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Unit 12 > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

What are some differential diagnoses for DVT?
What tests might you complete to rule them out?

A

Nephrotic syndrome - urine dip stick - protein in urine, hyperliduria
Ruptured Bakers cysts -
Compartment syndrome - history most common after tibial fracture.
Achilles tendon tear - Thompson test positive
Calf muscle haematoma - history, normal follows injury to limb.
Fracture - history, x-ray

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2
Q

What are some common differential diagnosis for a pulmonary embolism?

A

Chest infection/pneumonia
Exacerbation of COPD
Asthma
Pneumothorax
Congestive cardiac failure
Acute coronary syndrome
Costochondritis
Musculoskeletal pain or rib fracture

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3
Q

What is the difference between ischamie and information?

A

Ischaemia - deficient supply of blood to a body part
Infarction - injury od death of tissue resulting from poor blood supply.

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4
Q

Define thrombosis

A

Formation of presence of a bloot clot within a blood vessel

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5
Q

Define embolism

A

Sudden obstruction of a blood vessel by an abnormal circulating particle

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6
Q

Define shock

A

A state or profound depression of the vital processes associated with reduced blood volume and pressure.

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7
Q

Define congestion

A

An excessive accumulation especially of blood or mucus

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8
Q

Define odema

A

An abnormal infiltration and excess accumulation of serous fluid in connective tissue or in a serous cavity

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9
Q

Define haemorrhage

A

A sudden and heavy loss of blood from blood vessels.

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10
Q

What is the differential diagnosis of chest pain?

A

Acute coronary syndrome - MI and angina
Pericarditis
Myocarditis
GERD
Costochondritis
Pneumonia.

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11
Q

How commonly does atherosclerosis lead to stable angina?

A

70 to 75% narrowing of the lumen

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12
Q

Describe the process of atherosclerosis formation

A
  1. Endothelial injury due to hyperlipidemia, HTN, smoking, viruses etc.
  2. Endothelial dysfunction - resulting in increased permeability - leads to leukocyte and monocyte adhesion and migration, platelet adhesion to the surface
  3. Smooth muscle cell migration and proliferation - lipids mainly oxidised LDL accumulate in the vessel wall, Smooth muscle tries to migrate from the media to the intima, macrophages are activated
  4. Macrophages and smooth muscle cells engulf lipids - forming foam cells and fatty streaks develop.
  5. The plaque matures - smooth muscle proliferates, collagen and other ECM components are deposited, and extracellular lipids accumulate in the intima. Results in the formation of an outer fibrous cap and a soft inner necrotic lipid core.
  6. Atheromatous plaque formation - necrotic cell will also contain necrotic cell debris, calcium and may be neovascularised in the shoulder area.
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13
Q

What are the macroscopic features of atherosclerosis?

A

Yellow-like deposits which may have a white superficial layer indicate fibrous plaque - indicate lipid deposition in the arterial intima.

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14
Q

What is the microscopic appearance of atherosclerosis?

A

Intimal thickening
Atheromatous plaque thickening - occluding the lumen.
Lines of Zahn - alternatig pale pink bands of platetelts with fibrin (white) and rbs (red)

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14
Q

What investigatoins should be done when a patient presents with a 2hr history of chest pain, previous angina diagnosis?

A

Full blood count - to check if anemia may be exacerbating stable angina symptoms
Cardiac Markers:
Myoglobulin - earliest to detects but non-specific
Creatine protein kinase - MB
Troponin T/I - very specific and sensitive.
Echocardiogram
ECG - look for signs of ventricular hypertrophy, arrhythmia, pulmonary embolism, stable angina, acute coronary syndrome.

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15
Q

What is the usefulness of each cardiac marker in MI?

A

Troponin I is the golden standard - peaks around 22 hours after onset of chest pain
Myoglobin - peaks around 4 hours after pain onset, if the first marker to be seen but depletes rapidly and in first 10hrs and is not very specific.
CK-MB - peaks around 8 hours from pain onset, is more sensitive and specific.

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16
Q

What are the differential diagnosis of ST elevation on an ECG?

A

ELEVATIONS
Electrolyte (hyperkalemia)
Left bundle branch block
Early repolarisation
Ventricular hypertrophy
Aneurysmal left ventricular
Thrombotic occlusion (MI)
Inflammation (pericarditis)
Osborn (hypothermia)
Neurogenic
Sudden death (Brugada)

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17
Q

What is the most common pathology and anatomical location of it in an MI?

A

Coronary thrombosis in the left anterior descending artery.

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18
Q

What vessels are most commonly affected by an coronary occlusion in an MI?

A

4-50% is the LAD
30-40% is the right coronary artery - particularly the RPD
15-20% is the left circumflex coronary artery.

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19
Q

What is the macroscopic appearance of a coronary thrombosis?

A

Reddish or dark mass adeherent to the arterial wall, may occlude all of part of the vessel lumen
Surrounding tissue may show signs of ischaemia such as pallor or mottling.

20
Q

What is the microscopic appearance of a coronary thrombosis?

A

Line of Zahn - alternating red and white lines - white is platelets and fibrin, red is RBCs.
Thrombus - red-coloured occlusion
Thrombus normally overlies the atherosclerotic plaque
Fibrintimal proliferation with cholesterol clefts

21
Q

What is the microscopic apperance of an MI over time?

A

One day infarct - coagulative necrosis and wavy fibres
3-4 days old - odema and scattered neutrophils, surrounding nuclear fibres
7-10 days - removal of necrotic myocytes by phagocytosis
Granulation tissue and abundant capillaries
6 weeks - healed by myocardial infarct necrotic tissue replaced by dense collagen.

22
Q

What stain is used to identify collagen in a scar tissue after an MI on histological images?

A

Massons trichrome

23
Q

What are the different types of infarct in an MI?

A

Full thickness of transmural - involve the entire thickness of the ventricular wall, results from total occlusion of coronary vessel - STEMI

Subendocardial or laminar - infarction of the inner subendocardial healf of the myocardium - partial occlusion of coronary vessel - NSTEMI

24
Q

What are the different types of shock?

A

Cardiogenic - heart unable to deliver enough blood to ensure adequate tissue perfusion
Hypovolemic - insufficient circulating volume to reach oxygen demands.
Obstructive - obstruction of outflow tracts of the heart, reduced cardiac outflow
Septic - type of disruptive shock - insufficient intravascular volume due to venous or arterial vasodilation
Anaphylactic - type of disruptive shock - abnormal regional blood flow mediated by histamine in an allergic reaction.

25
Q

Describe the pathophysiology of cardiogenic shock.

A

Cardiac output falls
Reduced BP may cause poor myocardial perfusion and increase myocardial damage.
Right atrial pressure rises (due to compensatory mechanisms and increased preload)
Barorectpros and other responses activated by fall in BP and cardiac damage
Sympathetic ANS activation - vasoconstriction, increased venous return and stimulation of the heart
Reduced renal blood flow, reduced urine output and fluid retention.
Compensatory mechanism can initially help increase CO but in longer term such as in HF cases can become maladative by increasing workload of heart causing structural and functional changes. **

26
Q

What is the main functional effect by which MI causes cardiogenic shock?

A

Decreases contractility.

27
Q

What are the differential diagnosis of a patient coughing up sputum?

A

Pneumonia
Malignancy
Bronchiectasis
COPD
Asthma
Pulmonary edema
Pulmonary embolism

28
Q

What are the different types of sputum and their associated pathology?

A

Purulent - thick, yellow/green in colour - tends to be infectious such as pneumonia or an abscess
Mucoid - tends to be clear, grey or white - COPD and asthma
Serous - clear, frothy and may be pink - pulmonary oedema
Blood - malignancy, PE, clotting disorders or infection

29
Q

Describe the pathology of pulmonary odema in heart failure.

A

Occurs due to increased pulmonary hydrostatic pressure or increased capillary permeability
Norm - pulmonary hydrostatic pressure is lower than oncotic pressure
In LS HF their is an increase in pressure in the pulmonary veins which is transmitted to pulmonary capillaries.
This increased pulmonary hydrostatic pressure above oncotic pressure causing excess fluid to move out of pulmonary capillaries into interstitium of lungs.
The endothelium of capillaries develops fenestratsion allowing plasma proteins to travel into the interstitium.
Some fluid in the interstitum can be drained away into the lymphatics system in the bronchioles and vasculature.
However when lymphatic capacity is exceeded fluid accumulates in the interstitium, alveoli.
This reduces the efficiency of gas exchange.

30
Q

What is the macroscopic appearance of pulmonary odema?

A

Frothy and blood tinged fluid in lungs

31
Q

What are the microscopic changes in pulmonary edema?

A

Alveoli fill with a smooth to loosely aggregated with pink material
Capillaries within alveolar walls are congested, filled with many rbcs
May be associated with areas on inflammation - immune cell infiltrate
Is blood leaks into alveolar spaces get hemosiderin-laden macrophages contain brown cytoplasmic grnules from breakdown of RBCs.

32
Q

What is meant by heart failure cells?

A

Hemosidern-laden macrophages
Found in alveoli of lungs when pulmonary odema occurs as a consequence of left sided heart failure
Appear brown due to large hemosiderin granule content from breakdown of RBCs.

33
Q

What are some differential diagnosis of leg swelling?

A

Congestive cardiac failure
Renal failure
Cirrhosis
Drug side effect - mainly Ca2+ channel blockers

34
Q

What clinical signs can confirm right sided heart failure?

A

Peripheral oedema
Raised JVP
Hepatomegaly (nutmeg liver)

35
Q

What is shown in the images?

A

Nutmeg liver - mottled appearance to liver due to hepatic venous congestion
May show area of coagulative necrosis and hemorrhage in centriolobular regions- not in this image
Seen in right sides heart failure.

36
Q

What is the basic reasoning behind symptoms (and what are these symptoms) in right heart failure?

A

Reasons - congestion of peripheral tissues
Results in edema and ascities
Liver congestion - impaired liver function (jaundice)
GI tract congestion - weight loss, GI distress, appetite loss.

37
Q

What is the basic reasoning behind symptoms (and what are these symptoms) in left heart failure?

A

Reasoning - decreased cardiac output and pulmonary congestion causing pulmonary odema and impaired gas exchange
Symptoms - activity intolerance, cyanosis and signs of hypoxia, fought with a frothy sputum, otrhopnea, paroxysmal nocturnal dyspnea.

38
Q

What is the cyclical pathophysiological underpinning heart failure?

A
39
Q

What colour are infarcts in the lungs why?

A

Red - due to dual blood supply.

40
Q

What are the microscopic features of a pulmonary embolism?

A

Lines of Zahn - from thrmbus formed ar site of rapid arterial blood flow - laminatationof platelets and fibrin and rbcs
May have an hemorrhagic infarct marked by many red blood cells within surrounding alveolar spaces.

41
Q

What is shown in the image?

A

Cerebral haemorrhage - darkend area indicates accumulation of blood and tissue death.
Located in the parietal lobe

42
Q

What is shown in the brain in this image?

A

Liquifactive necrosis with beginning formation of cystic spaces (fluid filled cavities)
Ragged edges
Normally occurs 10 days to 2 weeks after the initial ischemic event.

43
Q

How common are complications after an MI?

A

80-90% of patients develop one or more major complications, do not make a full recovery, some complications can be fatal.

44
Q

What is the most common complication from an MI?

A

Arrhythmias

45
Q

What complications can arise from an MI?

A
  1. Death
  2. Arrhythmia (VT and VF cause most deaths)
  3. Rupture (5% of cases - can be fatal)
  4. Congestive heart failure
  5. Cardiogenic shock
  6. Pericarditis - fibrinious pericarditis associated with pericardial effusion triggered by DAMPs released by myocardium/pericardium
  7. Postmyocardial infarction syndrome
46
Q

What is postmyocardial infarction syndrome (Dressler syndrome)?

A

A form of secondary pericarditis with or without pericardial effusion resulting from injury to the heart or pericardium.
Fever, pleural pain
Usually occurs 1 to 6 weeks after MI.
If pericardium exposed to blood, antibodies form against pericardial antigens particularly from damaged tissue.
ECG - saddle shaped ST elevations.

47
Q

What layer of the blood vessel does atherosclerosis occur in?

A

The tunica intima.

48
Q

Describe the progressive changes in these images, over the aftermath of an MI.

A

a. one day after - loose irregularly shaped fibres (coagulative necrosis) and odema, may be some immune cells between dead fibres.
b. 3 to 4 days old necrosis and dense immune cell infiltrate
c. 7 to 10 days old immune cells phagocytosis of necrotic material
d. blood vessel formation and some new collagen deposition as scar forms, this is granulation tissue formation
e, six weeks - dense scar formation, lots of collagen and ECM deposition, this is a healed MI, residual cardiac muscle shown evidence of hypertrophy.

Unit 12 (23 decks)

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