3. Pathology of the heart

Question 1

constrictive pericarditis

Answer 1

-type of producte/prolif changes in pericarditis

• thickening and fibrosis of pericardium–>armoured apperance
  -cause dystolif function bc thickineng–>resutl expansion

-

Question 2

productive/prolif chnages in pericarditis

Answer 2

-fibriinous exsudate is prganized

What we get:

• fibrotic adhesions: focal or diffuse
  -non specific granulation tissue–>svcar=DIASTOLIC failure
  -Cor PETROSum->armoured heart

Question 3

what is not acute fomr of pericarditis

Answer 3

Pericardial plaques are localized thickening and calcification of the pericardium. They can be a result of healing from previous episodes of inflammation, such as in chronic pericarditis, tuberculosis, or after cardiac surgery

Question 4

most common cause of hemorragic peridcarditis (Exsudate cnages) is

Answer 4

Tumor infiltration of the pericardium

-basically TUMORS OF PERICADIUM, ikke infective greier

Question 5

characteristic for petrosa pericarditis

Answer 5

dystrophic calcification

-ofc leder også til armoured heart men tror at detn er mer riktig for constrictive

Question 6

tyep of esdative chnage of pericardtits

Answer 6

ususally seroufibrinos
-hemorrhagic
-purulent bactria–>purulent
-TB: specific infla
-dry: dry fibrinous infla

tamponade of heart if volume large

Question 7

what counts for ischemic coronary heart syndorme

Answer 7

Causes of ischemic heart diseases:
➢ 1) Principal (vascular, coronary) factors:
▪ ATS damage of coronary arteries
▪ Thrombosis or embolism of coronary arteries
▪ Non-ATS damage of coronary arteries (e.g. arteritis)
▪ Functional changes – spasm of coronary arteries

➢ 2) Additive factors:
▪ a) Myocardial – hypertrophy, reduced contractility of left ventricle, tachycardia,
aortic valve disorders, hypertension
▪ b) Extracardial – increased demands and decreased supply of oxygen,
hypotension, increased blood viscosity

Question 8

Ischmina/coronary heart diseasees include

Answer 8

1. asymptomatic stadium-mostly
   2: angina pectoris:stable, unstable, varinat
2. myocardiacl infarctiom
3. chroncik ischemic heart fisorder
4. sudden cardiac death

Question 9

chronicmanifestation of IHD

Answer 9

stabel angina pectoris
Chronic IHD

Question 10

acute manifestation of IHD/acute coronary syndorme

Answer 10

unstable angina pectoris
acute myocardial infarction
sudden death

Question 11

stable ATS plaque

Answer 11

a. Predictable -excersize
b. Triggers of stable AP
i. Physical, emotional exertion, hot & cold temp., heavy metals, smoking
c. Associated with stable ATS plaque
d. Short repeating episodes of chest pain (when resting or after intake of medicine it goes away)
e. ST-segment depression

fibromucsualr, low cont of lipids

Question 12

unstable ATS

Answer 12

a. Most severe form
i. called “pre-infarction state” -> very similar to MI
b. Chest pain lasts longer, comes more easily and occurs more often than stable AP
c. Associated with unstable ATS plaque
d. ST-segment depression

!Those that cause embolization of atheroma masses into the periphery!

LOOK: lipdi and necrotic core with fibromucuslar cap

Question 13

Variant (PIRZMETAL) AP

Answer 13

a. Due to endothelial dysfunction -> spasms
i. Spasms are not associated with physical exertion
b. Variant response to exertion (variant = sometimes we see ECG changes, sometimes we don’t)
c. ST-segment elevation

Question 14

typical site of involment of MI

Answer 14

Most commonly affected vessel = anterior interventricular a.
o Most commonly affected ventricle = left ventricle (because it’s larger + requires more blood supply)
o Most commonly affected atrium = right atrium (because it gets deoxygenated blood – LA gets oxygenated
blood which can help the LA to get oxygenated)

Question 15

type of MI

Answer 15

Transmural MI
▪ Also known as Q AMI
* “Q” – due to a very deep Q wave on ECG
* Deep Q wave = necrosis which after some time has changed into fibrous tissue
▪ Quite large – affects more than 50% of the valve of the heart
SEROUFIBRINOUS

o Subendocardial MI/laminar
▪ Also known as non-Q AMI
▪ Usually affects LESS THAN 50% of the valve of the heart
▪ Divided into STEMI and nonSTEMI
* STEMI = ST-Elevation Myocardial Infarction
* nonSTEMI = non-ST Elevation Myocardial Infarction

Question 16

morphology of MI

Answer 16

After 12 hours:
o Coagulative necrosis
▪ histomorphologically visible coagulative necrosis needs minimally 12 hours if patient survives
(doesn’t occur in dead people)
o Dead cardiomyocytes with
▪ Increased eosinophilia after death (hypereosinophilia) -> dark pink colour
▪ Disappeared nuclei (karyolysis + karyorrhexis)
▪ Loss of striation in their cytoplasm
▪ Thickening due to movement of remaining heart muscle

After 24 hours:non-specific grnaukation
Vital reaction: typical reaction for surviving tissue to necrosis
▪ Non-specific granulation tissue: mixture of endothelial cells, fibroblasts and some admixed
macrophages and inflammatory elements
▪ Fibrotic scar: hypovascular, hypocellular connective fibrotic tissue

1-7 days
o Macroscopically, necrotic tissue looks like yellow-brown soft tissue

basically
4-12h: necrosis
12-24 h:coagulation necroiss
3-7d: begining disintegration of dead myofibers, +dying neutro:early phagocysosi of dead cells by macropahes at infarct border
7-12 days: granulation tiise formation btw 3-10 d, vasculae prolif on 10-14d

Question 17

Left coronary artery (LCA):branches

Answer 17

Has 2 main branches:
* Left anterior descending (LAD) or anterior interventricular (AIB) artery
o Anterior part of left ventricle + anterior 2/3 of interventricular septum
* Circumflex artery
o Lateral wall of left ventricle

▪ Supplies:
* Left atrium
* Left ventricle + papillary mm. of the left ventricle
* Anterior 2/3 of interventricular septum
* Anterior wall of the right ventricle + anterior papillary muscle of the right ventricle
* Posterior papillary mm. in left ventricle

Question 18

Right coronary artery (RCA)

Answer 18

Has 1 main branch:
* Posterior descending artery
▪ Supplies:
* Right atrium
* Right ventricle + papillary muscles in right ventricle
* Posterior 1/3 of interventricular septum
* Posterior wall of left ventricle + posterior papillary muscle of left ventricle
* Anterior papillary muscle in right ventricle

Question 19

MI-consqeuence and complicaiton

Answer 19

Sudden cardiac death
* Arrythmias
o Very common
* Cardiac insufficiency
* Alveolar lung oedema
* Rupture of myocardium
o Rupture of free wall of LV – seen in 90% of cases (-> heart tamponade)
o Rupture of interventricular septum -> blood flows from the left side to the right side (due to pressure
differences)

• Rupture of papillary muscle, scar of papillary muscle -> valve insufficiency
• Myocardial aneurysm – acute/chronic
  o Affected tissue has changed to fibrous tissue -> more likely to form aneurysm
• Mural intracardial thrombosis -> arterial embolization
  o May embolize to systemic circulation (spleen, kidneys, intestines, brain,…)
  o May embolize to pulmonary circulation
• May embolize to coronary arteries again (vicious cycle)
• Pericarditis epistenocardiaca
  o Called “epistenocardiaca” after MI
  o Fibrinous pericarditis (aseptic form)
  o Usually forms on the 2nd day after MI
  o Usually resolves spontaneously
• Dressler’s syndrome

Question 20

infective endocarditis

Answer 20

-staphyococcus auresu
-INFECTIVE
-may lead to acute destruction of valve
-onsequence is either valvular stenosis or valvular insufficiency
-

complications
1.perforation of valve–>insufficency
2.large vegetations->stenosis
3. ulceration of valave->insud
4. enbolization of coronary aa->abseding mycoarditis
5.septic emboli->infarction+abscess
6. sepsis

cause:
-IV drug use
-prthetic valves
-congenital heart disease

Question 21

rheumatic heart disease

Answer 21

-streptococcus
-NOT INFECTIVE-more postinfective

Question 22

Libman sacks endocarditis

Answer 22

realetd to SLE
-NOT INFECTIVE
-STERILE VEGETATIONS

Question 23

non bacterial thrombotic endocarditis (NBTE

Answer 23

NON INFECTIVE

Question 24

acute/malignant/ulcerosa endocarditis

Answer 24

-affect healthy valves
-streptococci and staphylo
-BØ-HEMO
-NECROISS

-Development of thrombotic
vegetations composed of coagulated blood, necrotic tissue and colonies of
bacteria -> necrotisation -> development of ulcerative defect on the valve

• Rapidly progressing disease with fever and complication

Question 25

subacute endocarditis/maligant endocarditis lenta/polyposa

Answer 25

-not normal valves-fibrotic, calcification, ATS) -less virulent like a-hemo strep o Not normal valves (usually damaged by other changes (esp. fibrotisation, calcification, atherosclerotic o Development of thrombotic vegetation containing colonies of bacteria but no necrosis -> no ulcerative defect!!! of the valve o Thrombotic vegetations have time to grow -> proliferation of granulation tissue into thrombotic vegetation - > thrombotic vegetations can become very large EMBOLIZATION AND SEPSIS, no necrosis, large vegetation make stenosis

Question 26

criteria Rheutmatic fever

Answer 26

major: (Pan)carditis (Migrating) polyarthritis (inflammation of joints) Syndernham’s chorea minor (involvement of CNS) Development of subcutaneous painless rheumatic nodules Appearance of marginated erythema anulare on the skin minor: -fever -arthraglia -^sedimentation/CRP -rpolonged RQ interval -RH fever og carditis

Question 27

rheumatic fever micro:

Answer 27

Fibrinoid necrosis and fibrinoid dystrophy surrounded by large polygonal transformed histiocytes (called Aschoff’s cells) + caterpillar cells (Anitschkow cells) + inflammatory elements (lymphocytes, plasma cells, sporadic eosinophils) -small aseptic thrombotic vegetations are developing small aseptic thromotic vegetations (so-called verrucous endocarditis).

Question 28

concentric

Answer 28

pressuee so thicker wall but smaller dia

Question 29

eccentric

Answer 29

-volum thicker wall+larger dia

Question 30

cor hypertonicum/left ventricle hyperthorgu

Answer 30

-Isolated concentric hypertrophy of LV Causes: o Arterial hypertension (causes pressure overload) o Aortic stenosis o Both genetic and hemodynamic factors contribute to it (cardiiomyppathy) Microscopical features of cor hypertonicum o Beefy myocardiocytes o Foci of fibrosis basicallt: atrial hyeprtorphy aortal valve stenosis or dialtion MITRAL incompetens IHD aortal coarctation arteiovenous shunt hyperthyreoidism pheochormocytoma

Question 31

cor pulmonale (RV hypettorgy

Answer 31

* Isolated concentric hypertrophy of RV * Causes: o Disorders of lung Cor pulmonale acutum ▪ Occurs typically following massive pulmonary embolism -> sudden dilation of pulmonary trunk, conus, RV ▪ Ovoid dilation Cor pulmonale chronicum ▪ More common ▪ Thickness from 3-5 mm to 10 mm ▪ Concentric hypertrophy = compensated stage ▪ Excentric hypertrophy = decompensated stage ▪ Causes: * Pulmonary HYPERTENSION o Primary pulm. Hypertension = primary disease of pulmonary circulation o Secondary pulm. Hypertension = consequence of lung diseases (e.g., COPD); more frequent * Chronic emphysema * Bronchitis * TBC * Pneumoconiosis * Cystic fibrosis basically: -right valve disease and pulmonayr hypertensia -primary lung disease--obstructive -gibbus -kyphosccoliosis -MITRAL VALVE STENOSIS -succesive embolsiation to lunger small vv

Question 32

cor bovinum/cow heart

Answer 32

Hypertrophy + dilation of the heart (both ventricles and atria) Weight >500 g / >800 Mnemonic to Remember Causes: "High Volume COW" C – Chronic regurgitation   ↳ Aortic valve leaks → blood flows back into LV → volume overload → LV hypertrophy O – Overload (volume or pressure)   ↳ Think: Hypertension and IHD (Ischemic Heart Disease) → pressure overload → hypertrophy W – Weird infections (e.g., Tertiary Syphilis)   ↳ Affects aortic root → dilation → regurgitation → volume overload Pathophysiology Summary Volume overload = regurgitation, syphilitic aortitis Pressure overload = hypertension, IHD → LV hypertrophy and dilation → Eventually involves both ventricles and atria → Decompensated valvular disease = Cor Bovinum

Question 33

hypertrophic CMP

Answer 33

Primary (Intrinsic) Cardiomyopathy ✅ 100% genetic – caused by mutations in sarcomere proteins ✅ Affects especially the left ventricle (LV) and interventricular (IV) septum ✅ Leads to asymmetrical, concentric hypertrophy Manifestation of HCM A. IV Septum hypertrophy   → Can block the LV outflow tract (like sub-aortic stenosis) B. Disorganized cardiomyocytes   → “Myocyte disarray” (a classic microscopic feature) C. Fibrosis   → Both interstitial (between cells) and replacement (scar tissue) D. LV outflow tract plaque   → Further narrows the blood flow exit path E. Thickened small vessels in the septum   → May reduce perfusion Mnemonic: "HCM = H-FADS" H – Heart Failure F – Fibrosis & Flow obstruction A – Atrial Fibrillation D – Disarray of myocytes S – Sudden death

Question 34

primary cmp

Answer 34

hypertorphic restrictive arrythmogenic right ventricular cmp/dysplasia

Question 35

extrinsic /secondary cmp

Answer 35

-congenital heart disea -nutritional -ischemitc -hypertensive valvular inflammaotry alcholic diabetic

Question 36

dilated cmp

Answer 36

-most common- -Excentric hypertrophy with dilation (Heart is enlarged (remodelled)) -unspecific - Genetic cause = in 30-40% cases ▪ Mutations in sarcomere ▪ Mutations in cytoskeleton ▪ Mutations in nuclear envelope ▪ Mutations in mitochondria o Non-genetic causes -Inflammation (myocarditis) ▪ Peri partum ▪ Toxic (e.g., alcohol) ▪ Idiopathic Manifestation of DCM o Hypertrophy o Dilation o Fibrosis may develop in the myocardium (interstitial disseminated myofibrosis) o Intracardial mural thrombi may develop in enlarged chambers ▪ E.g., in apex of LV or in auricle of LA. * Clinical consequences of CMP o Heart failure o Sudden death o Atrial fibrillation o Stroke

Question 37

arryhtmogneic right ventricula cardiomyopathy

Answer 37

-form electrical disturbance of heart in which heart is replaced by fibrotis scar tissue RV

Question 38

restictrive CM

Answer 38

-wall of ventricles are stiff-may not be thickened and resist normla filling of heart -oblietraive CM is a type seen in hypereosinophlic syndorme

Question 39

risk factor ATS

Answer 39

age, gender, amoking, hypertension, hyperlipidemia, iactivity ad obesity, DM, fmaily historu

Question 40

stages of ATS

Answer 40

1. fatty streak and dots -flat ish -yellow=precursor lesions 2. gelatinous leasions -intima -first months -roung/oval -grye elevation 3. atheromatous plaques -fibrous cap -central core -cellular area under cap 4. complicated palques -calcificaiton -ulceration -thrombosis -haaemorrhage -aneurysm fomraiton

Question 41

vv typically affected by ats

Answer 41

Aorta * Renal and mesenteric aa. * Carotid aa. * Coronary aa. * Cerebral aa. * Arteries of lower limb

Question 42

sudan red

Answer 42

lipids se diff btw extracell and ontra cell accc of lipifd

Question 43

van gieson

Answer 43

colagen=red muscle=yellow

Question 44

lawson stain

Answer 44

elsatic =balcj

Question 45

von kossa impregnations

Answer 45

ats dystophic impregnantion=black or dark

Question 46

complications of ATS

Answer 46

Stenosis (an abnormal narrowing in a blood vessel or other tubular organ or structure) a. Stensosis -> ischaemia -> Wet gangrene (necrosis) 2. Dystrophic calcification 3. Intimal (recent) and wall (inveterate) ulceration 4. Thrombosis a. Atherosclerosis + thrombosis of coronary artery -> myocardial infarction 5. Haemorrhage into arteriosclerotic wall 6. Aneurysm

Question 47

Aneurysm and most common cause

Answer 47

Aneurysm = permanent abnormal dilation of a blood vessel due to a congenital or acquired weakening or destruction of the medial layer of the vessel wall. AORTA AND ITS MAJOR BRANCHE SMOSLTY: brachipcephalic->right common carotid and right subclavia, left common carotid, left sublacina Most common causes for aneurysms: 1. Atherosclerosis 2. Hypertension 3. Deep wounds 4. Infections

Question 48

what can aneurysm cause

Answer 48

Thrombosis and thromboembolism * Alteration in the flow of blood * Rupture of the vessel * Compression of neighbouring structures

Question 49

most common aneuryms based on ATS

Answer 49

Most common in Abdominal aorta —> infrarenal rr, bifurcation, aortic rr

Question 50

treu vs false anurysm

Answer 50

true: composed of ll layers of vv false: not all, trauma

Question 51

arterosclerotic aneuryms

Answer 51

-msot common -mostly in ABD arota: infrarenal and above bifurcation of aorta complication -rupture -compression arterial occlusion: inf mesenteric aa, collateral circulation developed

Question 52

syphilitis anurysm

Answer 52

-tertiary syphilis -THOTACIC AORTA-ASCENDING AORTA AND ARCH comlicaiton -rupture, compression, erosins, cardiac dysfunctuino

Question 53

Dissecting anurysm

Answer 53

-blood enter the speerated wall of vv and spred longituidnallt -bc weakenede aortic media(hypertnsion, MARFAN syndorme, truama, pregancnt) classificaiton - I. begins in ascending aorta and extend distally (75% of cases) - II. only in ascending aorta (5%) - III. begins in descending thoracic aorta and extends distally (20%) Stanford classification (based on clinical management) - type A (proximal dissection) – involves proximal aorta (I. + II. DeBakey) - type B (distal) – distal aorta and sparing the ascendent (III. DeBakey)

Question 54

mycotic aneuryms-berry

Answer 54

-small -asymptomatic -ruptur - circle of wills

Question 55

complication and consequens of aneurysm

Answer 55

Organ damage (e.g., kidney failure, or life-threatening intestinal damage) 2. Stroke 3. Aortic valve damage (aortic regurgitation) or rupture into the lining around the heart (cardiac tamponade) 4. Death (due to severe internal bleeding)

Question 56

systemic symptoms of vasuclits

Answer 56

Fever o Loss of appetite o Weight loss o Fatigue (feeling tired) and weakness o General aches and pains

Question 57

Immune-complex mediated vasculitis

Answer 57

– necrotic vessel wall is replaced by smudgy, pink “fibrinoid” material LEUKOCYSTOCLASTIC VACULITS - Polyarteritis nodosa o Henoch-Schönlein purpura o Microscopic polyangiitis o Hypersensitivity vasculitis o Henoch-Schönlein purpura

Question 58

Vasculitis due to cellular hypersensitivity (granulomatous vasculitis)

Answer 58

LARGE VV VASCULITIS - Giant cell arteritis o Takayasu’s arteritis SMALL VV VASUCLITUS o Churg-Strauss disease (ALSO EOSINOPHILIC= o Wegener granulomatosis (ALSO GRANULOMAOTUS)

Question 59

Small vessel vasculitis

Answer 59

o Microscopic polyangiitis o Leukocytoclastic vasculitis o Wegener granulomatosis o Churg-Strauss disease

Question 60

* Giant cell arteritis

Answer 60

Temporal arteritis o Takayasu’s arteritis

Question 61

consequence of vasculitis

Answer 61

Narrowing -> more difficult for blood to get through * Occlusion -> completely closed off * Aneurysm and even aneurysm rupture o In rare cases * Endothelial damage and thrombosis

Question 62

behcet dises-vasculitis

Answer 62

Can occur in vessels of any size or type -> can affect any part of the body o Commonly affects eye, mouth, and genitals * Epidemiology: o Patients are often younger (20s/30s)

Question 63

buerger disease-vasculitis

Answer 63

Typically affects blood flow to the hands and feet * Also known as thromboangiitis obliterans * More likely to occur in smokers than non-smokers

Question 64

churh strauss syndrome-vasculitis

Answer 64

Churg-Strauss syndrome * Affects many different organs, mostly lungs, skin, kidneys, and heart * Many people also have asthma (may be pre-existing, newly diagnosed, or recently worsened asthma)

Question 65

giant cell arthirits

Answer 65

Most common form of vasculitis in adults >50 yo. * More likely to occur in people of Scandinavian origin * Common symptoms: o Headache o Fever o Blurred vision o Pain in the jaw, shoulders, or hips TEMPORAL ARTERIES It is a segmental disease, and may lead to ipsilateral headaches and jaw claudication's

Question 66

Henoch-Schönlein purpura

Answer 66

Most common form of vasculitis in children o Often follows an upper respiratory infection in children * Not usually a chronic disease, and full recovery is common * Most commonly affects skin, kidneys, joints, and stomach

Question 67

6. Microscopic polyangiitis

Answer 67

Most commonly affects kidneys, skin, and nerves

Question 68

polyarteritis nodosa

Answer 68

Most common in people in their 30s and 40s * Most commonly affects the kidneys, skin, and nerves, but can affect any organ in the body * Men are 2x as likely as women to get polyarteritis nodosa * In some cases, it is associated with chronic hepatitis B infection or a very specific type of leukaemia (hairy cell leukaemia)

Question 69

rheumatoid vasculits

Answer 69

-patient with severe arthirtis -diff organs

Question 70

takaysasu arteritis

Answer 70

Typically occurs in Asian women <40 yo. * Affects the aorta and its branches !!!!!

Question 71

Wegener’s granulomatosis

Answer 71

Most common in middle-aged and older * Can occur anywhere in the body Most commonly affects upper respiratory tract (nose, sinuses, and throat), lungs, and kidneys

Question 72

vascular tumors bening and malignant

Answer 72

bening:haemangionma borderline malignant:hemanigiosarcoma

Question 73

DVT is initiated by triad changes:

Answer 73

Endothelial damage 2. Alteration in composition of blood 3. Venous stasis

Question 74

CLINICAL MANIFESTATIONS OF PHLEBOTHROMBOSIS/THROMBOPHLEBITIS

Answer 74

CLINICAL MANIFESTATIONS OF PHLEBOTHROMBOSIS/THROMBOPHLEBITIS May be local or systemic * Local effects of phlebothrombosis/thrombophlebitis o Oedema distal to occlusion o Heat o Swelling o Tenderness o Redness o Pain * Systemic effects of phlebothrombosis/thrombophlebitis o Pulmonary thromboembolism o Bacteraemia o Septic embolization to brain, liver,...

Question 75

phleothrombisis

Answer 75

Phlebothrombosis = occurs when a blood clot (thrombosis) in a vein (phlebo) forms without inflammation of the vein (phlebitis)

Question 76

thrombophelbitis

Answer 76

Thrombophlebitis = Thrombophlebitis is phlebitis (vein inflammation) related to a thrombus (blood clot).

Question 77

thrmbophlebitis migrans

Answer 77

-infla+mutliple venous thormbi from one site-->another -paraneoplastic syndrome or nonbacterial thrombocytic endocarditis

Question 78

thrmbosis vv gepaticea-BUDD CHIARI SYNDORME

Answer 78

Malignant tumour ingrowth into hepatic veins

Question 79

phlegmasia alba dolens

Answer 79

-Extensive swelling of the leg due toILIOFEMORAL venous thrombosis -Can be associated with late pregnancy or after extensive pelvic surgery -c. Complication = phlegmasia cerulea dolens -d. Treatment must start right away before it proceeds to phlegmasia cerulea dolens

Question 80

Phlegmasia cerulea dolens

Answer 80

Complication of massive iliofemoral thrombosis and decreased arterial blood flow -> ischaemia and gangrene Markedly swollen bluish skin with superficial gangrene d. Treatment = usually necessary to perform high amputation of lower extremity due to bacteraemia and sepsis which may lead to death

Question 81

SVC syndorme

Answer 81

Obstruction of the superior vena cava as a result of external compression or thrombosis b. Usually due to malignancies (esp. lung cancer and lymphoma) c. Symptoms: i. Dilated veins of neck and thorax ii. Oedema of face, neck and upper chest iii. Visual disturbances iv. Disturbed senses

Question 82

IVC syndrome

Answer 82

Obstruction of inferior vena cava b. Often a result from thrombosis by extension from iliofemoral veins i. Also caused by external compression and neoplastic invasion c. Symptoms i. Oedema of lower extremities ii. Dilated leg veins and collateral venous channels in the lower abdomen