Week 2: Cell death and adaptation workshop Flashcards

1
Q

What are the features in reversible cell injury?

A

Cellular swelling - small clear vacuoles may appear within the cytoplasm due to degeneration of the ER, more eosinophilic cytoplasm
Cell membrane changes- blebbing or loss of microvilli
Fat accumulation -typically in the liver
Mictochondrial swelling
Nuclear alterations - clumping of chromatin

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2
Q

What are the key morpholigical features of necrosis?

A

Darker staining cytoplasm
Vacuolated /moth eaten cytoplasm after enzymes have digested the cellular content
Discontinous plasma membrane
Calcium precipitates
Nucleus may shrink and darken or fragment or lighten

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3
Q

What are the cellular features of necrosis?

A

Swelling
Nucleus - pyknosis (condense), karyorrhexis (fragments), karyolysis (fades)
Plasma membrane is disrupted
Cellular contents, undergoes enzymatic digestion may leaks out of cell

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4
Q

What are the cellular features of apoptosis?

A

Shrinkage
Nucleus fragments
Plasma membrane is intact but has an altered structure
Cellular content is intact and released within apoptopic bodies

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5
Q

What are the signs of early ischemic damage in an MI?
(still reversible)

A

Cell nucleus is still present
Cells are lighter staining - reduction in sarcomeres
Patchy appearance
Cell swelling

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6
Q

What are the signs of coagulative necrosis in cardiacmyocytes in MI?

A

Lack of nucleus
Darker staining cytoplasm
No cellular content is visible

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7
Q

Define myocardial infarction

A

Death of cardiac muscle due to severe prolonged ischemic conditions

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8
Q

What are the primary diagnostic tests for MI?

A

ECG
Followed by serum cardiac enzymes

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9
Q

What are the normal serum cardiac enzymes that are tested for in a suspected MI?
What is their normal value?

A

Troponin 1 <0.03ng/mL
Troponin T <0.1ng/L
Creatine kinase MB isoenzyme <10mg/mL

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10
Q

When and what gross changes occur after an MI?

A

Visible ater 12hrs
Dark Mottling develops to a yellow core eventually becoming a scar

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11
Q

What is the time span of histological changes in MI?

A

take 6 to 12 hours to develop
- coagulative necrosis
- neutrophil influx after 12 to 24 hours
- loss of nuclei on day 1 to 3
-phagocytosis on day 3 to 7
- scar forms in 2 months

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12
Q

What is the primary goal in an MI patient?

A

Manage as soon as possible

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13
Q

What is the cause of cell injury in an MI?

A

Coronary artery occlusion leading to severe hypoxia and prolonged ischemic conditions for group of cardiac myocytes
Leads to inhibition of myocardial contractility - causing MI
Eventually tissue dies

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14
Q

Why is troponin T the most valued serum cardiac enzyme?

A

When cardiac myocytes are damaged is released through porous cell membrane
Is the most specific and sensitive for MI.
Can be detected after 2 hours
Is proportional to the degree of damage

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15
Q

What are the potential complications of acute MI?

A

Arrhythmias
Hypotension
Ventricular septal rupture
Left ventricular free wall rupture
Left ventricular aneurysm formation

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16
Q

What are the aims of percutaneous coronary intervention?

A

May be described as an angiogram and stent
Is a non-surgical intervention, by which a catheter is used to insert a stent into a narrowed coronary artery
Inflation of the stent widens the vessel helping to treat atherosclerosis, reducing the risk of MI by improving blood flow.

17
Q

Explain how pyrexia and raised white blood cell count may be related by MI?

A

Area of inflammation - response to necrotic tissue, recruitement of immune cells, acitvated immune cells may secrete pyrogenes causing fever

CRP is associated with inflammation and the formation of atherosclerosis - is elevated after MI along with fever.

Inflammation is implicated in the pathogenesis of atherosclerosis and acute conronary syndromes

Inwards migration of wbcs

18
Q

What are the outcomes of MI 12 weeks later?

A

Disturbance in rate, rhythm and conduction
Pericarditis
Ventricular Septal defect
Ruptured Papillary muscles
Dressler’s Syndrome - autoimmune reaction to myocardial neo-antigens

19
Q

What are some of the physiological purposes of apoptosis?

A

Endometrium - shedding of lining for menses
Embryogenesis - elimination of cells and tissues, prevent webbing in fingers and toes
Viral infections - eliminate infected cells
Normal lining epithelial cells (intesintal) - apoptosis to replace and regenerate the GIT lining

20
Q

What is the key difference between apoptosis and necrosis?

A

Apoptosis - pre-defined cell suicide, that is executed in a controlled way by an enzyme cascade. Physiological

Necrosis - uncontrolled cell death, no specific enzyme pathway or plan, pathological, has a negative effect on function

21
Q

What are some of the signs of acute kidney injury on imaging?

A

Micrscopic: pale swelling cells
Macroscopic - pale and enlarged kidney

22
Q

What is measured in a liver function test? How do the values change in liver damage?

A

ALT and AST - increase
Bilirubin - increase
Albumin - decrease (found normally in the blood is a protein produced by the liver)
Alkaline phosphate and y-glutamyltransferase: increase

23
Q

What are the cellular targets of cell injury?

A
  1. Cell membrane damage - resulting in H20 influx
  2. Mitochondrial damage resulting in Cytochomr C release
  3. Na+k+ pump damage - cell swelling
  4. Increased ROS - damage DNA, protein and lipids
  5. Protein misfolding and DNA damage - activates pro-apoptopic proteins
24
Q

What plasma elevation is a marker of kidney damage?

A

Creatinine
Urea

25
Q

What plasma elevation is a sign of muscle damage?

A

Creatine Kinase
Myoglobin

26
Q

What are some of the histological changes that occur in Alcoholic Liver Disease?

A

Lipids droplets accumulate in heptocytes, push nucleus to the periphery, result in pale white nucleus.
Other cells maintain a central nucleus, but appear a patchy white, may be from ER dysfunction, hepatocyte ballooning - sign of necrosis

27
Q

Is Alcoholic Liver Disease reversible?

A

At early stage yes - if the reversible stimuli is removed.

Also recommend maintaining a healthy weight and managing diabetes (if applicable)

If reverse all histological changes would revert to normal

28
Q

What cellular changes occur in the liver as a result of severe continued alcohol use?

A

Loss of hepatocytes - replaced by fibrotic tissue
Cirrhosis
Acute liver failure
Hepatocellular carcinoma

29
Q

What are the gross changes in a cirrhotic liver compared to a normal liver?

A

Loss of smooth surface - growth on cirrhotic liver nodules on the external and internal surface.
Increased yellowing of colour
Fibrosis of liver tissue

30
Q

What are the common histological changes in a cirrhotic liver?

A

Increased fibrous tissue deposition around hepatocyte nodules
Chronic inflammation results in excessive collagen production by hepatic stellate cells
Loss of specialised tissue features

31
Q

What type of epithelium is present in Barrets Oesophagus?

A

Specialised columnar epithelium - contains goblet cells and villi architecture or mimics gastric glands and contains mucus neck cells

32
Q

Is metaplasia reversible?

A

POtentially yes, if the damaging stimuli is reversed before the damage progresses to dysplasia

33
Q

Give three pathological examples of metaplasia.

A

Smoking - bronchi change from cilliated simple columnar to stratified sqaoumous cells, more resistant to chemical damage from cigarrete smoke but less mucocillary clearance.

Chronic endometriosis - uteurs lining changes from simple columnar to startified sqaoumous bettwe suited to chronic inflammation