward shift of passive diastolic pressure-volume curve
-> Increase LVEDP, decrease LVEDV, preserved EF
Relates to decrease in compliance
86
Cardiovascular Pathology:
How does heart failure present?
9 points
- pulmonary congestion
- low perfusion
- orthopnea (shortness of breath when supine)
- dyspnea on exertion
- Paroxysmal nocturnal dyspnea *breathless awakening from sleep
- fatigue
- PE shows rales, JVD, and pitting edema
- S3 or S4 may be present
- Microscopically intra-alveolar hemosiderin-laden macrophages (HF cells), alveolar edema, and cardiac myocyte hypertrophy are seen
87
Cardiovascular Pathology:
What are the complications to heart failure?
3 points
- Pulmonary congestion
- cardiogenic shock
- hyperaldosteronism secondary to RAAS
88
Cardiovascular Pathology:
Why does orthopnea and paroxysmal nocturnal dyspnea (PND) occur in HF?
When supine, venous return is increased for blood redistribution and the baseline pulmonary venous distention from pulmonary edema worsens. This leads to SOB. PND occurs 1-2 hours of sleeping and is less readily reversible by siting up compared to orthopnea.
89
Cardiovascular Pharmacology:
Which agents would you give to pts with HFrEF to reduce mortality?
- Beta blockers
- ACE inhibitors/ARBs
- mineralocorticoid antagonists
*More responsive to systolic failure
90
Cardiovascular Pharmacology:
How do ACE inhibitors help treat HF?
Decreases after load, reducing aldosterone-mediated salt an water retention
91
Cardiovascular Pharmacology:
How do diuretics help treat HF?
Preventing volume overload
92
Cardiovascular Pharmacology:
How do beta blockers help treat HF?
Augments cardiac output and stabilizes hemodynamics
93
Cardiovascular Pharmacology:
How does Digoxin help treat HF?
Inotropes alike improves contractility in the setting of systolic failure, not much helpful to improve diastolic function
94
Cardiovascular Pharmacology:
How do you treat acute heart failure?
Goal is to provide relief from dyspnea and congestion:
- Oxygen
- Diuretics
- Nitrates
- Morphine
95
Cardiovascular Pharmacology:
What is the treatment of acute HF due to MI?
Mneumonic: MOP LaNe
- Morphine
- Oxygen
- Position (sit upright)
- Loop diuretics
- Nitrates
96
Cardiovascular Pharmacology:
What is the treatment for right sided HF?
ACE inhibitors, decreases after load and prevents aldosterone-mediated salt and water retention. Cautious with pts with stiff LV's (very preload dependent)
97
Cardiovascular Pathology:
What are the complications to aneurysms?
- thrombus formation
- erosion into nearby structures
- rupture leading to hypotension, shock, and death
98
Cardiovascular Pathology:
What patient population would you see an Abdominal Aortic Aneurysm (AAA)?
Male smokers > 50 years old with atherosclerosis
99
Cardiovascular Pathology:
Where would suspect a AAA to occur?
Between the renal arteries (L1-L2) and the aortic bifurcation at the L4 level.
100
Cardiovascular Pathology:
Where would you see pooling if a AAA ruptured?
Peritoneal cavity
101
Cardiovascular Pathology:
How would you screen for a AAA?
Abdominal ultrasound for past or active male smokers between 65 and 75 years old
102
Cardiovascular Pathology:
How many different types of Thoracic Aortic Aneurysms are there?
3;
- Atherosclerotic
- Syphilitic
- Connective Tissue disorder
103
Cardiovascular Pathology:
How does a TAA to be caused by syphilis occur?
Tertiary syphilis damages the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of the aorta and valve ring. Calcification of the aortic root and ascending aortic arch causes a "tree bark" appearance. Valve involvement can lead to aortic insufficiency.
104
Cardiovascular Pathology:
How does a TAA to be caused by atherosclerosis occur?
Hx of atherosclerosis, CAD, HTN, and smoking
105
Cardiovascular Pathology:
How does a TAA to be caused by connective tissue disorders occur?
Acquired or congenital causes can lead to weakening and possible dissection.
106
Cardiovascular Physiology:
What is the formula of wall stress?
Law of Laplace
Wall stress = ( P * r)/ (2 * wall thickness)
107
Cardiovascular Pathology:
Which aneurysms are considered Miscellaneous?
3 points
- Berry aneurysms
- Mycotic Aneurysms
- Micro-aneurysms
108
Cardiovascular Pathology:
Where can you suspect a Berry aneurysm?
Bifurcations of cerebral arteries (PCA and ACA)
109
Cardiovascular Pathology:
What condition are Berry aneurysms associated with and what complication can it lead to?
Polycystic Kidney disease, can lead to subarachnoid hemorrhage
110
Cardiovascular Pathology:
Describe a Mycotic Aneurysm?
Usually due to a bacterial infection (Mc Salmonellosis) involving the wall of the abdominal aorta.
111
Cardiovascular Pathology:
Who would you seen micro aneurysms occur in?
DM and HTN patients
112
Cardiovascular Pathology:
What does an Aortic Dissection create?
A False Lumen, this is luminal blood dissecting the medial layers through a longitudinal intimal tear.
113
Cardiovascular Pathology:
What can an Aortic dissection progress to?
- 3 points
- Pericardial tamponade
- aortic rupture
- death
114
Cardiovascular Pathology:
How does an Aortic dissection occur?
Cystic medial necrosis, in which elastic tissue and muscle within the tunica media have degenerated.
115
Cardiovascular Pathology:
What are some predisposing factors to an Aortic dissection?
3 points
- HTN
- Bicuspid aortic valve
- Inherited connective tissue disorders (ie Marfan syndrome and Ehlers-Danlos syndrome)
116
Cardiovascular Pathology:
How does an Aortic dissection present?
3 points
- sudden onset tearing chest pain, radiating to the back
- +/- markedly unequal blood pressures in each arm, indicating the subclavian artery
- CXR showing mediastinal widening
117
Cardiovascular Pharmacology:
How do you treat an Aortic Dissection?
- if it's proximal Stanford Type A then surgery because of aortic valve involvement
- Distal Stanford Type B managed with Beta-blockers, then vasodilators
118
Cardiovascular Pathology:
What are some changes expected to see in a Arteriovenous fistula?
- diversion of blood can cause ischemic changes
- increase venous pressure causes aneurysm formation
- hypervolemia can lead to high-output cardiac failure associated with palpable thrill on PE (increased venous return -> increased preload -> increased CO -> HF)
119
Cardiovascular Pathology:
Which conditions are categorized as Systolic Murmurs?
- Mitral Regurgitation
- Tricuspid Regurgitation
- Mitral Valve Prolapse
- HCM
120
Cardiovascular Pathology:
Which conditions are categorized as Diastolic Murmurs?
- Aortic Regurgitation
- Pulmonic regurgitation
- Mitral stenosis
- Tricuspid stenosis
121
Cardiovascular Pathology:
Which conditions are categorized as Continuous Murmurs?
- PDA
- VSD
122
Cardiovascular Pathology:
What are the consequences of Mitral regurgitation?
3 points
- increased LA pressure and volume
- Increased LV Volume
- reduction of forward flow
123
Cardiovascular Pathology:
What are the causes of Acute Mitral regurgitation?
3 points
- Papillary muscle rupture
- endocarditis
- ruptured chord tendineae
124
Cardiovascular Pathology:
What are the causes of chronic Mitral regurgitation?
7 points
- rheumatic heart disease
- ischemic cardiomyopathy
- dilated cardiomyopathy
- HCM
- Mitral Valve prolapse
- endocardial fibroelastosis
- endocarditis
125
Cardiovascular Pathology:
What is the most common cause of Mitral regurgitation in the developed world?
Mitral valve prolapse
126
Cardiovascular Pathology:
How does an acute MR present?
Symptoms of pulmonary edema
127
Cardiovascular Pathology:
How does a chronic MR present?
- symptoms of low cardiac output (fatigue, weakness)
- pulmonary congestion (dyspnea, orthopnea, PND)
- RHF (peripheral edema, ascites) in severe cases
128
Cardiovascular Pathology:
What heart sounds would you hear in MR?
S3 and holosystolic, high-pitched, blowing murmur best heard at the apex, radiating toward the left axilla.
129
Cardiovascular Pathology:
How would you diagnose a Mitral Regurgitation?
- ECG includes LV Hypertrophy and LA enlargement
- Echocardiogram shows regurgitant mitral valve
- CXR may show pulmonary edema
- Pulmonary capillary wedge pressure tracing will show a prominent V wave (Tall) indicative of increased LA pressure
130
Cardiovascular Pharmacology:
How do you treat Mitral Regurgitation?
Goal is to increase forward flow, reduce regurgitation, and decrease pulmonary venous hypertension.
- Diuretics
- Vasodilators
- Digitalis (increases cardiac output)
- valve repair is symptomatically severe
131
Cardiovascular Pathology:
What patient population is at risk for Aortic stenosis?
- elderly because of age-related thickening and calcification
- younger patients (<65 yo) with a history of RHD and bicuspid aortic valve (anatomically disadvantage)
132
Cardiovascular Pathology:
How does an advanced Aortic stenosis present?
3 points
- SAD triad: Syncope, Angina, Dyspnea (ASD order)
- crescendo-decrescendo systolic ejection murmur
- Pulsus parvus et tarsus: weak and delayed pulse at the carotid artery due to stenosis
133
Cardiovascular Pathology:
How does a Tricuspid regurgitation sound?
A blowing holosystolic murmur heard at the left lower sternal border that increases with inspiration due to the increase in venous return to the right side of the heart.
134
Cardiovascular Physiology:
What is the formula for coronary perfusion pressure?
Aortic diastolic pressure - LVEDP
135
Cardiovascular Pathology:
How would an infant present if they had a VSD?
4 points
- harsh systolic murmur
- fatigue with feeding
- poor growth
- respiratory infections
136
Cardiovascular Pathology:
How would you diagnose a VSD?
Murmur that is harsh, non radiating holosystolic murmur best heard over the left sternal border at the third and fourth intercostal spaces. Intensity varies with the size of the defect.
137
Cardiovascular Pathology:
Describe Mitral Valve Prolapse:
aka Floppy valve disease
- autosomal dominant or acquired part of connective tissue disorders such as Marfan syndrome, SLE, the mucopolysaccharidoses, and Ehlers-Danlos syndrome
- Normal collagen and elastin have been replaced with myxomatous connective tissue
138
Cardiovascular Pathology:
How does a Mitral Valve Prolapse present?
- can be asymptomatic
- can cause chest pain, palpitation, labored breathing, or fatigue
- Murmur: Late systolic murmur preceded by a mid systolic click
139
Cardiovascular Pathology:
Describe how different maneuvers changes the intensity of the murmur in MVP:
3 points
- valsalva maneuver decreases preload, and squaring increases preload.
- Valsalva or standing decreases the volume of the LV, allowing the prolapse to occur sooner increasing the intensity
- Squatting increases VR, Ventricular Volume, helping maintain tension on the chord tendineae and allowing the valve to stay shut longer, decreasing the intensity
140
Cardiovascular Pharmacology:
How to treat an MVP?
Beta blockers to control pain and/or arrhythmias
141
Cardiovascular Pathology:
Why are MVP and HCM have paradoxical murmurs?
All other murmurs increase in intensity with increased preload (squatting) and decrease in intensity with decreased preload (Valsava)
142
Cardiovascular Pathology:
Describe the Grading system for systolic murmurs:
1. Barely audible
2. Faint but audible
3. Easily heard
4. Easily heard and associated with palpable thrill
5. Easily heard with stethoscope barely touching the chest
6. Easily heard without stethoscope touching the chest
143
Cardiovascular Pathology:
Describe some key PE finding seen in Aortic regurgitation:
1. Corrigan (water-hammer) pulse: marked distention and collapse
2. de Musset sign: Head bobbing with systole
3. Quincke sign: Capillary pulsation visible in nail beds
4. Bisferiens pulse: double systolic impulse in carotid or brachial artery
**all related to a widened pulse pressure
144
Cardiovascular Pathology:
What are the two diastolic murmurs?
Aortic Valve regurgitation and Mitral stenosis
145
Cardiovascular Pathology:
How does a widened pulse pressure occur in Aortic Regurgitation?
LV systolic pressure increases while aortic diastolic pressure decreases, coronary perfusion pressure decreases too
146
Cardiovascular Pathology:
What are the causes of Aortic Regurgitation?
6 points
- RHD
- Infection endocarditis
- Aortic dissection
- HTN
- Syphilis
- Marfan syndrome
147
Cardiovascular Pathology:
How does a Aortic regurgitation present?
- dyspnea on exertion
- angina due to shorter diastole and decreased coronary artery filling
- fatigue
- Wide pulse pressure
- S3 and a high-pitched, "blowing" early diastolic decrescendo murmur heard best at the second right intercostal space
- Austin Flint Murmur, a mid siadtolc low pitched rumbling from regurgitated blood hitting the MV leaflet during diastole, prevents the opening snap (vs MS)
148
Cardiovascular Pathology:
How would you diagnose an Aortic regurgitation?
- Echocardiography
- "pseudo valve" or "bird's nest deformity" on the ventricular septum
149
Cardiovascular Pharmacology:
How would you treat an Aortic Regurgitation?
Goal is afterload reduction.
- ACE inhibitors and Vasodilators
- Diuretics and digitalis
- Valve replacement if severe
150
Cardiovascular Pathology:
Describe a Pulmonic Regurgitation:
Usually due to PAH, also a decrescendo murmur and is heard best in the pulmonic area of the heart.
151
Cardiovascular Pathology:
What can mitral stenosis lead to?
- pulmonary edema
- hemoptysis due to bronchial vein rupturing
- RHF due to reactive pulmonary HTN
- Afib due to LA dilation disrupting the conducting system
152
Cardiovascular Pathology:
What is the most common cause of Mitral Stenosis?
- RHD, producing commissural fusion (fish mouth valve)
- less commonly is calcification in elderly patients, congenital stenosis, and endocarditis with large vegetations
153
Cardiovascular Pathology:
How does Mitral Stenosis present?
- dyspnea, fatigue, orthopnea, PND
- Signs of RHF if severe
- Afib
- Thromboembolism
- infective endocarditis
- Hemoptysis
- Murmur: high-pitched opening snap after S2, followed by a decrescendo "diastolic rumble" best heard at the apex, with an accentuation at the end of diastole
154
Cardiovascular Pathology:
How would you diagnose Mitral Stenosis?
- echocardiography:mthich MV leaflets and LA enlargement
- ECG shows P mitral (M shaped P wave) due to enlarged atrium
155
Cardiovascular Pharmacology:
What is the treatment for Mitral Stenosis?
- diuretics and salt restriction to control vascular congestions
- Warfarin to prevent thromboembolism
- Beta blockers to reduce HR and improve diastolic LV filling
- Mechanical option include percutaneous ballon mitral valvoplasty (crack open the stenosis), open mitral commissurotomy (cutting open the stenosis)
- Valve replacement
156
Cardiovascular Pathology:
What is a PDA communicating between?
Aorta and Pulmonary Artery
157
Cardiovascular Pathology:
How does a Patent Ductus Arteriosus present?
- CHF and Late cyanosis are often seen
- machine-like murmur
158
Cardiovascular Pathology:
How do u diagnose a PDA?
Doppler echocardiography
159
Cardiovascular Pathology:
What is the treatment for a Patent Ductus Arteriosus?
Indomethacin (NSAID) to close by decreasing cyclooxyrgenase-mediated production of PG.
160
Cardiovascular Pathology:
Describe a cardiac myxoma?
6 points
- most common primary cardiac tumor in adults
- found in the left atrium in 90% of affected adults
- arise from endocardial mesenchymal cells
- Microscopy will show myxomatosis cells, endothelial cells, and smooth muscle cells found in a mucopolysaccharide background
- presents with syncopal episode because of tumor emboli or ball-valve obstruction on the MV
- may produce a diastolic "plop" sound
161
Cardiovascular Pathology:
Describe a cardiac rhabdomyoma?
3 points
- most common primary cardiac tumor in children
- arises from the myocardium
- associated with Tuberous sclerosis
162
UWorld: Pathophysiology:
What is responsible for maintaining cardiac output in the setting of chronic aortic regurgitation?
Increase in LV SV
163
Uworld Anatomy:
Where is the atrioventricular node located?
Endocardial surface of the right atrium, near the insertion of the septal leaflet of the tricuspid valve and the orifice of the coronary sinus.
164
Uworld Pharmacology: Sympathomimetic agents
Pt develops venous blanching, induration, and pallor after a NE infusion, what is the antidote to prevent local tissue necrosis?
Phentolamine, an alpha receptor blocker leading vasodilation. Must be given within 12 hours of extravasation to be effective.
165
Cardiology Pathology:
What is the inheritance pattern of tuberous sclerosis? 1 point
What are its manifestations? 5 points
- Autosomal dominant
- Hamartomas (benign tumor-like growths) affecting several organ systems, with cortical tubers
- "ash leaf" skin lesions that are hypo pigmented
- facial angiofibibromas (adenoma sebaceous)
- renal angiomyolipomas
- cardiac rhabdomyomas
166
Cardiology Pathology:
How does a DVT present?
- asymptomatic or present with calf or thigh discomfort, unilateral leg, swelling, edema, erythema, and warmth or tenderness on palpation over the vein.
167
Cardiology Pathology:
How would you test for a DVT?
Homans sign; dorsiflexion of the foot produces calf pain. Often used but is unreliable.
168
Cardiology Pathology:
How would you diagnose a DVT?
- D-Dimer and Lower extremity venous duplex US
- Angiography is gold standard but is invasive
169
Cardiology Pharmacology:
What are the techniques and strategies used to treat a DVT?
Main objective is to prevent complications such as PE, and post-thrombotic syndrome (chronic venous insufficiency syndrome)
- extremely elevation helps reduce edema
- anticoagulation with heparin to prevent thrombus enlargement
- if pt can't tolerate anticoagulation, an intrascular filter is placed near the IVC to prevent the emboli from traveling to the lungs
170
Cardiology Pathology:
What is Migratory Thrombophlebitis (Trousseau Syndrome)?
Hypercoagubility secondary to malignancy, typically a paraneoplastic syndrome to lung, pancreas, and colon cancer. A venous thrombus will appear at one site, disappear, then reappear at another site.
171
Cardiology Pathology:
Explain SVC Syndrome:
Neoplasms compressing or invading the SVC impairing drainage. Symptoms include dyspnea, face and neck edema, dilation of head, neck, and arm veins, as well as collaterals of the chest. Often accompanied by respiratory distress (pulmonary venous compression).
Neoplasms are typically bronchogenic carcinoma and mediastinal lymphomas.
172
Cardiology Pathology:
Explain IVC syndrome:
- edema in the legs
- distention of the superficial veins of the lower abdomen
- proteinuria if the renal veins are involved
- Neoplasms are either liver and kidney cancers, or thrombi
173
Cardiology Pathology:
What kind of acid/base phenomena can you expect with a pulmonary embolism?
respiratory alkalosis
174
Cardiology Pathology:
What kind of symptoms would be shown in a PE if any?
6 points
- Tachycardia
- tachypnea
- dyspnea
- hemoptysis
- cough
- +/- chest pain
175
Cardiology Pathology:
How can you diagnose a pulmonary embolism?
6 points
- Test of choice is Spiral CT angiography
- V/Q scan is renal insufficient and/or cannot get contrast
- pulmonary angiogram
- Doppler US
- increased D-dimer
- Arterial blood gas showing reduced PaO2 and PaCO2 and resp. alk. secondary to hyperventilation
176
Cardiology Pathology:
How do arterial emboli arise usually?
Mural thrombus in the left atrium
177
Cardiology Pathology:
What coexisting defects typically coincide with Paradoxical emboli?
2 points
ASDs or Patent Foramen Ovale
178
Cardiology Pathology:
What three congenital heart defects that do not cause early cyanosis?
ASD, VSD, and PDA
179
Cardiology Pathology:
How would remember if an arterial embolism to an extremity is occurring?
5 P's
Pain
Pulselessness
Pallor
Paresthesias
Paralysis
180
Cardiology Pathology:
How do patients present with a Fat Emboli?
4 points
- Petechiae
- Neurologic abnormalities
- Pulmonary distress
- Look for severe long bone fractures
181
Cardiology Pathology:
What are the complications of an Amniotic Fluid embolism?
- Disseminated intravascular coagulation (DIC) (80%)
- death (20-90%)
182
Cardiology Pathology:
How many stages are there to shock?
3;
Compensation
Decompensation
Irreversible injury
183
Cardiology Pathology:
How different types of shock are there?
4;
Hypovolemic, Cardiogenic, Obstructive,, and distributive
184
Cardiology Pathology:
How is obstructive shock caused by?
Cardiac tamponade, PE
185
Cardiology Pathology:
How is distributive shock caused?
Sepsis, CNS injury, anaphylaxis
186
Cardiology Pathology:
What causes distributive shock caused by sepsis?
Nitric Oxide
187
Cardiology Pathology:
How does the skin appear in distributive shock compared to others?
Warm and dry
188
Cardiology Pathology:
How do the kidneys present in a "shock" state?
2 points
Acute tubular necrosis and oliguria
189
Cardiology Pathology:
How do the intestines present in a "shock" state?
3 points
- Mucosal ischemic necrosis
- patchy hemorrhages
- sepsis
190
Cardiology Pathology:
How do the brain present in a "shock" state?
1 point
Necrosis
191
Cardiology Pathology:
How do the liver present in a "shock" state?
1 point
Centrilobular necrosis "shock liver"
192
Cardiology Pathology:
How do the adrenals present in a "shock" state?
2 points
- Waterhouse-Friderichsen syndrome with acute hemorrhagic infarction
- adrenal insufficiency
193
Cardiology Pathology:
What are some key facts that an infarction of the left anterior descending (LAD) can cause?
3 points
- Left bundle-branch block
- anterior wall rupture
- mural thrombus
194
Cardiology Pathology:
What are some key facts that an infarction of the Right coronary artery (RCA) infarction can cause?
3 points
- LV papillary rupture
- posterior flail leaflet
- Mitral regurgitation
195
Cardiology Pathology:
What is the formula for systemic vascular resistance?
(MAP- CVP)/CO
196
Cardiology Pathology:
How does a Pericardial Effusion present?
7 points
- usually asymptomatic
- dullness over the posterior left lung
- dysphagia (compression of the esophagus)
- dyspnea
- hoarseness
- left sided chest ache
- soft heart sounds
197
Cardiology Pathology:
List some causes of an acute pericardial effusion:
-Pericarditis
- cardiac surgery
- uremia
- collagen vascular disease
198
Cardiology Pathology:
List some causes of a chronic pericardial effusion:
- TB
- cancer (lung, breast, or bone)
- SLE
- HIV
199
Cardiology Pathology:
Explain the triad of cardiac tamponade:
The Beck Triad
- Muffled heart sounds
- Elevated jugular venous pressure (JVP)
- Low systolic blood pressure
200
Cardiology Pathology:
What are the most common causes of cardiac tamponade and what does it lead to?
8 points
- neoplasms
- postviral
- uremia
- hemorrhage
- ruptured LV from LAD MI
- active TB
- dissecting aortic aneurysm
- leads to impaired cardiac filling
201
Cardiology Pathology:
Describe the presentation of Cardiac Tamponade:
8 points
- pulsus paradoxus
- JVD (systemic venous congestion)
- peripheral edema
- hepatomegaly
- crackles/rales on lung auscultation (pulmonary venous congestion)
- hypotension and tachycardia (decreased CO)
- elevated diastolic intracardiac pressure
- decreased heart sounds
202
Cardiology Pathology:
What other types of pathologies can we see pulsus paradoxus?
- status asthmaticus
- restrictive cardiomyopathy
- impaired outflow
203
Cardiology Pathology:
How would you diagnose Cardiac Tamponade?
4 points
- Echocardiography
- Cardiac catheterization is definitive, shows diastolic pressure equalization in all four chambers*
- ECG will show low voltage
- Electrical alternans*: beat-to-beat variation of the QRS complex amplitude with without a wandering ECG baseline. This occurs because the heart move more freely.
204
Cardiology Pathology:
How would you treat cardiac tamponade?
Pericardiocentesis
205
Cardiology Pathology:
What are the two locations for a pericardiocentesis can be performed?
- Between the fifth and sixth intercostal space along the left sternal border
- infrasternal approach inferior to the xiphoid process
206
Cardiology Pathology:
What must the needle pass through in a Subxiphoid pericardiocentesis?
8 points
- skin
- superficial and deep fascia
- pectoralis major
- external intercostal membrane
- internal intercostal membrane
- transversus thoracis muscle
- fibrous pericardium
- parietal layer of the serous pericardium
207
Cardiology Pathology:
What is the mnemonic to remember the causes of pericarditis?
CARDIAC RIND
- collagen vascular disease
- aortic aneurysm
- radiation
- Drugs (hydralazine)
- infections
- Acute renal failure
- Cardiac infarction
- Rheumatic fever
- Injury
- Neoplasms
- Dressler syndrome
208
Cardiology Pathology:
What is Dressler syndrome?
Delayed pericarditis that develops 2-10 wks after an MI. Believed to be AI reaction against cardiac antigens formed in inflammation during MI.
209
Cardiology Pathology:
What are the four subtypes of Pericarditis?
- serous
- fibrinous
- suppurative (production of pus)
- hemorrhagic
210
Cardiology Pathology:
How does acute pericarditis present?
6 points
- pericardial friction rub
- retrosternal chest pain (worse on inspiration or coughing; relief while sitting or leaning forward)
- fever
- hypotension
- JVD
- distant heart sounds
211
Cardiology Pathology:
What would ECG show with an acute pericarditis?
Diffuse ST segment elevations and PR depressions
212
Cardiology Pathology:
What is chronic constrictive pericarditis?
Fusion of the pericardial layers and scar formation with possible calcifications leading to stiffness
213
Cardiology Pathology:
What is the most common cause of chronic constrictive pericarditis worldwide?
- TB
- also secondary to pyogenic organisms or Staph. spp.
214
Cardiology Pathology:
How does chronic constrictive pericarditis present?
5 points
- Fatigue, hypotension, and reflexive tachycardia (reduced CO)
- JVD, peripheral edema, and hepatomegaly with ascites (elevated systemic venous pressures
- Kussmaul sign: failure of the jugular veins to collapse during inspiration
- distant heart sounds
- pericardial "knock": an early apical diastolic sound representing the sudden cessation of ventricular filling due to the stiffened pericardium
215
Cardiology Pathology:
How is chronic constrictive pericarditis diagnosed?
4 points
- CXR shows enlarged cardiac silhouette
- CT/MRI show pericardial thickening
- confirmation is by cardiac catheterization showing increased diastolic pressures
- Prominent y descent is visible in the atrial pressure curve
216
Cardiology Pathology:
How do you treat chronic constrictive pericarditis?
Pericardiectomy
217
Cardiology Pathology:
Describe Serous Pericarditis:
- Exudate: protein- rich, straw colored, few inflammatory cells
- Associated with SLE, rheumatic fever, uremia, viral infection (Caxsackie B)
218
Cardiology Pathology:
Describe Fibrinous Pericarditis:
- Exudate: fibrin-rich with plasma cells
- Associated with MI Dressler syndrome), uremia, RF, can lead to scar and diastolic filling defects
219
Cardiology Pathology:
Describe Suppurative Pericarditis:
- Exudate: cloudy fluid with many inflammatory cells
- caused by bacterial infection leading to erythematous serial surfaces
220
Cardiology Pathology:
Describe Hemorrhagic Pericarditis:
- Exudate: bloody and inflammatory fluid
- due to tumor invasion or TB
221
Cardiology Pathology:
Describe the Large-vessel vasculitis: Temporal Arteritis?
2 points
- aka giant cell arteritis affects medium to large arteries, particularly the carotid and aortic branches
- affects women more than 50 yo
222
Cardiology Pathology:
How is giant cell arteritis characterized?
3 points
- nodular inflammation
- intimal fibrosis
- granulomas containing multinucleate giant cells
223
Cardiology Pathology:
Describe the presentation of giant cell arteritis:
6 points
- often affecting the temporal artery (absent pulse on palpation)
- unilateral headache
- sudden onset vision loss
- facial pain
- jaw claudication
- Ophthalmic artery involvement can lead to blindness
224
Cardiology Pathology:
What can giant cell arteritis be associated with?
Polymyalgia rheumatica: severe stiffness and aches in the axial skeleton (neck, shoulder girdle, and pelvic girdle)
225
Cardiology Pathology:
How would you diagnose giant cell arteritis?
- biopsy the affected vessel, should show granulomatous inflammation
- Elevated ESR and CRP
226
Cardiology Pathology:
How would you treat giant cell arteritis?
High dose systemic corticosteroids
*administer after confirming elevated ESR to prevent blindness, bx can be taken after
227
Cardiology Pathology:
Describe the Large-Vessel Vasculitis: Takayasu Arteritis
3 points
- aka pulseless disease
- inflammation of elastic arteries, MC aorta and its upper branching vessels
- often occurring in Asian woman younger than 40 years old
228
Cardiology Pathology:
How does Takayasu Arteritis present?
3 points
- loss of the carotid, ulnar, and radial pulse
- inflammation of the vessels can lead to myocardial ischemia, HTN, and visual defects
- systemic inflammatory effects such as fever, nigh sweats, arthralgia, and weight loss
229
Cardiology Pathology:
How is Takayasu Arteritis diagnosed?
Angiography showing narrowing of the aortic arch and proximal great vessels due to granulomatous inflammation. Elevated ESR.
230
Cardiology Pathology:
How do you treat Takaysu Arteritis?
Steroids and cytotoxic drugs to reduce inflammation
231
Cardiology Pathology:
What is cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) associated with?
Granulomatosis with Polyangitis (GPA)
232
Cardiology Pathology:
What is Perinuclear antineutrophil cytoplasmic antibody (p-ANCA) associated with?
3 points
- Churg-Stauss syndrome
- Microscopic polyangitis
- Primary sclerosing cholangitis
233
Cardiology Pathology:
Describe the Medium-Vessel Vasculitis: Polyarteritis Nodosa
3 points
- a necrotizing, immune complex-mediated inflammation of small to medium arteries
- destroys the media and internal elastic laminate- affects middle-aged to older men, peaking around 50 years
- common in patients with hepatitis B infection ( up to 30% infected )
234
Cardiology Pathology:
How is Polyarteritis Nodosa presented?
8 points
- inflammation can lead to fever and MSK pain
- decreased organ blood flow can cause headache, abdominal pain, and hypertension
- ischemic heart disease *
- arthritis*
- renal lesions*
- mononeuritis multiplex* (motor peripheral neuropathy affecting at least two unrelated nerve regions
- Cutaneous symptoms: palpable purpura, livedo reticularis, subcutaneous nodules
- NO LUNG INVOLVEMENT
235
Cardiology Pathology:
Describe the medium vessel Vaculitis: Kawasaki Disease
- a mucocutaneous disease characterized by acute necrotizing inflammation of the small, medium, and larger arteries
- often seen in children younger than 4
- most serious sequelae include coronary vessel involvement, leading to aneurysm
236
Cardiology Pathology:
How does Kawasaki disease present?
7 points
- fever present for at least 5 days
- cervical lymphadenitis
- bilateral conjunctival injection
- red, fissured lips
- oral erythema ("strawberry tongue")
- diffuse maculopapular erythematous rash
- desquamation of the hands and feet
237
Cardiology Pathology:
How do you diagnose Kawasaki Disease?
2 points
- diagnosed clinically
- coronary angiogram is performed to dx coronary artery aneurysm
238
Cardiology Pathology:
How do you treat Kawasaki disease?
3 points
- ASA and IVIG for anti-inflammatory
- those with CAD need longterm ASA and anti platelet therapy
- anticoagulation for those with coronary aneurysms
239
Cardiology Pathology:
Describe the medium sized vasculitis: Thromboangiitis Obliterans
3 points
- aka Buerger disease
- full-thickness, segmental, thrombosing inflammation of the distal extremity medium sized arteries, veins, and nerves.
- strongly associated with young men who are heavy smokers
240
Cardiology Pathology:
How does Buerger disease present?
2 points
- triad: distal arterial occlusion, Raynaud phenomenon, and migrating superficial vein thrombophlebitis
- gangrene/autoamputation of the digits caused by intermittent claudication
241
Cardiology Pathology:
How is Buerger disease diagnosed?
- arteriography can show distal stenotic corkscrew vessels
- definitive diagnosis. involved a tissue biopsy
242
Cardiology Pathology:
How do you treat Buerger Disease?
Smoking cessation
243
Cardiology Pathology:
What is the mnemonic to remember Kawasaki disease?
CRASH and BURN; needs 4/5
- Conjunctivitis (with spraring of the limbus)
- Rash (truncal)
- Adenopathy (unilateral and cervical)
- Strawberry tongue (+/- dry, cracked lips)
- Hand and feet (edema followed by desquamation)
PLUS
- BURN= fever of at least 5 days
244
Cardiology Pathology:
Describe the small-vessel vasculitis: Granulomatosis with Polyangiitis
3 points
- necrotizing, granulomatous inflammation affecting small vessels in the renal system and respiratory tract
- triad of focal necrotizing vasculitis, necrotizing granulomas in the lungs and upper airways, and necrotizing glomerulonephritis
245
Cardiology Pathology:
How does Granulomatosis with Polyangitis present?
4 points
- renal: hematuria, red cell casts in the urine
- lower respiratory tract: hemoptysis, cough, dyspnea
- upper respiratory tract: nasal septum perforation, chronic sinusitis, otitis media, mastoiditis
- skin: purpura
246
Cardiology Pathology:
How do you diagnose granulomatosis with polyangitis?
4 points
- 90% of pts are c-ANCA/PR3-ANCA positive
- definitive diagnosis biopsy showing necrosis and granuloma formation
- CXR: shows nodular densities
- hematuria/red cell casts also aid in dx
247
Cardiology Pathology:
How do you treat granulomatosis with polyangitis?
Cyclophosphamide and corticosteroids
248
Cardiology Pharmacology:
How does Mesna treat cystitis after taking cyclophosphamide?
Binds to metabolite acrolein in the bladder
249
Cardiology Pathology:
Describe the small vessel vasculitis: Churg-Strauss Syndrome
Granulomatous, necrotizing vasculitis affecting small to medium sized arteries. Characterized by the presence of eosinophilia
250
Cardiology Pathology:
How does Churg-Strauss Syndrome present?
- Upper respiratory tract: sinusitis, allergic rhinitis
- lower respiratory tract: asthma and cough
- MSK: Arthralgias
- Dermatologic: Palpable purpura
- Neurologic: peripheral neuropathy (ie foot drop)
- GI: Melena, colitis
- Pauci-immune glomerulonephritis (cardiac and renal manifestations) can also be seen
251
Cardiology Pathology:
How do you diagnose Chirg-Strauss syndrome?
Criteria includes:
- asthma
- peripheral eosinophilia (increased IgE
- paranasal sinusitis
- pulmonary infiltrates
- histology showing vasculitis
- polyneuropathy
- often associated p-ANCA positive 70%
252
Cardiology Pathology:
How do you treat Churg-Strauss syndrome?
Supportive therapy and glucocorticoids
253
Cardiology Pathology:
Describe the small vessel vasculitis: Microscopic Polyangitis
Necrotizing vasculitis most commonly involving small vessels of the lungs, kidneys, and skin. Characterized by pauci-immune glomerulonephritis and palpable purpura
254
Cardiology Pathology:
How does Microscopic Polyangitis present?
Similar to GPA but lacking nasopharyngeal involvement
255
Cardiology Pathology:
How do you diagnose microscopic polyangitis?
Positive for p-ANCA/MPO-ANCA. No granulomas seen on bx
256
Cardiology Pathology:
How do you treat microscopic polyangitis?
Cyclophosphamide and corticosteroids
257
Cardiology Pathology:
Describe the small vessel vasculitis: Henoch-Schönlein Purpura
2 points
- most common childhood systemic vasculitis with inflammation secondary to IgA complex deposition affecting small vessels
- often follows an upper respiratory infection in children
258
Cardiology Pathology:
How does Henoch-Schönlein Purpura present?
- Classic triad: palpable purpura on the buttocks and legs, polyarthralgias, colicky abdominal pain
- edema, hematuria (due to IgA nephropathy), hypertension, and melon may also be seen
259
Cardiology Pathology:
How is Henoch-Schlönlein Purpura diagnosed?
Clinically since lab tests are normal
260
Cardiology Pathology:
How do you treat Henoch Schlönlein Purpura?
- supportive therapy with analgesics
- long term follow up to prevent CKD and/or HTN
- Corticosteroids
261
Cardiology Pathology:
Describe the small vessel vasculitis: Cryoglobulinemic Vasculitis
Small vessel disease in which serum proteins precipitate out in the cold
262
Cardiology Pathology:
How do you diagnose Cryoglobulinemic Vasculitis?
4 points
- often due to Hep C infection
- purpura
- low complement
- immune deposits in vascular walls
263
Cardiology Pathology:
How do you treat Cryoglobulinemic Vasculitis?
- plasmaphoresis
- Hep C tx: interferon alpha and ribavirin
264
Cardiology Pathology:
How does Ischemic heart disease present normally?
As angina pectoris or MI
265
Cardiology Pathology:
How does Angina Pectoris present?
- retrosternal chest pain or pressure that radiates
- episodic lasting 15 seconds to 15 minutes
- diaphoretic or nauseated
- similar to MI but without ECG findings
266
Cardiology Pathology:
What are some precipitating factors that lead to Angina Pectoris?
What are the relieving factors?
- Cold, food, and stress
- rest and nitroglycerin
267
Cardiology Pathology:
How many types of Angina Pectoris are there?
3;
- stable angina
- unstable anigina
- prinzmetal angina
268
Cardiology Pathology:
Describe Stable angina:
Most common form induce by exertion, relieved by rest or nitroglycerin.
Pain is though to be due to stenosis.
If pain occurs with exertion, the coronaries are generally > 70% stenotic.
269
Cardiology Pathology:
Describe Unstable angina:
Pain at rest and activity with increasing frequency and intensity. Induced by a ruptured atherosclerotic plaque that leads to thrombosis and embloization.
- More likely to lead to MI compared to stable angina.
- ECG may show ST depressions and T-wave inversions, but never ST elevations.
- Cardiac biomarker are normal
- if pain occurs at rest, the arteries are ?90% stenotic
- Treatment involves ASA, nitrates, beta-blockers, and statins for lipid management
- Heparin or glycoprotein IIb/IIIa inhibitors are also used
- pts often sent for coronary angiography
270
Cardiology Pathology:
Describe Prinzmetal angina:
- aka variant angina, presents as intermittent chest pain at rest
- not related to activity, stress, or BP
- known triggers include tobacco, cocaine, and triptans
- often occurs at night
- due to coronary artery vasospasm*
- ECG shows transient ST elevations
- Definitive diagnosis involves exaggerated spam of coronary arteries after injection with agents like ergonovine* during coronary angiography.
- Tx includes calcium channel blockers and nitrates
271
Cardiology Pathology:
How do you diagnose Angina Pectoris?
- ECG showing prior MI or signs of ischemia
- stress testing to induce ischemia visible by ECH or myocardial perfusion imaging
- cardiac catheterization can directly visualize coronary obstruction
272
Cardiology Pathology:
How do you treat Angina Pectoris?
- modification of risk factors
- Sx: Coronary artery bypass graft (CABG) and percutaneous transluminal coronary angioplasty
273
Cardiology Pathology:
What ST segment change would you see in transmural ischemia?
Elevation
274
Cardiology Pathology:
What ST segment change would you see in subendocardial/partial thickness ischemia?
Depression
275
Cardiology Pharmacology:
Why would you use Nitrates in Stable Angina Pectoris?
- Reason: venous dilation to decrease preload (main effect), arteriolar dilatation to decrease after load, and coronary after dilatation to increase O2 supply
- AE: orthostatic hypotension, reflex tachycardia, blushing, headache
276
Cardiology Pharmacology:
Why would you use Beta-blockers in Stable Angina Pectoris?
- Reason: decrease sympathetic drive will decrease myocardial O2 demand and improve survival
- AE: bronchoconstriction, insomnia, depression, GI disturbances
277
Cardiology Pharmacology:
Why would you use CCB's in Stable Angina Pectoris?
- Reason: decrease preload and after load
- AE: hypotension, reflex tachycardia, flushing, headache
278
Cardiology Patholgy:
How can Cocaine cause an MI?
Precipitates coronary vasospasm and thrombosis
279
Cardiology Pathology:
How does an MI present?
- Prolonged ( > 30-45 minutes ) crushing chasten pain similar to angina, not relieved by nitroglycerin
- nausea, vomiting, sweating, SOB, weakness
280
Cardiology Pathology:
Describe a Non-ST-elevation MI (NSTEMI):
- MI limited to the inner one-half to one-third of the LV wall
- ST-depression is seen on ECG
281
Cardiology Pathology:
Describe a ST-elevation myocardial infarct (STEMI):
- following atherosclerotic plaque rupture and thrombosis leading to complete vessel occlusion
- necrosis of the entire myocardial wall is seen
- Q waves may develop hours after and persist long after MI
282
Cardiology Pathology:
Coronary artery thrombosis affects which vessels from most to least likely?
LAD > RCA > LCX
283
Cardiology Pathology:
Why do ST elevations occur shortly after an MI?
Injury to myocytes
284
Cardiology Pathology:
Why do prolonged Q waves occur 1-4 days post-MI?
Coagulative necrosis
285
Cardiology Pathology:
Why do T wave inversion happen a day after an MI?
Signifies ischemia at the periphery of the infarct
286
Cardiology Pathology:
What would you seen on gross and microscopically in the first 4 hours post-MI?
Nothing
287
Cardiology Pathology:
What would you seen on gross and microscopically 4-24 hr post-MI?
- Cellular events: Early coagulative necrosis with edema, hemorrhage, and "wavy fibers." If repercussion occurs -> contraction bands (due to free radical damage)
- Neutrophilic infiltrate
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Cardiology Pathology:
What would you seen on gross and microscopically in 1-3 days post-MI?
- Cellular events: extensive coagulative necrosis and acute inflammation
- Neutrophilic infiltrate
289
Cardiology Pathology::
What would you seen on gross and microscopically in 3-14 days post-MI?
- Cellular events: continued inflammation, granulation tissue at margins
- Macrophagic infiltrate
290
Cardiology Pathology::
What would you seen on gross and microscopically 2 wks and onward post-MI?
A completely retracted scar with no cellular infiltrate.
291
Cardiology Pathology:
What are the two cardiac enzyme marker that help diagnose an MI?
Troponin and CK-MB
292
Cardiology Pathology::
What is the prognosis 0-3 days post MI?
- cardiac arrhythmias
- sudden cardiac death
- acute post-infarction fibrinous pericarditis (friction rub)
- Cardiogenic shock
293
Cardiology Pathology::
What is the prognosis 3-14 days post MI?
- ventricular free wall rupture resulting in cardiac tamponade (LAD)
- papillary muscle rupture resulting in acute mitral regurgitation (RCA)
- interventricular septum rupture resulting in VSD
- ventricular pseudo aneurysm resulting in reduced CO, arrhythmia, and risk of embolus from mural thrombus
294
Cardiology Pathology::
What is the prognosis 2 wks to months post MI?
- true ventricular aneurysm resulting in dyskinesia, associated with fibrosis
- Dressler syndrome or AI fibrinous pericarditis
295
Cardiology Pharmacology:
What is the mnemonic to treat an Acute MI?
MONA
- Morphine
- Oxygen
- Nitrates
- ASA
296
Cardiology Pathology::
Which lead has ST elevation with a anteroseptal (LAD) infarct?
V1-V2
297
Cardiology Pathology::
Which lead has ST elevation with a anteroapical (distal LAD) infarct?
V3-V4
298
Cardiology Pathology::
Which lead has ST elevation with a anterolateral (LAD or LCX) infarct?
V5-V6
299
Cardiology Pathology::
Which lead has ST elevation with a Lateral (LCX) infarct?
I, aVL
300
Cardiology Pathology::
Which lead has ST elevation with a inferior (RCA) infarct?
II, III, aVF
301
Cardiology Pathology::
Which lead has ST elevation with a Posterior (PDA) infarct?
V7-V9, ST depression in V1-V3 with tall R waves.
302
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the alpha-1 receptor is stimulated:
- increase in IP3
- causes peripheral vasoconstriction, urethral constriction, pupillary dilation
303
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the alpha-2 receptor is stimulated:
- decrease in cAMP
- causes CNS sympathetic inhibition, decreases insulin release and intestinal motility
304
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the beta-1 receptor is stimulated:
- increase in cAMP
- increases cardiac contractility and heart rate, also increases renin release by JG cells of the kidney
305
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the beta-2 receptor is stimulated:
- increase cAMP
- causes peripheral vasodilation and bronchodilation
306
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the Muscarinic-2 receptor is stimulated:
- decrease cAMP
- causes a decrease in cardiac contractility and heart rate
307
Pharmacology: Sympathetic agents
Explain the change in the secondary messenger and the primary effect when the muscarinic-3 receptor is stimulated:
- increases IP3
- causes bronchoconstriction, increases insulin release and intestinal motility, bladder contraction, pupillary constriction, and peripheral vasodilation via nitric oxide.
308
Pathology: Atherosclorosis
What causes a plaque to reduce in stability leading to rupture?
Inflammatory macrophages in the tunica intima secrete metalloproteinases which degrade the ECM proteins.
