Tutorials Flashcards
Most prominent cells?
Thin arrow?
Thick arrows?
Acute Inflammation
Neutrophils
Large macrophage
Red blood cell
Yellow star?
Large pink spots?
Acute inflammation
Oedema fluid
eosinipholic due to plasma proteins
Congested capillaries in alveolar walls
Black star?
Acute inflammation
eosiniphilic strands
mixed with fibrin and neutrophils
Chronic inflammation
Yellow: necrosis
Green: granuloma
What are the layers of a blood vessel from inside to outside?
- Tunica intima
- Internal elastic lamina (if present)
- Tunica media
- External elastic lamina (if present)
- Tunica adventitia
Which vessels contain smooth muscle?
elastic arteries
muscular arteries
arterioles
capillaries
post-capillary venules
collecint & muscular venules
small veins (<2mm)
large veins (>2mm)
SVC & IVC
small lymphatic vessels
large lymphatic vessels
elastic arteries
muscular arteries
arterioles
capillaries - no
post-capillary venules - no
collecint & muscular venules
small veins (<2mm)
large veins (>2mm)
SVC & IVC
small lymphatic vessels - no
large lymphatic vessels
How can a small arteriole be distinguished from a muscular venule?
Muscular venules have a larger lumen relative to their wall thickness.
Both have only one or two layers of SM.
What are fenestrated capillaires?
Greater permiability than that of continuous-endothelium type capillaries, permitting rapid passage of macrmolecules smaller than plasma proteins from the lumina into surrounding tissues
Where are fenestrated capillaries found?
Kidney (glomeruli), endothelium of the sinusoids of the bone marrow, spleen, and liver
Pericytes
supportive cells with a smooth muscle-like phenotype that are normally located in and around the basement membrane of arterioles and venules
What type of junctions hold together endothelial cells of blood vessels?
Fascia occludens - discontinuous tight junctions
zonula occludens
continuous tight junctions that form a rim around the circumference of cells
in brain blood vessels
Which cell types contain actin and myosin filaments?
a (skeletal muscle) and d (smooth muscle)
b - nerve
c - connective tissue of adventitia
e - blood
Which cell type is not typically found in atherosclerotic plaque?
Neutrophils
Atherosclerosis is a chronic inflammatory disease process, neutrophils are a feature of acute inflammation.
Plaques can contain macrophages, smooth muscle (migrating from media into intima), lymphocytes, small blood vessels (endothelial cells, RBCs), and RBCs from fissures or haemorrhage
What is the most important mechanism via which cardiac myocytes obtain additional oxygen at times of increased mycardial oxygen demand?
Autoregulation of vascular resistance leading to vasodilation
The micrograph is of infarcted myocardium. Which one of the following
processes is likely to have occurred in these cells contributing to the
development of this abnormality?
Increase in cytosolic calcium due to failure of ATP-dependent calcium pumps in ischaemia.
This is coagulative necrosis (cell structure is retained, nuclei lost)
When are caspases activated?
Apoptosis
A 65 year-old woman experiences transient episodes of central chest tightness and shortness of breath that settle on resting when undergoing an exercise stress test in the cardiac outpatients department. ECG during the episodes of pain shows ST depression in lateral leads. The most likely finding in the coronary artery supplying the area of myocardium ‘visualised’ by these leads is
Atherosclerotic narrowing of the lumen by >70%
The features are in keeping with stable angina, generally occurring when the diameter of the lumen of the artery is reduced by greater than 70% by atherosclerosis.
A 65-year-old woman presents to the Emergency Department with a several hour history of constant, severe central chest pain and shortness of breath. ECG shows ST elevation, loss of amplitude of the R wave and a small Q wave in the inferior leads. The most likely finding in the coronary artery supplying the area of myocardium ‘visualised’ by these leads is
Atherosclerosis with thrombosis
Pt has had an inferior MI; right coronary artery is likely narrowed by atherosclerosis and occluded with thrombus. (acute plaque event)
Which region of the heart is most susceptible to ischaemia and why?
Subendocardial muscle. Due to high intramyocardial pressure in this region)
Which coronary artery has been occluded to cause this infarct?
Left anterior descending. Supplies the anterior LV, the apex, and the anterior 2/3 of the IV septum.
This infarct is several days to a week or so old.
What is the fate of infarcted myocardial cells?
Myocytes cannot proliferate to replace them, therefore healing following coagulative necrosis involves removal and replacement with scar tissue.
Endocardium
Myocardium
Endocardium
Myocardium
Epicardium
Contractile cells.
Endothelial cells.
Blood cells.
What is indicated by D, and what is its function?
Desmosomes, provide anchorage for intermediate filaments of the cytoskeleton.
What is indicated by FA, and what is its function?
Fascia adherens, transmits contractile forces. Part of the intercalated disc, along with the desmosomes and gap/nexus junctions.
What is indicated by G, and what is its function?
Glycogen granules, substrate for energy production.
What is indicated by N, and what is its function?
Nexus junction (or gap junction), transmits electrical impulses. Mainly in longitudinal portions of the interdigitations of the intercalated disc.
What is indicated by SR, and what is its function?
Sarcoplasmic reticulum, stores and releases Ca2+ ions.
What is indicated by H? I?
H - myosin
I - actin
What abnormality is this, what is the likely cause, and how does it cause death?
Haemopericardium (blood in the pericardial sac) due to ventricular wall rupture following MI (5-10 days).
Causes death by cardiac tamponade.
Yellow star?
Green star?
Yellow star? Normal myocardium
Green star? Infarcted myocardium
The nuclei of healthy cardiac myocytes appear
- oval in shape
- fine chromatin
- inconspicuous or small nucleoli
Nuclei of infarcted cardiac myocytes demonstrate
Smudged blurred chromatin
Why is rupture more likely during 5-10 days post-MI?
Rupture is more likely at this time as the necrotic muscle is weak and being phagocytosed. As time goes on more collagen (or fibrous tissue) is laid down which strengthens the wall.
What is visible 1-4hrs post-MI?
Few changes, variable waviness of fibres at border of infarct
What is visible 4-12hrs post-MI?
Dark mottling (occasionally); early coagulative necrosis, oedema, hemmorrhage
What is visible 12-24hrs post-MI?
Dark mottling; Ongoing coagulation necrosis, pyknosis of nuclei, myocyte hypereosinophilia, marginal contraction band necrosis, early neutrophilic infiltrate
What is visible 1-3 days post-MI?
Mottling with yellow-tan infarct centre; coagulative necrosis, loss of nuclei and striations, brisk interstitial infiltrate of neutrophils
What is visible 3-7 days post-MI?
Hyperemic (increased blood flow) border, central yellow-tan softening; beginning of desintigration of dead myofibers with dying neutrophils (apoptosis, pynknosis), early phagocytosis of dead cells by macrophages at infarct border
What is visible 7-10 days post-MI?
Maximally yellow-tan and soft, with depressed red-tan margins; well-developed phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margins
What is visible 10-14 days post-MI?
Red-gray depressed infarct borders; well-established granulation tissue with new blood vessels and collagen deposition
What is visible 2-8 weeks post-MI?
Gray-white scar, progressive from border toward core of infarct; increased collagen deposition, with decreased cellularity
What is visible 2 months+ post-MI?
Scarring complete; dense collagenous scar
How old is this infarct?
- 24 hours
- patchy loss or blurring of cross-striations
- hypereosinophilic
- some capillary engorgement, interstitial oedema
- mild neutrophil infiltrate - early inflammatory response
How old is this infarct?
- 2-3 days
- intensely hypereosinophilic
- most nuclei lost
- marked neutrophils in oedemitous interstitium
- over next several days, necrotic myocardium undergoes autolysis and fragmentation
How old is this infarct?
- 10 days
- most necrotic muscle phagocytosed by neutrophils and macrophages
- infarcted area occupied by residual macrophages, some lymphocytes, and plasma cells in a loose oedematous mesh
- few capillaries and fibroblasts - earliest signs of granulation tissue formation
How old is this infarct?
- 14 days
- infarct almost wholly replaced by fibrovascular granulation tissue
- necrotic myocardium almost completely removed by phagocytosis by neutrophils and macrophages
- over succeeding weeks, GT becomes more fibrous and less vascular
- leads to formation of highly collagenous, relatively acellular scar by the end of the 2nd month post-MI
Green Star?
Yellow star?
What is the abnormality of the lumen?
Green star - intima
Yellow star - media
thrombus in lumen
Calcification (dystrophic)
Lymphocytes
Foam cells
Cholesterol clefts
Collagen
If a pt survives an atherosclerotic plaque event, what changes occur over time in the affected artery?
- Thrombus will undergo organisation and recanalisation
- Organisation is the process of the formation of scar tissue via the formation of granulation tissue, which in this case will replace the thrombus
- Recanalisation refers to the formation of new vessels in the granulation and later scar tissue through the occluded lumen
- Passage of blood will be limited, however, and in the case of occluded arteries, the tissues supplied will already be dead
What comprises granulation tissue?
macrophages, fibroblasts, capillaries
some scattered lymphocytes, some ECM
vessels in vascular GT
How does fibrinous exudate present on the epicardium?
disorganized layers and clumps of eosinophilic protein
network or mesh-like structure
occasional macrophages
Fibrinous exudate of the pericardium casues
Serousal inflammation, causing pericarditic pain (sharp, well localised, relieved by leaning forwards). Rub can sometimes be heard on ascultation of the left sternal edge.
What are some post-MI causes of death between 1-2 weeks?
- LVF and cardiogenic shock
- ventricular fibrillation
- LV rupture
- thromboembolism to the brain from thrombus in LV
Why do anterior myocardial infarcts tend to have a worse prognosis than inferior or lateral infarcts?
LAD supplies a larger volume of left ventricular muscle, tf greater risk of heart failure
What are the macroscopic abnormalities expected with inferior MI?
LV myocardium and posterior 1/3rd of the IV septum would be very pale, white, and the wall thinned
Which coronary is likely occluded in an inferior MI? What could be occluded in other individuals?
Right coronary gives off PDA; circumflex (~8%) that gives rise to PDA
Ruptured papillary muscle presents
Acutely developing shortness of breath and tachycardia due to mitral valve incompetence causing acute cardiac failure +/- pulmonary oedema.
Ruptured papillary muscle leads to
Dilation of the chamber e.g. LV. Mitral incompetence puts a volume load on the LV due to regurgitation in to LA. Initial overload increases contractility; over time chronic overloading leads to eccentric hypertrophy and eventual failure of the chamber.
