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Foundations Week 8 > Cell Differentiation I & II > Flashcards

Cell Differentiation I & II Flashcards

0
Q

What is replacement?

A

unable to make cells os same type as those lost. CT types “fill in” the space previously occupied by lost cells

Proliferation is controlled by variety of mediators (GF and inhibitors)

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1
Q

What is regeneration?

A

make new cells of same type as those lost. Depends on ability of cells to proliferate

Proliferation is controlled by variety of mediators (GF and inhibitors)

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2
Q

Regeneration involves what 2 types of tissues?

A

Renewing tissues (regeneration - skin & GI)

Compensatory growth (liver & kidney)

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3
Q

Replacement involves what 2 responses?

A

Wound - wound healing, scar formation

Chronic inflammation - fibrosis

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4
Q

What is labile?

A

constantly cycling the cell cycle

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5
Q

What is stable?

A

those cells in Go quiescent - hepatocytes

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6
Q

What are permanent cells?

A

cardiac myocyte & neurons

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7
Q

What is glioblastoma multiforme? What is the specific signaling pathway?

A

The malignant of astrocytes. Vascular that can be leaky.

Contrast enhancing mass

The malignant astrocytes produce VEGF in response to hypoxia.

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8
Q

What are examples of tyrosine kinase receptors?

A

EGF, FGF, VEGF, PDGF, TGF-beta. Found in wound healing

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9
Q

What is systemic sclerosis or scleroderma?

A

disease of chronic inflammation likely due to autoimmunity

involves widespread damage to small blood vessels

injured endothelium releases PDGF & TGF-beta (both are fibrogenic)

Patients develop progressive interstitial & perivascular fibrosis in skin & multiple organs (can have dyspnea)

sclera - hardening

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10
Q

What is the proposed mechanism for systemic sclerosis?

A

Immune system activation (effector T & other leuks (B)) create cytokines that injure & narrow blood vessels. Blood vessels then secrete PDGF & TGF-beta which entices fibroblasts to grow –> increases ECM –> fibrosis

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11
Q

What type of signaling do you see with systemic scleraderma?

A

cytokine signaling.

EPO (GF) & JAK (Janus kinase receptor) –> phosphorylates STAT (signal transducer & activator of transcription) –> gene transcription

Can also lead similar to RTK pathway – GRB2–>SoS–> Ras–> Raf —> MAPKK–> MAPK –> TF of gene transcription

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12
Q

What are examples of cytokine receptors?

A

Erythropoietin, IFN, IL2-IL4…

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13
Q

What is multiple myeloma?

A

plasma cell neoplasm - bone marrow disease

Patient can be tired - b/c crowding out other cell types

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14
Q

What increases with multiple myeloma? What can it lead to?

A

Increase IL6 production by osteoclasts
IL- stimulates the growth of multiple myeloma cells
Multiple myeloma increase bone resorption by osteoclasts
High serum levels of IL6 correlate with poor prognosis
Bone destruction can lead to hypercalcemia

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15
Q

What are the 4 ligand classes of G protein linked signaling? What are examples of each? What is their function?

A

Small biogenic amines - histamine - capillary dilation, smooth muscle contraction; epinephrine - vasopressor

Peptides - substance P - neurotransmitter; bradykinin - vasodilator

Glycoprotein hormones - parathyroid hormone - Ca homeostasis

Phospholipid signaling molecule - platelet activating factor - immune cell regulation

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16
Q

Known inhibitors of growth signaling include ___

A

Neurofibromin 1 & 2
TGF-beta
WT-1
Interferon-beta

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17
Q

What are features of neurofibromatosis type 1?

A

autosomal dominant disorder
1/3000
seen in individuals who inherit 1 mutant allele of NF1 gene
Multiple tumors of peripheral nerves (neurofibromas)
Numerous pigmented skin lesions
Pigmented iris hamartomas

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18
Q

The NF-1 gene product turns ___ off

A

Ras

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19
Q

ECM can contribute to different diseases

A

slide 36 - integrins communicate to basal membrane

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20
Q

What are functions of ECM?

A

provides water, minerals & GF to tissue
determines tissue architecture
basement membrane restricts cancer spread

21
Q

Successful reconstruction of tissue by regeneration of labile and/or stable cells require preservation of ___

A

stromal architectural support network – intact basement membrane is critical

22
Q

Chronic, irreversible injury to hepatocytes can lead to liver disease cirrhosis. Major causes of cirrhosis in the US include

A

excessive alcohol consumption
Hep B infection
Hep C infection
IV drug abuse

23
Q

What are the 5 types of cellular adaptations?

A

Atrophy, hypertrophy, hyperplasia, metaplasia & dysplasia

24
Q

What is hyperplasia?

A

Increase in # of cells as result of proliferation often with inrease in size of tissue/organ

25
Q

What is metaplasia?

A

one cell type being replaced by different cell type

26
Q

What causes hyperplasia?

A

hormonal stimulation/increased functional demand
may be physiologic
may be compensatory
may be pathologic

27
Q

Pathological forms of hyperplasia may provide setting for ____

A

neoplasia

28
Q

Hyperplasia is found in ____ & ____

A

endometrial hyperplasia & compensatory hyperplasia in liver

29
Q

__ signals activate growth response genes

A

priming.

30
Q

Gene expression initiates ____. GF promote ___.

A

cell growth; mitosis

31
Q

Hormones like ___ may facilitate in compensatory hyperplasia in liver. ___ stop liver cell proliferation

A

insulin; growth inhibitors

32
Q

What is a prostate? What pathology is common with prostate?

A

gland in male productive system - secretions contribute seminal fluid

Hyperplasia

33
Q

What is hypertrophy?

A

increase in cell size generally with increase in organ size; don’t have more cells

Hypertrophy & hyperplasia may occur together; however, in non-dividing cells only hypertrophy occur (DNA content of such cells may increase but they don’t undergo mitosis)

34
Q

What causes hypertrophy?

A

Increased hormonal stimulation/functional demand
Physiologic (increase in smooth muscle of uterus under hormonal influences of pregnancy)
Pathologic (increase in myocardial volume b/c of elevated systemic vascular P in HT against which heart must pump)

35
Q

Where is hypertrophy seen?

A

heart - hypertrophic cardiomyopathy - septal muscle bulges into left ventricular outflow tract

Disarray, extreme hypertrophy & branching of myocytes

Boxcar nucleus demonstrating increased DNA content

36
Q

What is the mechanism of cardiac hypertrophy?

A

signals may be mechanical/trophic
myocytes are stimulated to increase synthesis of myofilaments
long-term adaptation can involve change in type of contractile proteins

37
Q

What is atrophy?

A

decrease in cell volume due to loss of substance

represents new sate of EQ

38
Q

What causes atrophy?

A 
decreased workload
loss of innervations
diminished blood supply
inadequate nutrition
loss of endocrine stimulation
aging
local pressure
39
Q

Color change in aged liver is due to ___

A

lipofuscin

40
Q

CF causes what type of cellular adaptation?

A

atrophy
protein-calorie malnutrition

persistent diarrhea; disruption of normal ion flow eventually leads to pressure atrophy in pancreas

41
Q

What is metaplasia?

A

one cell type replaced by another. Progenitor stem cells express new characteristics that are better adapted to altered tissue environment

Most common form - glandular epithelium replaced with squamous epithelium

42
Q

What are examples of metaplasia?

A

respiratory epithelium becomes squamous epithelium in airways of smokers

Squamous esophageal epithelial ells replaced with intestinal like columnar cells (Barrett esophagus) - acid reflux - closely monitored - greater risk of carcinoma - 30-40% increase

43
Q

Barrett esophagus is the single most important risk factor for esophageal ____

A

adenocarcinoma; 30-40% increased risk for patient with >3cm of Barrett mucosa

Diagnosis - endoscopic evidence of columnar epithelial lining above Gastroesophageal junction & histologic evidence of intestinal metaplasia in biopsy specimen from columnar epithelium

potentially reversible

44
Q

What is dysplasia?

A

disordered growth - further loss in control of normal cells groth with possible progression to neoplasia

Marked by changes in nuclei & tissue architecture

45
Q

Dysplasia is a potentially reversible response to ___ or ___.

A

chronic injury or stimulation

46
Q

What are examples of dysplasia?

A

dysplasia of airway lining epithelium in smokers (usually occurs on background of squamous metaplasia

dysplasia of uterine cervical epithelium w/ HPV infection

47
Q

Dysplasia often occurs in ___ epithelium

A

metaplastic

Metaplastic epithelium can be seen WITHOUT dysplasia

Dysplasia can arise WITHOUT going through metaplasia

48
Q

Dysplasia is measured by __ & ___

A

low grade & high grade

49
Q

What is an example of dysplasia?

A

cervical dysplasia - can see mitotic figures

50
Q

Cervical dysplasia in Pap smear will show increase in ___

A

nuclear size; lower amount of cytoplasm by comparison

51
Q

What is neoplasia?

A

abnormal proliferation of cells whose growth is uncoordinated with response to host’s needs & generally continues despite removal of stimuli

Implies automonous cellular proliferation, without normal response to control mechanisms

Foundations Week 8 (8 decks)

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