Path - Sem 1 Flashcards

1
Q

Using H&E what colour will cell cytoplasm typically stain? why?

A

Pink. Eosin is negatively charged and cytoplasm is positively charged

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2
Q

The cytoplasm of cells with abundant rough endoplasmic reticulum typically what colour? rough endoplasmic reticulum has affinity for which dye?

A

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

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3
Q

Nuclei appear basophilic as haematoxylin binds to what?

A

phosphate groups of nucleic acids

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4
Q

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?

A

simple squamous. Mesothelium

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5
Q

components of the acute inflammatory response? (4)

A
  1. vasodilation with hyperaemia (more blood flow).
  2. Endothelial activation and increase vascular permeability.
  3. Neutrophil infiltration
  4. Macrophage infiltration
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6
Q

components of the acute inflammatory exudate? (3)

A

neutrophils, fluid and fibrin

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7
Q

which abnormal laboratory findings would you most expect in a patient with a florid acute inflammatory disease process? (3) and why?

A

increase neutrophils.
increase CRP (activates complement system).
increase ESR.

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8
Q

when is granulation tissue required?

A

when the injury, infection or acute inflammatory response results in destruction of connective tissue and/or the tissue type is unable to regenerate,

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9
Q

characteristic histologic features of plasma cells? (4)

A
  1. amphophilic cytoplasm (takes both up H & E) The 2. Eccentric Nucleus (cytoplasmic machinery pushes the nucleus away from the centre).
  2. Clockface ( number of nucleoli in nucleus).
  3. Perinuclear hof (pale area adjacent to the nucleus - well dveloped golgi)
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10
Q

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)

A

increase in Immature neutrophils released from the bone marrow. occurs in response to severe inflammation including severe infection.

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11
Q

Explain, including relevant cytokines, how this neutrophilia develops. (3 marks)

A

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.

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12
Q

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)

A

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.

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13
Q

Name the arteries in the body that are elastic in type?

A

major distribution vessels: the aorta, brachiocephalic, subclavian and common carotid, and most of the large pulmonary arteries.

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14
Q

Select the two most likely complications that could develop as a result of an aortic atherosclerotic plaque. why?

A

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.

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15
Q

Explain the pathogenesis of arteriolar hyalinisation in aging or systemic hypertension. (4 marks)

A

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.

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16
Q

Hyalinisation of arterioles leads to what

A

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).

17
Q

most common cause of MI?

A

atherosclerosis with thrombosis

18
Q

what is cardiac tamponade? consequences?

A

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

19
Q

Why is rupture more likely at 2-4 days with say 3 or 6 weeks following an infarct? (2 marks)

A

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.

20
Q

without intervention what changes would occur over time in the affected artery? (has a thrombus in it)

A

Over time, a thrombus will undergo organisation and recanalisation.

21
Q

what are organisation and recanalisation?

A

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.

22
Q

Explain the role of troponin (in general, needn’t give details of all 3 subunits) in normal contraction.

A

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.

23
Q

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)

A

The inferior left ventricular myocardium and posterior one third of the interventricular septum would be very pale, almost white and the wall thinned.

24
Q

Explain, including relevant cytokines, process of neutrophilia

A

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.

25
Q

Explain how the pattern of infection develops for each of lobar and bronchopneumonia?

A

In bronchopneumonia the bacteria infect bronchi and bronchioles in a patchy distribution and spread down to the related alveoli where they also induce inflammation. Alveolar involvement is thus patchy. In lobar pneumonia they directly infect the alveoli and spread from alveolus to alveolus by the pores of Kohn.

26
Q

In Bacterial pneumonia, especially bronchopneumonia (excluding TB) how may death occur? (2) What are other potential issues (3)?

A

death from hypoxaemia or septicaemia.

other complications include empyema, abscess formation, dissemination of bacteria to other organs.

27
Q

dif b/w empyema and abcess?

A

empyema is a collection of pus in a naturally existing anatomical cavity.
Abscess is a collection of pus in a newly formed cavity

28
Q

What features contribute to bronchial narrowing in an asthma attack? (3 marks)

A

Acute bronchial narrowing in an asthma attack is caused by smooth muscle contraction, increased mucus production and oedema of the airway wall.

29
Q

3 clinical features of chronic TB that not likely to be present in acute pneumonia

A

weight loss, night sweats, haemoptysis

30
Q

dif b/w serosa and adventitia?

A

Serosa is connective tissue covered by a layer of simple squamous epithelium (known as mesothelium) which lines a cavity while adventitia is connective tissue which merges with surrounding tissues.

31
Q

Desmoplastic stroma in a malignant tumour contributes to the? how?

A

firmness of the lesion.

induce the proliferation of fibroblasts (via TGFbeta) which deposit extracellular matrix as they invade.

32
Q

compare the glands in different parts of stomach

A

In the fundus and body the glands contain many parietal and chief cells.
Whereas the glands of the cardia, antrum and pylorus contain predominantly mucus-secreting cells.

33
Q

usual location of chronic benign gastric ulcers?

A

Antrum (on the lesser curve)

34
Q

Which region of the stomach would a gastroenterologist biopsy for histopathological diagnosis in a patient with suspected Helicobacter gastritis?

A

Antrum or pylorus

35
Q

Which region of the stomach would a gastroenterologist biopsy if a histopathological diagnosis was required in a patient with suspected pernicious anaemia?

A

fundus or body. Pernicious anaemia results from destruction of parietal cells by an autoimmune gastritis, with reduced production of intrinsic factor resulting in reduced absorption of vitamin B12.

36
Q

explain the inflammatory course and pain history in appendicitis. why is this? what causes the pain

A

The inflammation in acute appendicitis starts in the mucosa then spreads transmurally. Until the inflammation involves the serosa, pain is often initially dull and felt in the central abdomen. The appendix touches areas of parietal peritoneum. Inflammation of the visceral serosa or peritoneum of the appendix then spreads to involve adjacent parietal peritoneum where somatic pain fibres are located and the pain becomes more severe and localised. Inflammatory mediators such as bradykinin and prostaglandins cause the pain.

37
Q

Do all hepatocytes of the different histological units have the same function biochemically? Explain

A

functionally, zone I hepatocytes (of the hepatic acinus) are specialized for different functions from those in zone 3. For example, hepatocytes in zone 1 are specialised for liver functions such as gluconeogenesis and cholesterol synthesis while hepatocytes in zone 3 are more important for cytochrome P-450-based functions.

38
Q

If the right ventricle started to fail, in which sinusoids would vasocongestion be seen initially, those around central veins or portal tracts? why?

A

Blood from the liver drains via the central veins into hepatic veins then into the IVC. if the right ventricle fails, blood will initially build up in central veins and surrounding sinusoids (rather than those around portal tracts where it enters the liver).