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BMS 460 > Curricular Exercise #2 > Flashcards

Curricular Exercise #2 Flashcards

1
Q

The intima is comprised of _________ and is the innermost, the media is comprised of ________ and is the middle layer, and the adventitia is comprised of _______ to make up the outer layer.

A
  1. Intima is made of endothelial cells.
  2. Media is made of smooth muscle and elastic fibers.
  3. Adventitia is made of connective tissue.
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2
Q

As you move from artery to vein, what happens to the thickness of the intima, media, and adventitia?

A
  1. Thickness of the tunica intima will not change.
  2. Thickness of the tunica media will get thinner.
  3. Thickness of the tunica adventitia will get thicker.
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3
Q

Which specialized capillary arrangement occurs when a capillary bed pools into another capillary bed?
a. Glomerulus.
b. Hepatic portal system.

A

b. - hepatic portal system.

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4
Q

Pytoptosis is usually triggered by ___________, because it plays a role in ____________ defense against microbes.

A
  1. Infection or cellular damage.
  2. inflammatory.
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5
Q

Which of the following will present early loss of the plasma membrane integrity:
a. Apoptosis.
b. Pyroptosis.
c. Pyknosis.
d. Necrosis.

A

b. pyroptosis.
d. necrosis.

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6
Q

Pyroptosis results in the release of what from the lysed cell:

A

cytokines and pathogen-associated molecular patterns (PAMPs).

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7
Q

The purpose of pyroptosis is to:

A

eliminate infected or damaged cells and prevent further injury to the tissue.

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8
Q

Excess pyroptosis can cause:

A

Extreme inflammatory responses, resulting in autoimmune disease.

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9
Q

AAT is an __________ protein that acts on ________ to limit the destruction of proteins in the tissues.

A
  1. Inhibitory.
  2. Proteases.
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10
Q

If elastase is not inhibited in AAT defiecency, what will occur?

A

Destruction of the elastin fibers of the lungs, causing decreased respiratory function.

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11
Q

In AAT deficiency, the liver produces abnormal or insufficient AAT. This is due to what kind of mutation, in what gene?

A

A mutation in the SERPINA1 gene, that will be hereditary.

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12
Q

What is the leading cause of cirrhosis of the liver in children?

A

AAT deficiency.

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13
Q

Adult patients with AAT deficiency may experience:

A
  1. Cirrhosis of the liver.
  2. Lung disease.
  3. Hepatocellular cancer.
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14
Q

What is the primary function of alpha-a antitrypsin (AAT)?
a. activating proteases.
b. inhibiting neutrophil elastase.
c. Degrading elastin.
d. Enhancing inflammation.

A

b. inhibiting neutrophil elastase.

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15
Q

Necrosis is uncontrolled death to many cells or tissues, it can be caused by:
a. Endogenous factors.
b. exogenous factors.
c. Both endogenous factors and exogenous factors.

A

C - both endogenous and exogenous factors.

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16
Q

____________ necrosis is caused by ischemic cell injury, where tissue architecture may be preserved for a long time. Occurs mostly in the heart, kidneys, and spleen.

A

Coaugulative necrosis.

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17
Q

__________ necrosis: Dead cells will decrease the pH and activate lysosomal enzymes that will liquefy the injured tissue.

A

Liquefactive necrosis.

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18
Q

__________ necrosis: Is a combination of coagulative and liquefactive necrosis. Is typically found in granulomatous inflammation and is characterized by tuberculosis.

A

Caseous necrosis.

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19
Q

_________ necrosis: Occurs when adipose cells are destroyed, typically by physical trauma or release of pancreatic enzymes. Leads to chalky white calcification of the adipose tissue.

A

Fat necrosis.

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20
Q

Which type of necrosis is commonly associated tuberculosis?
Coaugulative necrosis.
Liquefactive necrosis.
Caseous necrosis.
Fat necrosis.

A

Caseous necrosis.

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21
Q

Efferocytosis is the process of:

A

Clearing away dying or dead cells by phagocytic cells, like macrophages or dendritic cells. This is intended to help resolve inflammation caused by cytokines released from injured cells.

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22
Q

Failure of efferocytosis will cause:

A

Secondary necrosis and un-mediated inflammation, often associated with autoimmune disease.

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23
Q

Which of the following is false regarding efferocytosis?

a. efferocytosis will cause the release of pro-inflammatory cytokines.

b. If this process is defective, it can be linked to many autoimmune diseases.

c. Is the process of clearance of apoptotic cells by means of phagocytosis.

d. Increased cytoplasmic calcium concentrations will help digest phagocytosed cells.

A

a - efferocytosis will cause the release of proinflammatory cytokines.

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24
Q

Neutrophil - important azurophilic granules:

A
  1. Phosphoslipase A2
  2. Type IV collagenase.
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25
Q

Neutrophil important specific granules:

A
  1. Phospholipase A2.
  2. Elastase.
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26
Q

Neutrophil - Tertiary granules:

A

Metalloproteinases

27
Q

Eosinophils - Important azurophilic granules:

A

Collagenase.

28
Q

Eosinophils - Important specific granules:

A
  1. Histamine.
  2. collagenase.
29
Q

Basophils - important azurophilic granules:

A

Acid hydrolases.

30
Q

Basophil - Important specific granules:

A

Histamine.

31
Q

Histamine is found in:

A

Specific granules of basophils and eosinophils.

32
Q

Which granules in neutrophils contain phospholipase A2?

a) Specific granules
b) Azurophilic granules
c) Basophilic granules
d) Eosinophilic granules

A

B.) azurophilic granules of neutrophils.

33
Q

Acute-phase proteins are produced by the ________, when stimulated by cytokines ___, ___, and ____.

A
  1. Produced by the liver.
  2. IL-1, IL-6, TNF-a
34
Q

Types of acute-phase proteins released by the liver:

A
  1. C-reactive proteins.
  2. Serum amyloid A.
  3. Protease inhibitors - such as a1-antitrypsin (AAT).
  4. Fibrinogen.
35
Q

C-reactive protein facilitates _________ of bacterial cells, by binding to __________ in their lipid bilayer.

A
  1. Phagocytosis.
  2. Phospholipids.
36
Q

Effects of fibrinogen in the inflammatory response:

A

Causes coagulation of RBCs by lowering surrounding them and lowering their charges allowing them to aggregate. This allows for blood clotting.

37
Q

Function of protease inhibitors in the immune response:

A

Minimize the amount of damage done to the effected tissue.

38
Q

Which of the following acute-phase proteins is involved in clot formation and wound healing?
a) CRP
b) Heptaglobin
c) Serum Amyloid A (SAA)
d) Fibrinogen

A

d - fibrinogen.

39
Q

Which of the following is not a cytokine released by immune cells to stimulate the liver to produce acute-phase proteins?

a. IL-8
b. IL-1
c. TNF-a
d. IL-6

A

a - IL-8

40
Q

Gram-negative bacteria will release ______________, which will cause the release of __________ in the endothelium in sepsis.

A
  1. Lipopolyscharrides (LPS)
  2. Cytokines (IL-1 IL-6 and TNF-a)
41
Q

Gram-positive bacteria will release __________

A

Exotoxins.

42
Q

Sepsis will cause:

A
  1. Hypotension.
  2. vascular instability.
  3. Microvascular occlusions.
  4. widespread inflammation.
  5. Multiple organ failure.
43
Q

Exotoxins and endotoxins (LPS) are considered to be:

A

Very strong pro-inflammatory toxins.

44
Q

Both gram-positive and gram-negative bacteria will produce:

A

Peptidoglycans - a moderate pro-inflammatory molecule.

45
Q

LPS and exotoxins will act on the endothelium to cause the production and release of -

A

IL-1, IL-6, and TNF-A

Plasminogen and tissue factor will also be released by damaged endothelium to assist with clotting.

46
Q

What is the most potent and important in recruiting cytokines to perform an inflammatory response in sepsis:

a. Lipopolysaccharides (LPS)
b. Exotoxins.

A

a - lipopolysaccharides (LPS)/Endotoxins.

47
Q

True or false: Sepsis is caused by an underreaction of the immune system, causing a lack of inflammatory response to bacterial infection.

A

FALSE - Spesis is an overreaction of the immune system.

48
Q

Define shock:

A

When the circulatory system fails to provide oxygen and nutrients to the body, leading to cellular dysfunction and organ failure under hypoxic conditions.

49
Q

____________ shock occurs due to a decrease in cardiac output.

A

Cardiogenic shock.

50
Q

_________ shock occurs due to a significant decrease in blood volumes - often due to hemorrhaging or burns.

A

Hypovolemic shock.

51
Q

___________ shock occurs due to massive vessel dilation, increasing the capacitance of vessels and decreasing the cardiac output - Is seen in septic shock.

A

Disruptive shock.

52
Q

_________ shock is caused by the release of endotoxins (LPS) that has a major effect on dilating the arterioles, capillaries, and venules, as a response to inflammatory processes.

A

Septic shock.

53
Q

Which of the following is a characteristic feature of septic shock?

a) Increased systemic vascular resistance (SVR)
b) Decreased cardiac output with normal vascular tone
c) Widespread vasodilation and decreased SVR
d) Adequate tissue perfusion despite hypotension

A

c - widespread vasodilation and decreases SVR.

54
Q

Features of malignant tumors:

A
  1. Invasive of tissue.
  2. Invasive of lymphatic vessels.
  3. Invasive of blood vessels.
  4. Metastasis.
  5. Hemorrhage.
  6. Non-homogenous cut surface.
55
Q

Both malignant tumors and benign tumors are classified as -

A

Neoplastic - Uncontrolled growth of cells.

56
Q

___________: is the uncontrolled growth of cells that are characterized by a lack of differentiated features, where new features did not originate in the affected tissue. Highly associated with malignant tumors.

A

Anaplasia.

57
Q

Hallmarks of anaplasia:

A
  1. Pleomorphism - Nuclei vary in shape and size.
  2. High mitotic activity - High rate of proliferation.
58
Q

Which of the following is a hallmark in anaplastic malignant tumors:

a. Apoptosis.
b. Normal mitotic figures.
c. Pleomorphism.
d. Good response to growth inhibitors.

A

c - pleomorphism.

59
Q

_____________: are genes that regulate normal cell growth.

A

proto-oncogenes.

60
Q

_____________: are mutated genes that allow for malignant transformation of cells, that allow for excessive proliferation of cells.

A

Oncogenes.

61
Q

Burkitt’s lymphoma:

A

Is caused by an oncogene due to translocation of gene c-Myc between chromosomes 8 and 14.

62
Q

True or false: Benign tumors are not associated with any chromosomal abnormalities

A

True.

63
Q

What is the difference between an oncogen and a proto-oncogene.

a. Oncogenes and proto-oncogenes are both associated with malignancy, but relate to different types of cancer.

b. Oncogenes are normal genes that maintain cellular growth, while proto-oncognes are associated with malignancy.

c. Proto-oncognes are normal genes that maintain cellular growth, while oncogenes are associated with excess proliferation.

d. Oncogenes and protooncogenes are both associated with normal cellular growth, that stimulate different growth factors.

A

C- proto-oncogenes are normal genes that maintain cellular growth, while oncogenes are associated with excess proliferation.

64
Q
A

BMS 460 (13 decks)

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