Question

2. Sarp, a second year medical student in Marmara University, wants to go to Baba-Zula Concert in İstanbul, that is sponsored by Pathology Society. Due to Covid 19 days, the entrance to the concert hall is limited and the only way to participate is to figure out a puzzle based on the knowledge of etiopathogenesis, clinical findings and complications of hemodynamic disorders. Maybe you are not a fan of Baba-Zula, but Sarp is your best friend. In the entrance hall a puzzle is given to Sarp with the following list and asked to select only five items and create a group related to the following patients.

Patient 1: A 72 year old obese female patient with varicous veins.

Patient 2: A 48 year old male patient with renal infarction.

a) Please, select only 5 items for each patient from the following list (you can use an item only once). (3 points)

1) venous thrombosis

2) arterial thrombosis

3) arterial embolism

4) systemic embolism

5) venous embolism

6) stasis in the flow of blood

7) turbulance in flow of blood

8) edema due to increased venous hydrostatic pressure

9) edema due to decreased extravascular hydrostatic pressure

10) edema due to increased extravascular oncotic pressure

11) edema due to decreased intravascular oncotic pressure

12) hyperemia

13) localized congestion

14) systemic congestion

15) vegetations on the mitral valve

16) myocardial infarction

For patient 1, the selected items are venous thrombosis , venous embolism, stasis in the flow of blood …………………………

For patient 2, the selected items are ………………………...

b) Please write the logical sequence of events for each of the above patients using the items that you have selected. (2 points)

3. Please fill in the blanks.

a) Membrane dysfunction and mitochondrial membrane damage are 2 critical events to ………………………………………. (1 point)

b) The most common type of ischemic necrosis is ………………………………….....…. (2 points)

c) Caseification necrosis is typical for …………………………………………………..……… (2 points)

Answer 1

3. A. Alzheimer's and Parkinson's disease

Abnormal interactions and misfolding of synaptic proteins in the nervous system are being extensively explored as important pathogenic events resulting in neurodegeneration in various neurological disorders. These include Alzheimer’s disease (AD), Parkinson’s disease (PD), and dementia with Lewy bodies (DLB). In AD, misfolded amyloid β peptide 1–42 (Aβ), a proteolytic product of amyloid precursor protein metabolism, accumulates in the neuronal endoplasmic reticulum and extracellularly as plaques. In contrast, in PD and DLB cases there is abnormal accumulation of α-synuclein in neuronal cell bodies, axons, and synapses. Furthermore, in DLB, Aβ 1–42 may promote α-synuclein accumulation and neurodegeneration. The central event leading to synaptic and neuronal loss in these diseases is not completely clear yet; however, recent advances in the field suggest that nerve damage might result from the conversion of nontoxic monomers to toxic oligomers and protofibrils. The mechanisms by which misfolded Aβ peptide and α-synuclein might lead to synapse loss are currently under investigation. Several lines of evidence support the possibility that Aβ peptide and α-synuclein might interact to cause mitochondrial and plasma membrane damage upon translocation of protofibrils to the membranes. Accumulation of Aβ and α-synuclein oligomers in the mitochondrial membrane might result in the release of cytochrome C with the subsequent activation of the apoptosis cascade. Conversely, the oxidative stress and mitochondrial dysfunction associated with AD and PD may also lead to increased membrane permeability and cytochrome C release, which promotes Aβ and α-synuclein oligomerization and neurodegeneration. Together, these studies suggest that the translocation of misfolded proteins to the mitochondrial membrane might play an important role in either triggering or perpetuating neurodegeneration. The insights obtained from the characterization of this process may be applied to the role of mitochondrial dysfunction in other neurodegenerative disorders, including AD. New evidence may also provide a rationale for the mitochondrial membrane as a target for therapy in a variety of neurodegenerative diseases.

B. ischemic necrosis. A condition in which there is a loss of blood flow to bone tissue, which causes the bone to die. It is most common in the hips, knees, shoulders, and ankles. It may be caused by long-term use of steroid medicines, alcohol abuse, joint injuries, and certain diseases, such as cancer and arthritis.

C.Caseous necrosis is a condition of cellular death that usually occurs in the lungs. When the lung cells die, they begin to take on a crumbly, dull white appearance that resembles cheese. Although caseous necrosis most often occurs in the lungs, it can also happen in other locations of the body such as the kidneys.