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Human Pathology > Lecture Exam 1 > Flashcards

Lecture Exam 1 Flashcards

1
Q

contains DNA/RNA

A

cell nucleus

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2
Q

ribosomes on outer surface synthesize proteins

A

endoplasmic reticulum

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3
Q
  • production of steroid hormones

- synthesize glycogen

A

smooth endoplasmic reticulum

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4
Q

packages proteins and lipids in vesicles

A

golgi bodies

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5
Q

produces cell energy (ATP) via respiration

A

mitochondria

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6
Q

myeloid cell that targets bacteria and fungi

A

neutrophil

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7
Q

myeloid cell that targets parasites and allergic inflammatory response

A

eosinophils

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8
Q

myeloid cell that releases histamine for inflammatory responses

A

basophil

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9
Q

myeloid cell that migrates from vasculature to tissue and differentiates in macrophages

A

monocyte

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10
Q

lymphoid cell that binds tumors and virus-infected cells without antigen stimulation and kills them by granule insertion

A

natural killer cell

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11
Q

lymphoid cell that directly kills infected cells by injecting proteins
-produces proteins that regulate immune system to kill pathogens and can distinguish between self and non-self

A

T lymphocytes

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12
Q

lymphoid cell that recognizes surface antigens on bacteria and viruses to produce antibodies to activate the immune system and destroy pathogens

A

B lymphocyte

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13
Q

B lymphocyte that differentiates into a plasma cell with help from T-cells. Ab it produces is similar to receptor on B lymphocyte. Abs released to bind to antigen to cause its destruction.

A

Plasma cells

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14
Q

intracellular stores of calcium

A

mitochondria and endoplasmic reticulum

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15
Q

increases in intracellular calcium triggers what enzymatic pathways that can be injurious to the cell?

A

ATPase = no ATP, no energy
phospholipase and protease = cell membrane damage
endonuclease = nuclear chromatin damage

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16
Q

anoxia

A

no oxygen delivery

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17
Q

asphyxia

A

no oxygen delivery due to an interruption of breathing

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18
Q

what are examples of reversible cell injury

A
  • decreased respiration and loss of ATP
  • glycogenolysis and glycogen depletion
  • reduction in intracellular pH (lactic acid)
  • failure of membrane transport systems (cellular edema - H2O accumulation due to increase in intracellular Na+)
  • detachment of ribosomes and decreased protein synthesis
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19
Q

irreversible cell injury

A
  • massive influx of calcium
  • membrane damage (phospholipases, ROS)
  • intracellular release of lysosomal enzymes (RNAases, DNAases, proteases)
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20
Q

coagulative necrosis

A
  • preservation of cell outlines and tissue structure

- prototype - myocardial infarction

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21
Q

liquefactive necrosis

A
  • insult leading to an influx of neutrophils releasing catalytic enzymes
  • loss of cell outlines and tissue structure
  • ex: bacterial abscess, brain
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22
Q

early changes in coagulative necrosis

A
  • hypereosinophilia (more red “red means dead”)
  • cytoplasmic vacuolization
  • nuclear changes: 1) pyknosis (shrunken and hyperchromatic)
    2) karyorrhexis (fragmented)
    3) disappearance
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23
Q

granuloma is different from granulation tissue

A

granulation tissue: new tissue that forms as part of the healing of an injury
granuloma: chronic area of inflammation

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24
Q

saponification

A

pancreatic enzymes break down fat tissue around the pancreas, which then complexes with cations and essentially forms soap

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25
Q

inducers of apoptosis (programmed cell death)

A
  • cytochrome C is released from mitochondria > induces caspases that break down protein and DNA
  • engagement of death receptors on cell (TNF) which is a ligand that directly activates caspases
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26
Q

regulatory protein of apoptosis that inhibits the release of cytochrome C from mitochondria?

A

bcl-2 in cytoplasm

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27
Q

only in dividing cells, usually cells under hormonal control - increase in cell number

A

hyperplasia

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28
Q

alzheimers diseases is an example of ________

A

brain atrophy

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29
Q

differentiation of one cell type by another, often replacing a whole tissue

A

metaplasia

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30
Q

earliest step in atherosclerosis development

A

abnormal accumulation of cholesterol in macrophages on the inner lining of arterial walls

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31
Q

major leukocytes for inflammatory response

A

monocytes (macrophages), neutrophils, antigen-specific lymphocytes

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32
Q

hallmark of inflammation

A

infiltration of tissue with any of the classes of leukocytes

  • neutrophils: acute inflammation
  • lymphocytes and monocytes: chronic inflammation
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33
Q

sequence of events in acute inflammation

A

1) increased blood flow to area
2) extravasation and deposition of fluid and plasma proteins
3) emigration of neutrophils from microcirculation and their accumulation at the site of injury

34
Q
  • secreted by mast cells (and basophils), present in most tissues
  • causes vasodilation and increased permeability
  • results in fluid leak
  • prominent role in allergic response, causing edema
A

histamine

35
Q

regulator of vascular permeability similar to histamine, present in circulating platelets

(extra: acts as neurotransmitter in CNS)

A

serotonin

36
Q

C3a and C5a protein function

A

vasodilation and permeability

37
Q

complement protein that is a powerful chemotactic agent for neutrophils

A

C5a

38
Q

prostaglandins and leukotriene function

A

mediators of acute inflammation

  • prostaglandins inhibited by aspirin (an anti-inflammatory)
  • leukotrienes involved in immune response
39
Q

characteristics of chronic inflammation

A
  • infiltration by monocytes and lymphocytes
  • 24 hours for maximum infiltration, persists for weeks
  • functions: phagocytosis, secrete cytokines, kill virus-infected cells, etc
  • often due to immune response
40
Q

all leukocyte traffic requires adhesion between:

A
  • leukocytes and surface of opposing cells
  • leukocytes and extracellular matrix proteins
  • mediated by cell surface adhesion molecules
  • requires cytokines (chemotactic) as initial step
41
Q

______ on neutrophils and monocytes bind to _____ on endothelial cells

A

Mac-1 on neutrophils and monocytes bind to ICAM-1 on endothelial cells
(integrins that help leukocytes exit the bloodstream to find the area of inflammation)

42
Q

integrin presented by lymphocytes in order to bind to ICAM-1 on endothelial cells

A

LFA-1 is the integrin shown on lymphocytes

Mac-1 is shown on neutrophils and monocytes

43
Q

selectin function

A

mediates adhesion to ligands shown on endothelial cells at sites of inflammation

44
Q

key features of selectin-mediated adhesion

A
  • rapid on-rate

- low bind affinity, too weak to stop cells in shear of flowing blood (hence the rolling)

45
Q

major regulatory molecule of angiogenesis

A

VEGF

Vascular Endothelial Growth Factor

46
Q

major stimulatory molecule of fibrogenesis

A

TGF-beta

Transforming Growth Factor-beta

47
Q

characteristics of neoplasms

A

clonal - derived from a single cell

proliferative - they grow

48
Q

HER2 is overexpressed in what cancers? How is it activated?

A

HER2 is an oncoprotein that is overexpressed in breast and gastric cancers.
Activated by amplification

49
Q

genetics of gametes (sperm or ovum) that can be passed down (also non-tumor cells)

A

germline

50
Q

refers to the genetic composition of cells other than gametes, cannot be passed to offspring

A

somatic

51
Q

condition that occurs in families - can be genetic or lifestyle-related

A

familial

52
Q

present at birth (may or may not be genetic)

A

congenital

53
Q
  • chromosomal germline disease
  • most common genetic cause of developmental delay
  • sporadic (meiotic nondisjunction in ovum in 95% of cases - low risk of recurrence)
A

trisomy 21 - down syndrome

54
Q

describe marfan syndrome

A
  • mendelian autosomal dominant disorder
  • if heterozygous, can result in haploinsufficiency, dominant negative effect, and gain-of-function

-mutation in fibrillin gene (FBN1) that then decreases structure of connective tissue and allows TGF-beta to destroy ECM

55
Q

advantages of next generation sequencing

A
  • highly multiplexed sequencing
  • higher analytical sensitivity
  • markedly decreased cost per base sequenced
56
Q

autosomal dominant mendelian disorders

A

if the trait is carried in heterzygous fashion, the disease may manifest
haploinsufficiency
dominant negative effect
gain of function

If one parent is affected, 50% chance of offspring will be affected

57
Q

the amount of wild-type protein is insufficient to perform normal function

A

haploinsufficiency

58
Q

mutant protein is nonfunctional and interferes with the function of the wild-type protein

A

dominant negative effect

59
Q

mutation introduces new function of the altered protein or increases wild type function with deleterious sequelae

A

gain-of-function

60
Q

Liver function tests

A

Transaminases - AST and ALT
Biliary enzymes - Alk Phos, GGT

-not true tests of liver function - liver enzymes that are released when it is damaged

61
Q

chronic hepatitis B histology

A
  • ground glass hepatocytes
  • sanded nuclei hepatocytes
  • portal inflammation
62
Q

chronic hepatitis C histology

A
  • macrovesicular steatosis (fat droplets)
  • portal lymphoid aggregates
  • bile duct injury/damage
63
Q

gallstone risk factors

A

fair: white population
fat: BMI >30
female
fertile: one or more children
forty: age > 40

64
Q

conditions for pathologic autoimmunity

A
  • presence of autoimmune rxn
  • evidence that it is not due to tissue damage
  • absence of another cause of disease
65
Q

breakdown in self-tolerance

A

pathologic autoimmunity

66
Q

classic example of type 2 cytotoxic reaction

A

blood transfusion reaction

67
Q

Goodpasture’s disease

A

aka Anti-GBM antibody disease
-patients make an ab to alpha-3 chain of type 4 collagen
-collagen is present in the lung
Patients have glomerulonephritis and pulmonary hemorrhage

68
Q

what are the type 2 cytotoxic diseases

A
  • pemphigus vulgaris
  • bullous pemphigoid
  • dermatitis herpetiformis
  • anti-GBM/Goodpasture’s
69
Q

what are the non-cytotoxic reactions?

A

1) thyrotoxicosis (Grave’s)

2) myasthenia gravis

70
Q

clinical features of grave’s disease (type 2 non-cytotoxic rxn)

A

increased thyroid hormone (T3, T4) secretion > hypermetabolic state:
heat intolerance, weight loss, hyperreflexia, protruding eyes

71
Q

clinical features of myasthenia gravis (type 2 non-cytotoxic rxn)

A

skeletal muscle acetyl choline receptors are blocked or bound by ab.
This causes blocking of neuronal impulse transmission across neuron-muscular junction = muscle weakness

72
Q

clinical features of systemic immune complex diseases (type 3)

A
  • fever
  • urticaria (itchy, swollen skin)
  • arthralgias (joint pain)
  • proteinuria and hematuria (glomerular injury)
  • lymphadenopathy
73
Q

describe type 3 immune complex rxn

A
  • abs (IgG, M or A) form against foreign or self antigens in circulation or localized in tissue
  • complement system is activated > PMNs, swelling, tissue destruction, positive feedback loop
74
Q

examples of Type IV T-cell mediated rxns

A

effector cells: t-cell-activated macrophages

ex: TB skin test rxn, TB, fungal infections

75
Q

Type IV delayed hypersensitivity time course:

A

local erythema and induration occurs after 8-12 hours

-rxn peaks after 2-7 days and slowly subsides

76
Q

type IV granulomatous hypersensitivity time course

A

requires weeks to months to develop and may resolve slowly or persist indefinitely (ex: TB granuloma)

77
Q

autoantibodies in SLE (systemic lupus erythematosus)

A

ANA - present in 95% lupus pts, diagnostic criterion.

Anti-native DNA and anti-Sm: specific for SLE

78
Q

granulomatosis with polyangiitis

A
  • type II
  • aka ANCA-associated vasculitis
  • anyone can get it
  • mostly white
  • median age 41
  • Wegener’s triad:
    1) necrotizing granulomatous vasculitis
    2) focal segmental glomerular nephritis
    3) necrotizing vasculitis of median and small vessels
  • open lung biopsy gold standard for diagnosis
79
Q

test for granulomatosis with polyangiitis

A

ANCA- antineutrophil cytoplasmic antibody test

-90% is c-(cytoplasmic)ANCA

80
Q

example of mendelian autosomal recessive disease

A

cystic fibrosis
-blocked airway, pancreatic duct, bile canaliculi, decreased Cl reabsorption in sweat ducts
Testing: next gen sequencing

81
Q

fragile X syndrome

A
  • X-linked genetic disorder
  • aka trinucleotide repeat disorder
  • 2nd most common genetic cause of developmental delay (1st is trisomy 21)

Human Pathology (2 decks)

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