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DIT > 1G Foundations 7 - Inflammation > Flashcards

1G Foundations 7 - Inflammation Flashcards

1
Q

What are the characteristics of a cell undergoing apoptosis?

A
  • Cellular shrinkage
  • Nuclear shrinkage (pyknosis)
  • Karyolysis (fading of the nucleus)
  • Apoptotic bodies
  • Membrane blebbing
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2
Q

What are some of the substances that can trigger apoptosis?

A
  • Deprivation of cell signals (growth factors)
  • Cell stress
  • DNA repair process fails –> triggers apoptosis
  • Cytokines (TNF)
  • Cytotoxic T cells can insert Granzyme B into cells
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3
Q

What neural crest derivatives are found in this adult structure? PNS

A
  • ANS
  • Dorsal root ganglia
  • CNs
  • Schwann cells
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4
Q

What neural crest derivatives are found in this adult structure? Ear

A

Bones of the middle ear

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5
Q

What neural crest derivatives are found in this adult structure? Eye

A

Structures of the anterior chamber

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6
Q

What neural crest derivatives are found in this adult structure? Adrenal gland

A

Chromaffin cells in medulla

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7
Q

What neural crest derivatives are found in this adult structure? Mouth

A

Odontoblasts

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8
Q

What neural crest derivatives are found in this adult structure? Heart

A

Aorticopulmonary septum (spiral septum)

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9
Q

What neural crest derivatives are found in this adult structure? Digestive system

A
  • Enteric nervous system
  • Celiac ganglion
  • Enterochromaffin cells
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10
Q

What neural crest derivatives are found in this adult structure? Thyroid

A

Parafollicular cells (C cells)

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11
Q

What neural crest derivatives are found in this adult structure? Skin

A

Melanocytes

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12
Q

Inflammation is characterized by?

A
  • Rubor
  • Dolor
  • Calor
  • Tumor
  • Functio laesa
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13
Q

Acute inflammation: Release of which inflammatory mediators?

A
  • IL-1
  • IL-6
  • TNF-alpha
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14
Q

Acute inflammation: Vasodilation and increased vascular permeability fluid exudation is mediated by?

A
  • Histamine
  • Serotonin
  • Bradykinin
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15
Q

Acute inflammation: Fibrosis. Fibroblasts lay down BLANK and requires BLANK

A

Collagen, vitamin C

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16
Q

Acute inflammation: Tissue remodelling by BLANK which contain BLANK

A

Metalloproteinases, Zinc

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17
Q

Intermediary stage in wound healing. Occurs 3-5 days into the healing process?

A

Granulation tissue

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18
Q

Fibrotic shell that seals inflammatory process off. (body considers this as a success outcome)

A

Abcess

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19
Q

Acute inflammation is mainly mediated by which cell type?

A

Neutrophils

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20
Q

Chronic inflammation is mainly mediated by whuich cell type?

A

Mononuclear cells (like macrophages and lymphocytes)

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21
Q

Multi nucleated giant cells are what?

A

Several macrophages that have connected their plasma membranes and cytoplasms to create one cell

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22
Q

What is a granuloma

A

Nodule of macrophages found in chronically inflamed tissue

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23
Q

Chronically inflamed tissue is characterized by which two processes?

A

Ongoing cycles of tissue damage and tissue repair

24
Q

Meaning of the word extravasation

A

something is leaving the circulation to enter a tissue

25
Q

What cells can be involved in leukocyte extravasation?

A
  • Neutrophils
  • Polymorphonuclear cells (PMNs)
  • Granulocytes
  • Monocytes
  • Certain types of T-cells
26
Q

Steps in leukocyte extravasation. What’s the role of E- and P-selectin?

A

They are expressed on endothelial cells lining the inside of vasculature and adhere to leukocytes

27
Q

Outcomes of chronic inflammation?

A

Scarring and Amyloidosis

28
Q

Steps in leukocyte extravasation. Where can you find L-selectin?

A

On leukocytes

29
Q

Steps in leukocyte extravasation. How is expression of selectins triggered in the endothelium?

A

By acute-phase cytokines

  • IL-1
  • IL-6
  • TNF-alpha
30
Q

Steps in leukocyte extravasation. Tight binding. Surface receptor involved?

A

ICAM-1

31
Q

Steps in leukocyte extravasation. Tight binding. Leukocyte protein involved?

A

LFA-1 (an integrin)

32
Q

Steps in leukocyte extravasation. Diapedesis, what is it?

A

Leukocyte travels between endothelial cells and exits blood vessel

33
Q

Steps in leukocyte extravasation. Diapedesis. Protein involved?

A

PECAM-1 (on the intercellular junctions between endothelial cells)
-Also found on Neutrophils, Monocytes, platelets)

34
Q

Steps in leukocyte extravasation. Migration-inducing signals?

A
  • Chemotactic signals

- Neutrophil chemotactic factors: C5a, IL-8, LTB4, Kallikrein

35
Q

Binding, diapedesis and migration is enhanced by?

A

Platelet activating factor

36
Q

Leukocyte adhesion deficiency syndrome is characterised by?

A
  • Abnormal integrin molecules
  • Delayed separation of the umbilicus
  • Recurrent bacterial infections
37
Q

Describe transudate

A
  • Mostly water
  • Decreased cells
  • Decreased protein
  • Low specific gravity due to:
  • Increased hydrostatic pressure
  • Decreased oncotic pressure
38
Q

Describe exudate

A
  • Rich in proteins and cells
  • Inflammatory cells due to:
  • Lymphatic obstruction
  • Inflammation
39
Q

List the three basic forms of inflammation

A
  • Serous
  • Fibrinous
  • Suppurative
40
Q

Feature of serous inflammation

A

Transudate

41
Q

Feature of fibrinous inflammation

A

Exudate

42
Q

Feature of suppurative (purulent) inflammation

A

Pus

43
Q

Granuloma?

A

-Collection of macrophages that make TNF-alpha – > maintains granuloma

44
Q

What does Infliximab block?

A

TNF-alpha

45
Q

What does blocking of TNF-alpha lead to (in a granuloma context)?

A

Breakdown of granuloma

46
Q

Why do you have to be careful before giving anti-TNF-alpha drugs?

A

It might breakdown latent granulomatous abcesses (i.e. TB) leading to disseminated disease

47
Q

Name granulomatous diseases

A
  • Mycobacterium Tuberculosis (caseating)
  • Fungal infections (blastomycosis, histoplasmosis, coccidiomycosis)
  • Sarcoidosis
  • Granulomatosis with polyangiitis (Wegener’s)
  • Berylliosis (people who work in Beryllium mines get this)
  • Treponema Pallidum (syphilis)
  • M. leprae (leprosy)
  • Bartonella henselae (cat scratch disease)
  • Crohn’s disease
  • Churg-Strauss syndrome
  • Silicosis
  • Listeria
  • Chronic granulomatous disease
  • Foreign bodies
48
Q

Is ESR high or low in inflammation?

A
  • Higher (products of inflammation e.g. fibrinogen coat RBC’s –> aggregation –> They fall faster)
  • It’s very non-specific
49
Q

Potential causes of elevated ESR (“sed rate”)

A
  • Polymyalgia rheumatica
  • Temporal arteritis
  • Disease activity in RA and SLE
  • Infection, inflammation (e.g. osteomyelitis)
  • Malignancy
  • Pregnancy
50
Q

How can we classify C-Reactive Protein?

A
  • Acute phase protein synthesised in the liver
  • Part of the innate immune system
  • An opsonin as it binds to microbial surfaces (opsonizes and activates complement)
51
Q

Acute phase proteins?

activated during acute inflammation

A
  • ESR
  • CRP
  • Fibrinogen
  • Ferritin
52
Q

In active inflammation you can see?

A

(Factors mediated by cytokines, non-specific)

  • Elevated ESR
  • Elevated CRP
  • Fever
  • Leukocytosis
  • Elevated HR and BP
53
Q

Information about CRP

A
  • Can be secreted from cells within atherosclerotic plaques to activate local endothelial cells to induce a prothrombotic state and increase the adhesiveness of the endothelium to leukocytes
  • Elevations are a strong predictor of MI, stroke, PAD, and sudden cardiac death
  • Can be lowered by smoking cessation, exercise, weight loss, and statins
54
Q

Reasons for decreased ESR?

A
  • Sickle cell (altered shape)
  • Polycythemia (too many)
  • CHF (unknown)
55
Q

Steps in Leukocyte extravasation and what the steps are mediated by

A
  • Rolling: selectins
  • Tight binding: Integrins
  • Diapedesis: PECAM-1
  • Migration: IL-8, LTB4, C5a, Kallikrein
56
Q

What cytokine is particularly important in the formation of granulomas?

A

TNF-alpha

57
Q

What cell type plays a role in inflammation by generating both fibrinogen and C-reactive protein?

A

Hepatocyte

DIT (11 decks)

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