Cardio: Pathology Flashcards
(51 cards)
1
Q
- Ischemia, Hypertension, Dilated cardiomyopathy, Myocardial infarction, and Restrictive cardiomyopathy
- Decreased forward perfusion
- Pulmonary congestion –> Pulmonary edema
- Dyspnea, Paroxysmal nocturnal dyspnea (increased venous return), Orthopnea, Crackles
- Bursting of congested capillaries –> intraaveolar hemorrhage w/ hemosiderin-laden macrophages (‘Heart-failure cells’)
- *Decreaesd *flow to Kidneys –> Renin-angiotensin system –> exacerbates CHF
- Tx: ACE inhibitor
A
Left-sided Heart Failure
2
Q
- Most commonly due to Left-sided heart failure but also include Left-to-right shunt and Chronic lung disease (cor pulmonale)
- Jugular venous distention
- Painful hepatosplenomegaly –> ‘Nutmeg Liver’ –> cardiac cirrhosis
- Dependent pitting edema (‘Dropsy’) due to increased hydrostatic pressure
A
Right-sided Heart Failure
3
Q
- Due to coronary artery vasospasm
- Represents reversible injury to myocytes (no necrosis)
- EKG shows ST-segment elevation due to transmural ischemia
- Relieved by Nitroglycerin or Calcium channel blockers
A
Prinzmetal Angina
4
Q
- Necrosis of cardiac myocytes (irreversible)
- Rupture of atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery
- vasospasm, cocaine use, emboli, vasculitis (kawasaki disease)
- Severe, crushing chest pain > 20 minutes that radiates to the left arm or jaw, diaphoresis, and dyspnea
- Symptoms not relieved by nitroglycerin
- LAD –> anterior and anterior septum (most common)
- RCA –> posterior wall and posterior septum and papillary muscles of LV
- Left Circumflex –> lateral wall of LV
A
Myocardial Infarction
5
Q
- Unexpected death due to cardiac disease; occurs without symptoms or < 1 hour after symptom arise
- Usually due to fatal ventricular arrhythmia
- Most common etiology is acute ischemia; 90% of patients have preexisting sever atherosclerosis
- Less common causes include Mitral valve prolapse, **Cardiomyopathy, ** and Cocaine abuse
A
Sudden Cardiac Death
6
Q
- Poor myocardial function due to chronic ischemic damage (with or without infarction)
- Progresses to congestive heart failure (CHF)
A
Chronic Ischemic Heart Disease
7
Q
- Defect in the Septum that divides the Right and Left Ventricles → Left to Right shunt
- Most common congenital heart defect and may be asymptomatic at birth
- A/w Fetal alcohol syndrome
- Size of defect determines extent of shunting and age at presentation
- Large defects –> Eisenmenger syndrome –> Right ventricular hypertrophy, LV overload, and Heart Failure
- Tx: surgical closure; small defects may close spontaneously
A
Ventricular Septal Defect (VSD)
8
Q
- Defect in interatrial septum that divides Right and Left atria; most common type is Ostium Secundum (90%)
- **Ostium primum **type is associated with Down syndrome
- Results in Left-to-Right shunt w/ Loud S1 and **Split S2 **on auscultation (increased blood in right heart delays closure of pulmonary valve)
- Paradoxical emboli are an important complication –> Right sided embolie –> arrive at brain or distal extrudate
- Usually occurs in Septum Secundum or Septum Primum w/ other anomalies
A
Atrial Septal Defect (ASD)
9
Q
- Failure of closure is associated with congenital rubella
- Results in Fetal R2L shunt, Neonatal w/ ↓ lung resistance L2R** shunt** between the Aorta and the Pulmonary artery → RVHand/orLVH, Heart Failure
- The ductus arteriosus normally shunts blood from the pulmonary artery to the Aorta, bypassing lungs
- Asymptomatic at birth w/ continuous ‘machine-like’ murmur; may lead to Eisenmenger syndrome, resulting in lower extremetiy cyanosis
- Tx: Indomethacin, which **decreases PGE, resulting in PDA closure (PGE K’EEEE’Ps open patency**)
A
Patent Ductus Arteriosus (PDA)
10
Q
- Pulmonary infundibular stenosis (most imporant) → forces Right to Left flow across VSD → cyanotic ‘tet spells’
- VSD
- Overiding Aorta of the VSD
- Right-to-Left shunt leads to early Cyanosis, degree of stenosis determines the extent of shunting and cyanosis
- Patients learn to squat in response to a cyanotic spell; increased arterial resistance decreasing shunting and allows more blood to reach the lungs
- RVH → ‘Boot-shaped’ heart on CXR
A
Tetralogy of Fallot
11
Q
- Characterized by pulmonary artery arising from the Left Ventricle and Aorta arising from the Right Ventricle
- A/w maternal diabetes
- Presents w/ **early cyanosis; **pulmonary and systemic circuits do not mix
- Creation of Shunt (allowing blood to mix) after birth is required for survival
- PGE can be administered to maintain PDA until difinitve surgical repair is performed
- Hypertrophy of RV and Atrophy of LV
A
Transposition of the Great Vessels
12
Q
- Characterized by a single large vessel arising form both ventricles
- Truncus fails to divide
- Presents with early cyanosis; deoxygenated blood from right ventricle mixes with oxygenated blood from left ventricle before pulmonary and aortic circulations separate
- Most patients have accompanying VSD
A
Truncus Arteriosus
13
Q
- Absence of Tricuspid valve or Tricuspid valve orifice fails to develop
- Hypoplastic Right ventricle
- Often associated with ASD, resulting in a Right-to-Left shunt; presents with early cyanosis
- Requires both ASD and VSD for viability
A
Tricuspid Atresia
14
Q
- Narrowing of the Aorta; classically divided into infantile and adult forms
-
Infantile form a/w PDA; coarctation lies after (distal to) the Aortic arch, but before (proximal to) the PDA
- Presents as lower extremity cyanosis in infants at birth; a/w Turner syndrome
- Tx: PGE2<strong></strong>
A
Infantile Coarctation of the Aorta
15
Q
- Pharyngitis due to **Group A β-hemolytic streptocci **affects children 2 - 3 weeks after an episode of streptococcal pharygitis ‘strep throat’
- **Molecular mimicry; **of bacterial M protein resembles proteins in human tissue –> Type II hypersensitivity
- J♥nes criteria (Joints migratory polyarthritis, ♥ pancarditis, Nodules subcutaneous, Erythema marginatum, Sydenham chorea (St. Vitus’ dance), *Increased *ESR
- Pancarditis w/ pericarditis, Endocarditis, and Myocarditis w/ Aschoff bodies (granuloma with giant cells), **Anitschkow cells **(enlarged macrophages)
- Repeat exposure results in relapse of the acute phase –> chronic disease –> antistreptolysin O titer increase
A
Acute Rheumatic Fever
16
Q
- Valve scarring that arises as a consequence
- Stenosis w/ classic ‘Fish-mouth’ appearance
- Almost always involves the Mitral valve; leads to thickening of Chordae tendineae and Cusps
- Occasionally involves the Aortic valve; leads to fusion of the commissures
- Other valves are less commonly involved
- Complications include infectious endocarditis
A
Chronic Rheumatic Heart Disease
17
Q
- Narrowing of the Aortic valve orifice
-
Fibrosis and Calcification from “wear and tear”
- Late adulthood (> 60 y.o.)
- Chronic rheumatic valve disease; coexisting mitral stenosis and fusion of the aortic valve commissures
- Systolic ejection click followed by a crescendo-decrescendo murmur
- Concentric left ventricular hypertophy
- Angina and Syncope with exercise
- Microangiopathic hemolytic anemia - RBCs damaged producing Schistocytes while crossing the calcified valve
- Tx: Valve replacement after complications onset
A
Aortic Stenosis
18
Q
- Backflow of blood from Aorta –> Left Ventricle during Diastole
- Aortic root dilation (**syphilitic aneurysm **and aortic dissection) or **Valve damage **(inf. endocarditis) –> isolated root dilation
- Blowing diastolic murmur
-
Hyperdynamic circulation due to increased pulse pressure
- Increase Systole, *decrease *Diastole
- Bounding pulse (water-hammer) Pulsating nail bed (Quincke pulse), and Head bobbing (De Musset’s sign)
- LV dilation and Eccentric hypertrophy (volume overload)
- Tx: valve replacement once LV dysfunction develops
A
Aortic Regurgitation
19
Q
- Ballooning of Mitral valve into LA during Systole
-
Myxoid degeneration (accumulation of ground substance) of the valve, floppy
- Marfan syndrome or Ehlers-Danlos syndrome
- Incidental mid-systolic ‘click’ followed by regurgitation murmur
- ‘Click’ softer with squating
- Complications include Infectious endocarditis, Arrhythmia, Severe Mitral regurgitation
- Tx: valve replacement
A
Mitral Valve Prolapse
20
Q
- Reflux of blood from LV –> LA during Systole
- Arisises as a complication of Mitral valve prolapse
- LV dilation (Left-sided cardiac failure)
- Inf. endocarditis
- Acute rheumatic heart disease
- Papillary muscle rupture after myocardial infarction
- **Holosystolic ‘blowing’ murmur – louder w/ squating **and **expiration **(increased return to LA)
- Volume overload and Left-sided heart failure
A
Mitral Regurgitation
21
Q
-
Narrowing of the Mitral valve orifice
- Usually due to Chronic rheumatic valve disease
- Opening snap followed by Diastoloic rumble
-
Volume overload –> dilation of LA which results in:
- Pulmonary congestion w/ edema and alveolar hemorhage
- Pulmonary hypertension –> Right-sided heart failure
- Atrial fibrillation w/ risk of Mural Thrombi due to stasis of valvular wall
A
Mitral Stenosis
22
Q
- The most common cause overall - low-virulence organism infecting **previously damaged valves **(e.g. chronic rheumatic heart disease and mitral valve prolapse)
-
Small vegetations that DO NOT destroy the valve
- Damaged surface develops thrombotic vegetations (platelets and fibrin) to exposed collagen
- Transient bacteremis leads to trapping of bacteria in the vegetations
A
Endocarditis:* Streptococcus viridans*
23
Q
- Most common cause in IV drug users
- **Pseudomonas **and Candida
- High-virulance organsim that infects normal valves
- Commonly seen in the Tricuspid valve
- Large vegetations that destroy the valve
- Chordae rupture, glomerulonephritis, suppurative pericarditis, emboli
A
Endocarditis: Staphylococcus aureus
24
Q
- Associated with Endocarditis of Prosthetic valves
A
Endocarditis: Staphylococcus epidermidis
25
* Associated with patients with underlying **Colorectal carcinoma**
**Endocarditis: *Streptococcus bovis***
26
HACEK organisms:
* **HACEK organisms**
* **Haemophilus**
* **Actinobacillus**
* **Cardiobacterium**
* **Eikenella**
* **Kingella**
* **A/w Negative blood cultures --\> difficult to grow**
27
* Acute, Subacute, Culture negative
* Hypercoagulable state, SLE (marantic / thrombotic)
* Mitral valve is most common
* Murmur due to **vegetations on heart valve** --\> septic embolizations
* **♥ FROM JANE ♥; F**ever**, R**oth spots** **(emb. of sep. vegt.) , **O**sler nodes (Fingers and Toes), **M**urmur, **J**aneway Lesions (eryth. Palms and Soles), **A**nemia, **N**ails: Splinter hemorrhages, **E**mboli
* * *Decreased *Hb, MCV, TIBC, Serum Iron, % Sat.
* *Increased *Ferritin
**Bacterial Endocarditis**
28
* **Sterile vegetations** that arise in a/w **SLE**
* Vegetations are present on the **surface and undersurface of the Mitral valve** --\> Mitral regurgitation
**Libman-Sacks Endocarditis**
29
* **All four chambers** of the Heart
* Systolic dysfunction (ventricles cannot pump)
* CHF: **Mitral** **and** **Tricuspic valve regurgitation**
* Arrhythmia, S3, Baloon appearance on CXR
* **A**lcohol abuse, **B**eriberi, Myocarditis (**C**oxsacki A or B), **C**hagas (*Trypanosoma cruzi*), Drug use (**C**ocaine, **D**oxorubicin,) Autosomal Dominant, (ABCCCDD)
* Lymphocytic infiltrate in the myocardium, Pregnancy, Hemochromatosis
* Tx: Na+ restriction, ACE, β-blockers, diuretics, digoxin, ICD, Heart Transplant
**Dilated Cardiomyopathy**
30
* Massive **Hypertophy** of the **Left Ventricle**
* Genetic mutation in **Sarcomere proteins** (Autosomal dominant) --\> **β-myosin heavy chain**
* Decreased cardiac output - LV hypertrophy --\> dysfunction (ventricle cannot fill)
* Ventricular arrhythmias --\> sudden death in young
* **Syncope w/ exercise** - Subaortic hypertrophy of Ventricular septum --\> functional aortic stenosis
* **Biopsy** shows myofiber hypertrophy w/ disarray
**Hypertrophic Cardiomyopathy**
31
* **Decreased compliance** of the ventricular endomyocardium --\> restricts filling during diastole
* Causes include: **Hemochromatosis**, Amyloidosis, Sarcoidosis, Endocardial fibroelastosis (children), and Loeffler syndrome (endomyocardial fibrosis w/ eosinophilic infiltrate and eosinophilia)
* Presents w/ **Congestive Heart Failure; **
* **Low-voltage EKG** w/ **Diminished QRS amplitude**
**Restrictive Cardiomyopathy**
32
* **Benign** **mesenchymal tumor** with a **gelatinous** appearance and abundant **ground** substance on histology
* Most common primary cardiac tumor in **adults**
* Usually forms a **Pedunculated mass** in the **Left Atrium** (90%) that causes **syncope** due to _obstruction_ of the **Mitral Valve**
* Described as a **"Ball valve" **obstruction w/in Left Atrium
* Multiple **syncope** episodes
**Myxoma**
33
* Benign **hamartoma** of cardiac muscle
* Most common primary **cardiac tumor in children**
* a/w **Tuberous sclerosis**
* Usually arisises in the ventricle
**Rhabdomyoma**
34
* Commonly involve the **pericardium**, resulting in a **pericardial effusion**
* Sources include:
* Breast
* Lung
* Melanoma
* Lymphoma
**Metastasis**
35
* **Sharp pain**, aggrevated **by inspiration**, relived by sitting-up and leaning forward
* Pericardial **friction rub**
* ECG: widespread **ST-segment elevation** and/or **PR depression**
* _Fibrinous_ - Dressler syndrome, Uremia, XRT
* _Serous_ - Viral, noninfectious inflammatory diseases
* _Suppurative / purulent_ - bacterial infections
* _Hemorrhagic_ - metastatic carcinoma and *tuberculosis*
**Acute Pericarditis**
36
* **Compression** of the **heart by fluid** (blood, effusions, etc.) in pericardium --\> *decreased* CO eq. of diastolic pressure
* **Beck Triad** (HypoTN, JVD, Distant heart sounds)
* *Increased *HR
* **Pulsus paradoxus** (*decrease* of 10 mmHg on inspiration)
* **Kussmaul sign** (*increase *in JVP on inspiration)
* **Low-voltage QRS** and electrical alternans (due to **"swinging of heart"** w/in the effusion)
**Cardiac tamponade**
37
* **Disruption** of the **vasa vasorum** of the **Aorta** w/ consequent atrophy of the vessel wall and **dilation of the Aorta and Valve ring**
* **Calcification** of the Aortic root and Ascending Aortic arch
* **"Tree bark"** appearance of the Aorta
* Aneurysm of the Ascending Aorta or Aortic arch
* Aortic insufficiency
**Syphilitic Heart Disease**
38
* ***Increase* in JVP --\> JVD on Inspiration** _instead_ of normal *decrease*
* Inspiration --\> negative intrathoracic pressure not transmitted to heart --\> impaired filling of RV --\> blood backs up into Venae cavae --\> JVD
* May be seen w/ Constrictive pericarditis, Restrictive Cardiomyopathy, RA or RV tumors
**Kussmaul Sign**
39
* ***Decrease* blood flow** to the skin due to **Arteriolar vasospasm** in response to cold temperature or emotional stress
* Most often in **Fingers** and **Toes**
* Primary --\> Idopathic
* Secondary --\> Mixed Connective tissue disease, SLE, CREST syndrome (systemic sclerosis)
**Raynaud Phenomenon**
40
Right to Left Shunts Pathologies
* Early cyanosis - "blue babies" Often diagnosed pernatally or become evident immediately after birth
* Usually require urgent surgical correction and/or maintenance of a PDA
* The **5 T's**
* **T**runcus Arteriossus (1 vessel)
* **T**ransposition (2 switched vessels)
* **T**ricuspid atresia (3 = Tri)
* **T**etralogy of Fallot (4 = Tetra)
* **T**APVR (5 letters in the name)
41
* Aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) → separation of Systemic and Pulmonary circulations, two non-mixing systems
* Not compatible with life unless a shunt is present to allow mixing of blood (e.g. VSD, PDA, or Patent Foramen Ovale)
* Due to **failure** of the **Aorticopulmonary septum** to **spira**l
* Without surgical intervention, most infants die wihtin the first few months of life.
D-transposition of the Great Vessels
42
* Congenital defect. Pulmonary veins not connected to LA
* **Pulmonary veins** **drain** by a abnormal connecting vein to the SVC and oxygen rich blood enters the **Right heart** circulation (SVC, coronary sinus, etc.)
* Oxygen rich blood being divirted away from the body
* **A/w ASD** and sometimes **PDA** to allow for Right to Left shunting to maintain CO as a portion of oxygen rich blood enters the LA via the RA → ASD → LA
Total Anomalous Pulmonary Venous Return
| (TAPVR)
43
* Uncorrected **Left to Right shunt** (VSD, ASD, PSD)
→ ↑ pulmonary blood flow
→ pathologic remodeling of vasculature
→ Pulmonary arteriolar HTN
* RVH occurs to compensate
→ shunt becomes **Right to Left shunt**
→ causes late cyanosis of lips, fingers, toes, clubbing, syncope, and polycythemia (too many RBCs)
* Age of onset varies
Eisenmenger syndrome
44
* Adult form is not a/w a PDA; **coarctation** lies after (distal to) the Aortic arch **distal to Ligamentum Arteriosum**
* **HTN in Upper extremities** and **HypoTN w/ weak pulses in Lower extremities** (**radiofemoral delay**); adulthood
* Collateral circulation develops actoss the intercostal arteries --\> engorded arteries --\> **'notching' of ribs**
* A/w **Bicuspid Aortic Valve**
Adult Coarctation of the Aorta
45
22q11 Syndrome
* Truncus arteriosus
* Tetralogy of Fallot
46
Down Syndrome
* ASD
* VSD
* AV Septal defect (endocardial cushion defect)
47
Congenital Rubella
* ASD
* VSD
* PDA
* Pulmonary artery stenosis
* Cataracts, Deafness, Microcephaly, Encephalitis, and a Blueberry muffin rash
48
Turner Syndrome
* Bicuspid Aortic valve
* Coartation of the Aorta (preductal)
49
Marfan Syndrome
* Mitral Vavlve Prolapse (MVP)
* Thoracic Aortic Aneurysm
* Thoracic Aortic Dissetion
* Aortic Regurgitation
50
Infant of Diabetic Mother
* Transposition of Great Vessels
51
* Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI)
Dressler Syndrome
