Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology 1 > Unit Test 1 > Flashcards

Unit Test 1 Flashcards

1
Q

Agranulocytes

A

Monocytes/Macrophages

Lymphocytes, T-cells, B-cells, NKC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Macrophages that live in connective tissue

A

Langerhan cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cells that secrete mucous in nose and upper respiratory tract

A

Goblet cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Complement system

A

> 20 plasma proteins made by Liver (C1-C9)
Bind to microbial invaders
Form membrane attack complex
Attract phagocytosis cells (macrophages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Neutrophils

A

1st responders
Most abundant
Fungal, bacterial infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Eosinophils

A

Destroy parasitic worms

Elevated in allergic reactions(secrete histaminases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Basophils

A

Secrete histamine
Similar to mast cells
Receptors for IgE antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Monocytes/Macrophages

A

Phagocytosis
Act as antigen presenting cells (take to T helper cells)
Arrive after neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Natural Killer Cells

A

Part of innate
Recognize and kill tumor cells, cells infected with virus
As oppose to free floating pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lymphocytes

A

T and B cells (acquired immunity)
NKC (innate)

Most active in viral and chronic infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

CD4 T helper cells

A

Recognize pathogen, secretes cytokines

Activates B cell and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CD8 T killer

A

Cell mediated immunity
Similar to NKC but acquired
Eliminates intracellular pathogens such as virus by destroying cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T-suppressor cells

A

Suppress immune response

Possibly not working in autoimmune

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

B Lymphocytes

A

Humoral (antibody-mediated) immunity

T helper cells instruct B cell to differentiate into plasma cell and produce antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IgM

A

First responder

Acute problem, current infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IgG

A

Produced after IgM, well designed for pathogen
Lifelong immunity
Cross placenta, don’t last but help for 6 mo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IgA

A

Mucosal secretions: saliva, breast milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

IgE

A

Mediates inflammatory, allergic, parasitic response

Binds to and activates MAST cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

IgD

A

Not in blood stream, membrane bound to B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Granulocytes

A

Neutrophils, Eosinophils, Basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

5 signs of inflammation

A 
Heat
Swelling
Redness
Pain
Loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of atrophy

A

Disuse, dennervation, inadequate nutrition, loss of endocrine stimulation, ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hyperplasia

A 
Increase in number of cells
Physiological
-hormonal: increase in breast tissue
-compensatory: wound healing
Pathological
-often hormonal, benign prostatic hyperplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Metaplasia

A

Change from one mature, well differentiated cell type into another
Often result of chronic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Dysplasia

A

Immature/undifferentiated cells replace mature cells
Result of chronic inflammation
Often precursor to cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Apoptosis

A

Programmed cell death
Does not activate immune response
No cell debris

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Necrosis

A

Unregulated digestion of cell
Activates immune response
Products of cell death released into extra cellular space
Large area=gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dry gangrene

A

Interference with arterial blood supply to area
Line of demarcation
Area becomes dry, shrinks, and wrinkle
Slow progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Wet gangrene

A 
Interference with venous return
Area becomes swollen
Susceptible to bacteria infection
Must amputate
No line of demarcation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

4 steps of acute inflammation

A
  1. damaged tissues secrete cytokines>cause cells to produce cell adhesion molecules>damaged mast cells secrete histamine
  2. histamine causes quick transit constriction>dilation>capillaries become more leaky
  3. immune cells enter tissue
  4. platelets seal wound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hallmarks acute inflammation

A

rapid, transient response to injury
generally beneficial
predominance of neutrophils followed by macrophages

32
Q

Hallmarks of chronic inflammation

A 
self perpetuating(inflammation itself causes tissue damage)
predominance of macrophages and lymphocytes
proliferation of blood vessels
damaging: tissue destruction, fibrosis (scar tissue), loss of organ function, calcification
33
Q

Dystrophic Calcification

A

deposition of calcium salts in injured tissue
Ca comes from surrounding dead cells, blood, interstitial fluid
athlerosclerosis, hardening of arteries

34
Q

Metastatic Calcification

A

deposits of Ca occur in normal tissue due to high serum Ca

kidney stones

35
Q

Type I Hypersensitivity

A

Allergy
requires sensitization
involve IgE bond to mast cells and basophils
antigen binding triggers histamine release

36
Q

Type II

A

antigen = fixed & intrinsic to tissue where reaction occurs
IgG and IgM
eg autoimmune, blood transfusion, tissue transplant

37
Q

Type III

A

antibody, antigen complexes
free exogenous or endogenous antigen
IgG, IgM
eg strep complexes get stuck in KD

38
Q

Type IV

A

Not antibody mediated

eg TB, CD8 try to kill infected macrophages, tissue in surrounding area ends up getting damaged

39
Q

hypertrophy

A

increase in cellular size
from increased work load
physiological or pathological
skeletal and cardiac tissue(high BP)

40
Q

Prion

A 
protein without genome
B sheath shape cellular proteins that we can't break down
accumulate in the brain
eg BSE-mad cow
no treatment
41
Q

virus

A

DNA or RNA, NOT BOTH surrounded by protein coat

eg polio

42
Q

Bacteria

A

prokaryotic
both RNA and DNA
cell wall made of peptidoglycan (targeted by antibiotics)

43
Q

Bacteria naming by growth pattern

A

Strepto- chains
Diplo- pairs
Staphylo- clusters

44
Q

Bacteria by shape

A
  • cocci: round
  • bacilli: rod shaped
  • vibrio: curved like boomerang
  • spirilla: spiral
45
Q

Diptheria

A

corynebacterium diphtheria spread by water droplet
binds to cells of respiratory tract and releases exotoxin that leads to cell death
layer of dead tissue develops in upper respiratory tract

46
Q

Tetanus

A

Clostridium tetani (bacteria found in soil, dust, animal feces
exotoxin blocks inhibitory neurotransmitter release from spinal cord
spastic paralysis, “lock jaw”

47
Q

Lyme Disease

A 
Borrellia Burgdorferi (bacteria transmitted via tick bite)
antigen/antibody complexes get lodged in vessels, nerves, joints
classic lesion: bulls eye
cardias, neuro, arthritic problems
48
Q

Impetigo

A

caused by staph or strep infection
common in kids
red sores on face, honey crusted lesions, itchy

49
Q

fungus

A 
eukaryotic
cell walls made of chitin
cell membrane made of ergosterol (targeted by antifungals)
yeasts=unicellular, ie Candida
molds=multicellar
50
Q

Tinea or ring worm

A

superficial fungal infection

51
Q

Parasites

3 types

A
  1. Protozoa: eukaryotic, unicellular, human to human contact, i.e. malaria
  2. Helminths: wormlike, ie roundworms, tape worms
  3. Arthropods: ticks, mosquitos, lice, fleas, mites
52
Q

Incubation Period

A

pathogen is replicating b4 sx appear

53
Q

5 infectious disease stages

A

incubation
prodrome: vague sense of not feeling well
acute stage: max impact
convalescent stage: containment, repair
resolution stage: elimination of pathogen if possible,

54
Q

HIV/AIDS

A

retrovirus(RNA)
bodily secretion
attacks anything with CD4 marker: T helper cells and macrophage/monocytes

55
Q

HIV enzymes

A

Reverse transcriptase
Integrase
Protease

56
Q

HIV proteins

A

p24: used for testing, our body makes antibodies to this
GP 120: attachment, binds to CD4 marker
GP41: helps fuse membranes

57
Q

Seroconversion

A

enough antibodies to be detectable in HIV test, nothing to do with sx

58
Q

window period

A

time btw infection and seroconversion

59
Q

incubation period

A

time btw infection and sx

60
Q

HIV progression

A

acute flu like infection 1-4wk after infection
latent period: 5-10yrs
overt AIDS: opportunistic infections, ie pnuemonia

61
Q

Oral-Fecal Hepatitis

A

HAV, HEV

62
Q

Blood Borne Hepatitis

A

B, C, D

63
Q

HAV

A

abrupt onset, self-limiting, doesn’t become chronic
incubation: 15-50 days
vaccine available but not heavily pushed

64
Q

HBV

A

blood born, very contagious
can become chronic and lead to cirrhosis
vaccine available
incubation: 45-160 days

65
Q

HCV

A

blood to blood (IV)
chronic right off the bat, 85% develop cirrhosis
no vaccine
incubation: 14-180days

66
Q

HDV

A

need HBV to develop

common in IV drug users

67
Q

HEV

A

no chronic state

mostly in developing nation

68
Q

mechanisms of tumor development

A

increase proto-oncogenes, decrease tumor suppressor genes
abnormality in apoptosis
dont respond to cell density limitations
telomerase re-elongates telomeres

69
Q

benign neoplasia

A

well differentiated, slow dividing, non-invasive, enclosed in fibrous capsule

70
Q

malignant cells

A

undifferentiated, rapidly dividing, no fibrous capsule, invade surrounding tissues, metastasis via blood and lymph

71
Q

General sx, red flags of cancer

A

explained deep body pain, weightloss, fatigue, unexplained bleedin

72
Q

naming benign tumors

A

-oma

ie osteoma, adenoma

73
Q

naming cancerous tumors

A

ie adenocarcinoma, sarcoma

74
Q

metastasis

A

spread via blood and lymph systems leading to secondary tumors

75
Q

Paraneoplastic syndromes

A 
disease or sx beyond actual tumor site due to:
hormones secreted by tumor
cytokines released in response to tumor
production of clotting factors
neurotransmitter interference

Pathophysiology 1 (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions