Path - Sem 1 Flashcards
Using H&E what colour will cell cytoplasm typically stain? why?
Pink. Eosin is negatively charged and cytoplasm is positively charged
The cytoplasm of cells with abundant rough endoplasmic reticulum typically what colour? rough endoplasmic reticulum has affinity for which dye?
purple. All the RNA from the RER will stain blue. As the cytoplasm will normally stain pink due to its positive charge, the mixture of pink and blue will give the cytoplasm a purple appearnce
Nuclei appear basophilic as haematoxylin binds to what?
phosphate groups of nucleic acids
What epithelial subtype lines the pericardial, peritoneal and pleural cavities ie. serous body cavities? What specific name is given to these cells in this situation?
simple squamous. Mesothelium
components of the acute inflammatory response? (4)
- vasodilation with hyperaemia (more blood flow).
- Endothelial activation and increase vascular permeability.
- Neutrophil infiltration
- Macrophage infiltration
components of the acute inflammatory exudate? (3)
neutrophils, fluid and fibrin
which abnormal laboratory findings would you most expect in a patient with a florid acute inflammatory disease process? (3) and why?
increase neutrophils.
increase CRP (activates complement system).
increase ESR.
when is granulation tissue required?
when the injury, infection or acute inflammatory response results in destruction of connective tissue and/or the tissue type is unable to regenerate,
characteristic histologic features of plasma cells? (4)
- amphophilic cytoplasm (takes both up H & E) The 2. Eccentric Nucleus (cytoplasmic machinery pushes the nucleus away from the centre).
- Clockface ( number of nucleoli in nucleus).
- Perinuclear hof (pale area adjacent to the nucleus - well dveloped golgi)
What does the term ‘left shift” or “shift to the left” mean in relation to the appearance of a blood film and why does it occur? (2 marks)
increase in Immature neutrophils released from the bone marrow. occurs in response to severe inflammation including severe infection.
Explain, including relevant cytokines, how this neutrophilia develops. (3 marks)
Cells, predominantly macrophages, in the acute inflammatory response release IL-1, IL-6 and TNF. These circulate systemically and cause the bone marrow to release some of its reserve pool of neutrophils such that more are available for the inflammatory response. In more severe and prolonged acute inflammatory responses it may also increase its production of neutrophils.
How does the morphology of the cells in the germinal centres differ from the surrounding cells? What is happening in a germinal centre? (3 marks)
The cells in the germinal centre are generally larger than the surrounding lymphocytes with more cytoplasm and larger paler nuclei. These cells are B cells that are actively dividing and differentiating into plasma cells.
Name the arteries in the body that are elastic in type?
major distribution vessels: the aorta, brachiocephalic, subclavian and common carotid, and most of the large pulmonary arteries.
Select the two most likely complications that could develop as a result of an aortic atherosclerotic plaque. why?
thrombosis (loss of endothelium over plaque may activate haemostasis leading to thrombus formation over the plaque,).
Embolism - Bits of plaque may flick off and embolise into bloodstream.
Explain the pathogenesis of arteriolar hyalinisation in aging or systemic hypertension. (4 marks)
Haemodynamic stress (with advancing age and aggravated by systemic hypertension), results in increased endothelial permeability to plasma proteins e.g. albumin and fibrinogen which deposit in the arteriole wall. Also stress and age lead to deposition of more extracellular matrix. Over time the build up thickens the wall and can narrow the lumen.
Hyalinisation of arterioles leads to what
Hyaline arteriolosclerosis can lead to narrowing and/or weakening of the vessel wall. Narrowing occurs gradually and can lead to chronic ischaemia with subsequent atrophy. Weakening can lead to rupture (and/or exudation of fluid).
most common cause of MI?
atherosclerosis with thrombosis
what is cardiac tamponade? consequences?
In cardiac tamponade, also known as pericardial tamponade, blood enters the pericardial sac and causes an increase in pericardial and thus intracardiac pressures. This impairs filling and cardiac output becomes inadequate
Why is rupture more likely at 2-4 days with say 3 or 6 weeks following an infarct? (2 marks)
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.
without intervention what changes would occur over time in the affected artery? (has a thrombus in it)
Over time, a thrombus will undergo organisation and recanalisation.
what are 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.
Explain the role of troponin (in general, needn’t give details of all 3 subunits) in normal contraction.
Troponin (3 subunits), tropomyosin, actin and myosin are regulatory and contractile proteins involved in contraction. Troponin and tropomyosin are linked and lie along the actin filaments. Tropomyosin inhibits the interaction between actin and myosin. Calcium released from the sarcoplasmic reticulum by depolarisation binds to one of the subunits of troponin, inducing a conformational change in tropomyosin, enabling interaction between actin and myosin and thus contraction.
A 74-year-old man with an old inferior myocardial infarction died of unrelated causes. Describe the macroscopic abnormalities expected to be seen in this man’s left ventricular myocardium. (3 marks)
The inferior left ventricular myocardium and posterior one third of the interventricular septum would be very pale, almost white and the wall thinned.
Explain, including relevant cytokines, process of neutrophilia
macrophages release IL-1, IL-6 and TNF> bone marrow to release some of its reserve pool of neutrophils.
In more severe and prolonged acute inflammatory responses it may also increase its production of neutrophils.
