Herz, Gefässe

Question 1

Myocardial infarction - Pathology

Accepted Answer

0-24 hrsMicroscopic: Early coagulative necrosis (> 4 hrs) → release of content from necrotic cells → release of inflammatory cytokines → recruitment of neutrophils (granulocytes). Hypercontraction of myofibrils and wavy fibers (1-4 hrs).Macroscopic: No gross changes (0-12 hrs), dark mottling (12-24 hrs) 1-3 daysMicroscopic: Coagulative necrosis (4-72 hrs), neutrophilic infiltrate (1-3 days)Macroscopic: Hyperemia, yellow pallor 3-14 daysMicroscopic: Macrophages and granulation tissue around the margins (3-10 days), proliferation of blood vessels into the granulation tissue (10-14 days)Macroscopic: Hyperemic border, central yellow pallor (yellowest at ∼10 days), softening 2 weeks to several monthsMicroscopic: Granulation tissue becomes denser and forms a collagenous scar.Macroscopic: Grayish-white fibrosis

Question 2

Myocardial infarction

Accepted Answer

Etiology:- Plaque rupture → acts as a nidus for the formation of thrombus - EmbolismNSTEMI = inner wall infarctionSTEMI = transmural infarction - Left anterior descending (LAD): 40-50%- Right coronary artery (RCA): 30-40%- Left circumflex artery (LCX): 15-20% Complications:- Heart failure- Cardiac arrhythmia: may be seen within minutes after MI or years later- Left ventricular (LV) failure and pulmonary edema: happens after left ventricular infarction, free wall rupture, ventricular septal defect, papillary muscle rupture with mitral regurgitation- Postinfarction pericarditis, papillary muscle rupture (might lead to acute, severe mitralregurgitation), interventricular septal rupture, ventricular pseudoaneurysm formation, ventricular free wall rupture (might lead to ventricular free wall rupture leading to pericardial tamponade/ventricular pseudoaneurysm), true ventricular aneurysm, Dressler syndrome Therapy: Fibrinolytic therapy, angiotherapy, percutaneous coronary intervention Reperfusion injury: - Blood flow back into the cells brings influx of calcium → contraction and can't relax → contraction band necrosis- Oxygen is converted to ROS → damage heart cells

Question 3

Duke criteria

Accepted Answer

The Duke criteria help to diagnose infective endocarditis. To confirm the diagnosis, one of the following requirements must be met:- Two major criteria- One major and three minor criteria- Five minor criteria Major diagnostic criteria- Two separate blood cultures positive for typical pathogens - Evidence of endocardial involvement in echocardiography- A new valvular regurgitation (worsening of a pre-existing murmur is not sufficient) Minor diagnostic criteria- Predisposition: underlying heart disease or IV drug abuse- Fever ≥ 38°C (100.4F)- Vascular abnormalities- Immunologic disorder (Glomerulonephritis, Osler nodes, Roth's spots, positive rheumatoid factor)- Microbiology (Positive blood cultures for atypical pathogens)

Question 4

Infective endocarditis

Accepted Answer

Etiology:- Staphylococcus aureus (45-65%): Most common cause of acute IE for all groups- Viridans streptococci (30%): S. sanguinis, S. mutans, S. mitis: Most common cause of subacute IE, especially in predamaged native valves and in prosthetic valves, common cause following dental procedures- Staphylococcus epidermidis: Common in patients with prosthetic heart valves or pacemakers/ICDs- Enterococci (< 10%): Common cause following nosocomial urinary tract infections (UTIs), following gastrointestinal or genitourinary procedures- Streptococcus gallolyticus: associated with colorectal cancer- Gram-negative HACEK group - Candida species, Aspergillus fumigatus: immunosuppressed patients, IV drug abusers Clinical features:- Signs of progressive heart failure (e.g., dyspnea, edema)- Signs of acute cardiac decompensation (pulmonary edema)- Arrhythmias- Nail-bed splinter hemorrhages - Janeway lesions: non-tender, erythematous lesions due to microemboli - Osler nodes: painful immune-complex depositions on pads of the fingers and toes- Roth spots: retinal hemorrhages with pale centers- Signs of acute renal injury, including hematuria and anuria Diagnosis: Duke criteria Therapy:- Initial empiric antibiotic treatment with vancomycin IV → adapt according to resistogram→ Native valve: 4-week treatment with penicillin G→ Prosthetic valves: 6 week treatment→ IV drug use: 2-week treatment with nafcillin

Question 5

Nonbacterial thrombotic endocarditis

Accepted Answer

Rare, non-infectious form of endocarditis due to sterile platelet thrombus formation on the heart valves (usually aortic and mitral valves). Etiology:- Underlying malignancy- Hypercoagulable states- Rheumatologic conditions (SLE, rheumatoid arthritis, etc.) Compared to infectious endocarditis, vegetations are easily dislodged and embolization is common. Clinical manifestations indicate systemic emboli:- Kidney: flank pain, hematuria- Skin: rash, digital ischemia- Cardiac/central nervous system (CNS): chest pain, stroke Definitive diagnosis can only be made pathologically: - Vegetations on either surface of the valve - Composed of immune complexes, mononuclear cells, and thrombi interwoven with fibrin strands. Libman-Sacks endocarditis: describes especially large vegetations, also referred to as verrucous vegetations. Treatment: Anticoagulants

Question 6

Infektiöse Endokarditis ulcero-polyposa

Accepted Answer

1. Bakterienrasen: Teils herdförmige, teils lang gestreckte Ansammlungen von dunkelblau gefärbten Bakterien. 2. Zerstörte Klappengeröst: Kernarm (nekrotisch), fibrös und von Leukozyten infiltriert. 3. Fibrinfilm: Auf der Oberfläche erkennt man homogene, eosinrote Fibrinauflagerungen.

Question 7

Abakterielle Endocarditis verrucosa

Accepted Answer

1. Verruköse, aus Fibrin und Thrombozyten bestehende Auflagerungen. 2. Vernarbtes Klappengerüst. 3. Evtl. Zeichen einer Klappenvorschädigung.

Question 8

Giant cell arteritis

Accepted Answer

Type of vasculitis, which causes chronic inflammation of large and medium-sized arteries.- Peak incidence: 70-79 years- 40-50% of patients with giant cell arteritis also have PMR Clinical features:- Constitutional symptoms: Fever, weight loss, night sweats- New onset pulse-synchronous, throbbing, dull headache, typically located over the temples- Hardened and tender temporal artery- Tenderness of the temples or the scalp- Jaw claudication: jaw pain when chewing- Amaurosis fugax or permanent loss of vision - Diplopia Diagnostics: ACR criteria (3 of the 5 criteria are required)1. Age at disease onset ≥ 50 years2. Headaches3. Abnormalities of the temporal artery4. Elevated ESR (≥ 50 mm/h)5. Histopathological abnormalities in the temporal artery Pathology:- Panarteritis of the large and medium-sized arteries- Proliferation of the intima (and subsequent stenosis of the artery)- Fragmentation of the internal elastic lamina- Predominantly mononuclear infiltration of the vessel wall with formation of giant cells

Question 9

Myxoma

Accepted Answer

- Most common type of primary tumor of the heart- Most common location: left atrium (∼75% of all cases)- Sex: F > M (3:1)- Peak incidence: 40–60 years Etiology:- Most cases are sporadic- Familial inheritance: ∼10% of all cases Clinical features:- General: Weight loss, fever, pallor, clubbing of the fingers- Dyspnea on exertion, paroxysmal nocturnal dyspnea, and/or orthopnea- Dizziness or syncope- Palpitations- Auscultatory findings: Mid-diastolic rumbling murmur over apex (similar to mitral stenosis)- “Tumor plop”: a sound related to movement of the tumor- Symptoms due to embolization (eg, transient ischemic attack, stroke, visceral infarction) Diagnostics: Echocardiography Pathology:- Microscopic appearance: Scattered mesenchymal cells within mucoid, gelatinous material. - Produce VEGF- Macroscopic appearance: often pedunculated, gelatinous consistency Treatment: Resection

Question 10

Cardiac tumors

Accepted Answer

Primary tumors (rare):- Myxoma→ From mesenchymal connective tissue→ Pedunculated→ Gelatinous in consistency (abundance of ground substance)→ Bloodflow blocked → syncope- Rhabdomyoma→ Most common in children→ Usually affects ventricles→ Considered hamartomas (abnormal formation of normal tissue)→ Seen in tuberous sclerosis→ Often regress spontaneously- Fibroma- Hemangiomas- Lipoma Secondary (metastatic) tumors: ∼ 30x more common than primary cardiac tumors!- Most common primary cancers: Lung cancer > lymphoma > breast cancer > melanoma

Question 11

Vascular tumor

Accepted Answer

1. Kaposi sarcoma- Malignant tumor linked to HHV-8.- Cancer of the blood vessel endothelial cells.- Seen in patients with suppressed immune systems (HIV, organ transplant patients)- Skin lesions that don't blanch in mucosa, nose, throat, lymph nodes, lungs, gastrointestinal tract- Treatment: Cryotherapy, adjust immunosuppressants, radiation + chemotherapy, interferon-α 2. Hemangioma- Benign tumor of the endothelial cells.- Found in skin but can happen anywhere.→ Pyogenic granuloma (pregnancy tumor): Most often on face and hands, often bleeds→ Capillary hemangioma (strawberry hemangioma): Most common type, raised and lumpy, usually subside by age 10→ Cavernous hemangioma: Deeper 3. Angiosarcoma- Malignant cancer that involved the endothelium of the blood vessels- Most common in dogs- Aggressive, can affect liver- Risk factors: Vinyl chloride, arsenic insecticides

Question 12

Angiosarcoma

Accepted Answer

A malignant cancer of the endothelial wall lining blood vessels (hemangiosarcoma) or lymphatic vessels (lymphangiosarcoma).- Metastasizes quickly, especially to the lungs. Can occur anywhere in the body.- Skin: Often on head or neck, raised purplish skin area, may bleed, may be painful- Bone: Multifocal and affects multiple bones- Soft tissue, breast tissue, liver, lungs Etiology:- Chronic lymphedema (eg, surgically removed, destroyed by trauma)- Liver angiosarcoma: Vinyl chloride, arsenic Symptoms:- Soft tissue: Pain and swelling, can compress peripheral nerves- Breast: Rapid-growing palpable masses- Liver: Fatigue, abdominal pain- Metastasis to lung: Chest pain, difficulty breathing Diagnosis:- Biopsy- MRI/CT Treatment: Surgery, chemotherapy, radiotherapy

Question 13

Arteriosclerosis

Accepted Answer

Hardening of arteries, with arterial wall thickening and loss of elasticity. Arteriolosclerosis- Affects small arteries and arterioles. Two types:1. Hyaline: thickening of vessel walls in essential hypertension or diabetes mellitus.2. Hyperplastic: “onion skinning” in severe hypertension with proliferation of smooth muscle cells. Mönckeberg sclerosis (medial calcific sclerosis)- Affects medium-sized arteries. - Calcification of internal elastic lamina and media of arteries → vascular stiffening without obstruction. - “Pipestem” appearance on x-ray.- Does not obstruct blood flow; intima not involved. Atherosclerosis- Build-up of atheromatous plaques in medium to large arteries.

Question 14

Peripheral vascular disease

Accepted Answer

Insufficient tissue perfusion due to atherosclerosis in the aorta and peripheral arteries- Often coexists with coronary artery disease (CAD), stroke, atrial fibrillation, and renal disease. Classification: FontaineStage I: Asymptomatic PADStage II: Pain on exertion - IIa: claudication at a walking distance > 200 m- IIb: claudication walking distance < 200 mStage III: Ischemic pain at restStage IV: Necrosis/gangrene/ulcers- IVa: dry necrosis, trophic disorders- IVb: infection of necrotic tissue, humid gangrene Clinical presentation:- Silent disease: Up to 20-50% of patients with PAD are asymptomatic!- Intermittent claudication (10-35% of patients)→ Femoropopliteal disease (most common) → calf claudication→ Aortoiliac disease (Leriche's syndrome): Level of the aortic bifurcation or bilateral occlusion of the iliac arteries: Triad of bilateral buttock, hip, or thigh claudication; erectile dysfunction; and absent/diminished femoral pulses→ Tibiofibular disease→ foot claudication- Absent or diminished pulses- Trophic changes: ↓ Skin temperature, ↓ hair, dry atrophic and shiny skin Diagnosis:- Ankle-brachial index:>1.3 = medial sclerosis with incompressible vascular wall (generally calcified vessels)1.0-1.30 = normal value0.91-0.99 = borderline0.40-0.90 = mild to moderate PAD → claudification<0.40 = severe PAD → resting pain, gangrene (critical limb ischemia)- Digital subtraction angiography (DSA): gold standard Treatment:- Smoking cessation!- Supervised graded exercise therapy- For all patients: long-term antiplatelet therapy with aspirin, clopidogrel, or ticagrelor- Lipid-lowering agent (usually statins)- Antihypertensive treatment- Hyperglycemia control- PDE inhibitors (i.e., cilostazol)

Question 15

Myocarditis

Accepted Answer

- Average age: ∼40 years- ∼10% of sudden deaths in young adults Etiology:- Viral: Coxsackie B, parvovirus B19, HHV-6, adenovirus, HIV, influenza A - Bacterial: Streptococcus group A (acute rheumatic fever), Corynebacterium diphtheriae, Borrelia burgdorferi- Protozoan: Chagas disease, caused by Trypanosoma cruzi- Parasitic: Trichinella, echinococcus- Connective tissue diseases (eg, systemic lupus erythematosus)- Vasculitis syndromes (eg, Kawasaki disease)- Toxic: Radiation therapy, medication (eg, sulfonamides), chemotherapy (e.g., anthracycline), cocaine- Giant-cell myocarditis: Unknown Clinical presentation:- Preceding (1-2 weeks) flulike symptoms indicates possible viral cause - Fatigue, weakness, dyspnea, nausea, vomiting - Positional chest pain: indicates pericardial involvement (perimyocarditis)- Arrhythmias- Acute decompensated congestive heart failure with dilated cardiomyopathy- Cardiogenic shock Diagnositics:- ECG/24-hour Holter monitoring: Tachycardia, arrhythmias, heart block- ↑ Cardiac enzymes (CK, CK-MB, troponin T), ↑ ESR (and CRP), leukocytosis, ↑ BNP- Chest x-ray and CT: cardiac enlargement, pulmonary congestion, pleural effusions- Echo: Inflammed muscle wall- Biopsy: Possible detection of viral DNA/RNA; Immunohistochemical detection of inflammation (with lymphocytic infiltrates in a viral etiology)

Question 16

Vorhofmyxom

Accepted Answer

1. Stark aufgelockertes teils fibröses, teils myxoides Stroma 2. Nester von spindelförmigen Tumorzellen 3. Fokale Stromablutungen 4. Eingestreute Entzündungszellen

Question 17

Arteriosklerose

Accepted Answer

- Verdickte Intima - Intima: Angelehnt an die Media amorphe Massen mit Cholesterinkristall-Lücken, z.T. aufgebrochen, blutdurchsetzt (= Atherom) - Schaumzellen, vor allem subendothelial - Atherome überdeckt durch eine wechselnd dicke, teils eingerissene Kollagenfaserschicht - Media: Parallellaufende Elastikalamellen

Question 18

Koronararterie - Hard plaque

Accepted Answer

- Atherom aus hyalinisierten Kollagenfasern (diese Polster können nicht aufbrechen; hard Plaque). - Atheromherde sind der Media angelagert und werden von einer dicken Kollagenfaserschicht lichtungswärts abgedeckt; auch hier ist die Gefahr des Polsteraufbruchs gering - Media geringgradig atroph

Question 19

Frischer Myokardinfarkt

Accepted Answer

- Im inneren Teil blasse Herde mit basophilem Saum - Blasse Herde: Kernarm, z.T. auffallend schlanke und gewellte Muskelfasern - Basophiler Saum: Demarkation der helleren (Nekrose-)Herde durch dichtliegende, teils zerfallende Granulozyten - Hypereosinophiles Myokard (Koagulationsnekrose) - Herzmuskelzellen mit Kontraktionsbandnekrosen - Die unmittelbar subendokardial gelegenen Herzmuskelzellen sind vital (erhaltene Zellkerne), zeigen aber ein blasig vakuolisiertes und aufgehelltes Sarkoplasma (= tubuläre Degeneration) als Zeichen eines chronischen Sauerstoffmangels (sogenannte Holundermarkzellen).

Question 20

Subakuter Herzinfarkt

Accepted Answer

- Koagulationsnekrose (Hypereosinophilie, fehlende oder abgeblasste Zellkerne) ohne granulozytäres Entzündungsinfiltrat. - Die Koagulationsnekrose wird auf allen Seiten gesäumt von einem breiten Granulationsgewebssaum mit Gefässen, Entzündungszellen (v.a. Makrophagen mit gelbbraunem Siderinpigment und Lipofuszinpigment, wenig Lymphozyten und Plasmazellen) und Fibroblasten.

Question 21

Pyämische Myokarditis

Accepted Answer

- Blaue Flecken in der Übersicht. Diese entsprechen Ansammlungen von neutrophilen Granulozyten (Mikroabszesse). - Mehrere Arterien mit intra- und perivaskulären Kokkenbakterien und neutrophilen Granulozyten erkennbar.

Question 22

Aortic dissection

Accepted Answer

Tear in the inner layer of the aorta which leads to a progressively growing hematoma between in the intima-media space.- Peak incidence: 60-80 years; in Marfan syndrome at the age of 30-50 Localization: - Ascending aorta: ∼65% of cases - Descending aorta, distal to the left subclavian artery: 20% of cases- Aortic arch: 10% of cases- Abdominal aorta: 5% of cases Etiology:- Hypertension (most common)- Trauma- Vasculitis with aortic involvement (eg, syphilis)- Use of amphetamines and cocaine- Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome)- Bicuspid aortic valve- Coarctation of the aorta Stanford classification:- Type A (proximal): ascending aorta dissection, including retrograde extension from the descending aorta - Type B (distal): descending aorta dissection, originating distal to the left subclavian artery Clinical presentation:- Sudden and severe tearing/ripping pain- Location: Anterior chest (ascending) or back (descending)- Interscapular or retrosternal pain- Neck and jaw- Abdomen or periumbilical, colicky pain- ↑ BP (if the patient is hypotensive, consider shock from blood loss or a cardiac tamponade)- Asymmetrical blood pressure and pulse readings between limbs- Syncope, diaphoresis, confusion or agitation Diagnostics:- Initial imaging: Chest x-ray (AP view) showing a widened mediastinum (> 8 mm)Definitive diagnostic tests:- In stable patients → Contrast-enhanced CT angiography (gold standard)- In unstable patients, renal insufficiency, contrast allergy → Transesophageal echocardiography (TEE) Treatment:- Sedation and analgesia (eg, morphine) - Adequate resuscitation- Control hypertension: Target value of the systolic blood pressure is ∼90-120 mm Hg→ IV labetalol, esmolol, or propanolol (best initial)→ Followed by IV sodium nitroprusside (vasodilator) Complication:- Aortic rupture and acute blood loss- Pericardial tamponade- Aortic regurgitation

Question 23

Aortendissektion

Accepted Answer

1. Pathologische Tunica media: amorphe extrazelluläre Matrix, verminderte elastische Faser 2. Geteilte Tunica media mit falschem Lumen: Thrombus mit Erythrozyten, Fibrin, Leukozyten- Kein Endothel → akuter Thrombus 3. Hämorrhagische Adventitia

Question 24

Pericarditis

Accepted Answer

Acute pericarditis is inflammation of the pericardium that either occurs as an isolated process or with concurrent myocarditis.Constrictive pericarditis is characterized by compromised cardiac function caused by a thickened, rigid, and fibrous pericardium secondary to acute pericarditis. Cause:- Infectious: Viral (most common), bacterial (eg, tuberculosis), fungal, toxoplasmosis- Myocardial infarction: pericarditis may occur either within 1-3 days as an immediate reaction (i.e., post-infarction fibrinous pericarditis), or weeks to months following an acute myocardial infarction (Dressler syndrome).- Postoperative (post-pericardiotomy syndrome): blunt or sharp trauma to the pericardium- Collagen vascular disease: systemic lupus erythematosus, rheumatoid arthritis- Other causes: renal failure (uremia), tumors (Hodgkin lymphoma), radiation Clinical presentation:- Low-grade intermittent fever, tachypnea, dyspnea, nonproductive cough- Chest pain: often sharp, pleuritic; improves on sitting and leaning forward- Pericardial friction rub: high-pitched scratching sound best heard on auscultation over the left sternal border during expiration while the patient is sitting up and leaning forward- Pericardial effusionConstrictive pericarditis:- Jugular vein distention, ↑ jugular venous pressure, Kussmaul sign- Hepatic vein congestion → hepatomegaly, painful liver capsule distention, hepatojugular reflux- Peripheral edema or anasarca, ascites with abdominal discomfort- Fatigue, dyspnea on exertion, tachycardia- Pulsus paradoxus: ↓ blood pressure amplitude during deep inspiration Diagnosis:- ECG changes:Stage 1: initial diffuse ST elevations; PR segment depressionStage 2: ST segment normalizes in ∼1 week.Stage 3: inverted T wavesStage 4: ECG returns to normal baseline- Pericardial effusion → Low-voltage, electrical alternals Treatment:- Acute pericarditis: often self-limiting and resolves within approx. 2-6 weeks. NSAIDs, colchicine, glucocorticoids.- Constrictive pericarditis: Symptomatic therapy (manage fluid overload with diuretic therapy), pericardiectomy

Question 25

Rheumatic fever

Accepted Answer

Inflammatory sequela involving the heart, joints, skin, and CNS that occurs 2-4 weeks after an untreated infection with group A streptococcus.- Peak incidence: 5-15 years Jones criteria: two major OR one major plus two minor criteria are required for diagnosis.Major: J = Joints (migratory), ♥ = Pancarditis, N = Nodules, E = Erythema marginatum, S = Sydenham choreaMinor criteria: Arthralgia, fever, ↑ acute phase reactants (ESR, CRP), prolonged PR interval- ↑ Antistreptolysin O titer (ASO) When only a subset of symptoms present, classified as: Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) Pathology:Aschoff bodies: - Granuloma of rheumatic inflammation- Central area of fibrinoid necrosis- Surrounded by characteristic multinucleated giant cells (Aschoff's cells) and other inflammatory cells (mononuclear cells, plasma cells, and T lymphocytes)Anitschkow cells:- Cardiac histiocytes (mononuclear cells) appearing in Aschoff bodies- Large and elongated cells- Longitudinal section: ovoid nucleus containing wavy, caterpillar-like bar of chromatin (“caterpillar cell”) Treatment: oral penicillin V

Question 26

Koronararterie - Soft plaque

Accepted Answer

- Atherom mit lanzettförmigen Aussparungen (Cholesterinkristalle) und Schaumzellen, z.T. von Blut durchsetzt - In der Restlichtung ein geschichteter Thrombus, z.T. durchsetzt von Cholesterinnadeln und Schaumzellen (aufgebrochene Plaque) - Atrophe Media - Adventitia verbreitert

Question 27

Riesenzellarteriitis

Accepted Answer

- Granulomatöse Entzündung der Arterienwand mit Zerstörung von Muskulatur und elastischen Lamellen - Lumen gefüllt mit einem organisierten Thrombus - Lamina elastica interna und Mediamuskulatur zerstört, nur noch wenige Muskelfaser erhalten - Zellreiches, granulomatöses Gewebe aus Fibroblasten, Histiozyten, mehrkernigen Riesenzellen, Lymphozyten, Plasmazellen

Pathologie (Fach) / Herz, Gefässe (Lektion)