Brainscape's Knowledge GenomeTM

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


See full index

PHRM824 > Exam 4 General Info > Flashcards

Exam 4 General Info Flashcards

1
Q

What is cell injury?

A

When the cells are stressed to the point that they are unable to adapt

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

What is apoptosis?

A

A programed cell death

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

What is necrosis?

A

A injury causing cell death that isn’t planned after the point of irreversibility

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

What is hypertrophy?

A

An increase in cell size

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

Where does hypertrophy occur?

A

It occurs in cells that are incapable of dividing (striated muscle cells in the skeletal muscles and the heart)

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

What commonly causes increased workload in hypertrophy?

A

Physiological stimuli or pathological conditions

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

Hypertrophy is characterized by what 2 protein synthesis?

A

Mechanical triggers such as stretching
Hormonal triggers such as adrenergic hormones (fight or flight)

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

What changes in the uterus during pregnancy?

A

The cells go through hypertrophy and become enlarged

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

What is hyperplasia?

A

An increase in the number of cells but not size

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

What are 3 physiological examples of hyperplasia?

A

Proliferation of the female mammary epithelium during puberty
Profiferation of connective tissue cells during wound healing
Regeneration of the liver (physiologic compensatory hyperplasia)

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

Physiological hyperplasia in female hormones?

A

Estrogen, progesterone, prolactin

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

Pathological hyperplasia in female hormones and male

A

Can cause cancer with hormone imbalances

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

What is atrophy?

A

Shrinkage of the cell size by the loss of cell substance

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

What are the 5 things cause atrophy?

A

Decreased workload
Loss of innervation
Reduced blood supply
Inadequate nutrition
Aging (senile atrophy)

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

Atrophy causes a decrease in cell size which is caused by?

A

Increased protein degradation
Or reduced protein degradation

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

What is metaplasia?

A

One cell type is replaced by another cell adult type

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

What 2 things usually causes metaplasia?

A

Chronic irritation
Inflammation

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

Examples of metaplasia?

A

Ciliated columnar epithelial cells of the trachea and bronchi help clear foreign matter and mucus
In smokers and vitamin A deficiency ciliated columnar cells are replaces by squamous epithelial cells which are more rugged and not ciliated
This leads to coughing and an increase in infections
Another example is Barretts esophagus

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

What does metaplasia usually lead to?

A

usually a precursor for cancer
can be reprogramming a stem cell and dosent replace (they keep dividing)

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

What is dysplasia?

A

Organization of cell is lost, they vary in size, number, shape and organization

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

What is dysplasia associated with?

A

Chronic irritation
Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Dysplasia is a precursor for what?

A

Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q
  1. oxygen deprived (causes of cell injury)
A

Hypoxia - oxygen deficiency
Ischemia - loss of oxygenated blood supply to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q
  1. cause of cell injury
A

Chemical agents - posions, air pollutants, CO, asbestos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q
  1. cause of cell injury
A

Infectious agents - viruses, bacteria, fungi, parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q
  1. cause of cell injury
A

immunological reactions - autoimmune diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q
  1. cause of cell injury
A

genetic defects - sickle cell anemia, familial hypercholesterolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
  1. cause of cell injury
A

physical agents - trauma, heat, cold, electrical shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
  1. Nutritional imbalances (causes of cel injury)
A

nutritional deficiencies - calcium or vitamin
Excess nutrition
Diabetes - can be causes by obesity - excess blood sugar levels can damage cells
Atherosclerosis - can be caused by diet rich in fats - can result in blockage of arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
  1. cause of cell injury
A

Aging - accumulation of damaging reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does ischemia mean?

A

Decreased oxygen to a tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the characteristics of reversable injury?

A

Cells start to swell and get larger
Fatty change - see lipid vacuoles starting to form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the characteristics of ireversible injury?

A

Mitochondria dysfunction - no ATP
Membrane dysfunction - around organelles and around the whole cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Free radical formation leads to ?

A

Oxidation of cell structures and nuclear and mitochondrial DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Intraceullular Ca increase leads to ?

A

Enzyme, organelle, cytoskeleton depeltion / injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

ATP depletion leads to ?

A

Detachement of ribosomes from ER
Decreased protein synthesis
lipid deposition
Increase in anarobic metabolism
Glycogen storage and intracellular pH drops
decrease in sodium potassium pump
Increase of sodium and water in the cell
BAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

2 pathways of damage to the mitochondria

A

Apoptosis - by cytochrome c and other preapoptic proteins
Necrosis - mitochondrial membrane gets breached, inability to produce ATP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does cytochrome c do?

A

Precursor for apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Increase of ca in the cell?

A

Very bad causes many things to go wrong

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ROS (reactive oxygen species) impact what in the cell

A

Fatty acids
Proteins
DNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Can ROS be expelled?

A

Yes by SOD
Glutathione peroxidase
Catalase (in peroxisomes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Sequstration of free ionized iron and copper in ROS

A

Free ionized iron and copper can casue ROS and oxygen free radical production via Fenton reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What happens when there is a defect in membrane permeability?

A

Plasma membrane damage
mitochondrial membrane damage
lysosomal membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What happens when Bax or Bak gets oligomerizised or dimerized?

A

They lead to cytochrome c release after pore formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Bcl-2 family proteins

A

Bax, Bak and Bad proteins increase mitochondrial membrane permeability which are called pro-apoptotic proteins
Bcl-2 and Bcl-x are inhibitors of these which they are anti-apoptotic proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

When activated caspases active proteases what happens?

A

Degradation of cytoskeletal proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

2 things inflammation is responsible for?

A

inflammation is responsible for eliminating infection
inflammation is responsible for repairing damages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the classical signs of acute inflammation (5)

A
  1. heat (warmth)
  2. redness (erythema)
  3. swelling (edema)
  4. pain
  5. loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What happens inside of the capillary that can tell you there is inflammation (2)

A
  1. vascular changes
  2. cellular events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Functions of inflammation

A
  1. to improve the delivery of inflammatory cells to the injured/infected area tissue
  2. Vascular changes associated with inflammation
    A) Changes in vascular diameter and flow that results in reduced
    blood velocity
    a)vasodilation
    b)increased viscosity (thickness)
    c)margination - when the leukocytes slow down and gives it
    more chance to bind and help the site of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Functions of inflammation (part 2)

A

B. Increased vascular permeability
a) endothelial cells contraction/retraction leading to intercellular
gaps that leak fluid
b) direct endothelial injury
c) leukocyte dependent damage because of toxic mediators
released by leukocytes
d) increased fluid flow through endothelial cells is called (transcytosis) from vascular to tissues on the other side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What does transcytosis mean?

A

An increased fluid flow from vascular side to the tissues on the other side

53
Q

What are 2 effects of vascular changes

A
  1. Release of transudate (small holes)
  2. Release of exudate (bigger holes / proteins can escape)
    -> these events result in edema
54
Q

What does the Sialyl-Lewis X modified glycoprotein bind to

A

P-selectin or E-selectin

55
Q

What does the integrin on the leukocyte bind to?

A

Integrin ligand (ICAM-1)

56
Q

What does PECAM-1 do?

A

Helps aid the leukocytes into the site of infection

57
Q

What are the 4 receptors that lead to leukocyte activation?

A

GPCRs, Toll-like receptors, Cytokine receptors, Phagocytic receptor

58
Q

What does LPS do when bound to toll-like receptor?

A

Casues the production of downstream mediators

59
Q

What are the steps of phagocytosis?

A
  1. Recognition and attachment to the receptors
  2. Engulfment as the phagocyte zips up around the microbe
  3. Microbe becomes ingested and fuses with the lysosome to make a phagolysosome
60
Q

What is the pH of the lysosome

A

Very acidic ~4

61
Q

Full events through cellular inflammation

A
  1. migration and rolling (margination, rolling, p-selecting)
  2. Adhesion is mediated by Sialyl-Lewis glycoproteins and selectins
  3. firm adhesion (ICAM-1 and VCAM-1 help bind more tight)
  4. Transmigration (when the leukocyte goes through the vascular endothelial cells to the site of action)
  5. chemotaxis and activation (they keep releasing more chemokines to call more leukocytes to the affected area
  6. Phagocytosis (goes through the process of engulfing and fusing with the lysosome to degrade)
  7. Degranulation (When phagosome and lysosome fuse together and break down the contents)
  8. Phagocytosis stimulates an oxidative burst (results in OFR and ROS) They can make very strong agents which can break stuff down
  9. Proteins present in the lysosome also help destroy foreign bodies
    (lysozyme, hydrolases and elastases, defensins
62
Q

What are opsonins

A

key to a process called opsonization, they coat microbes and target them for phagocytosis

63
Q

What does nitric oxide produce?

A

Arginine production

64
Q

What inhibits phospholipase?

A

Steriods inhibit

65
Q

What inhibits cyclooxyrgenase ?

A

COX-1 and COX-2 inhibitors like aspirin

66
Q

What are COX1/2 inhibitors

A

Aspirin, ibuprofen, naproxen

67
Q

What are the COX-2 inhibitors

A

Celebrex, vioxx (more cronic pain)

68
Q

What does singular act as an agonist on?

A

It is a leukotriene receptor antagonist (causes vasoconstriction)

69
Q

What do TNF/IL1 increase?

A

Endothelial effects, fibroblast effects, systemic effects, and leukocyte effects

70
Q

Outcomes of acute inflammation

A

Can lead to chronic inflammation over time but most likely it gets resolved, can also lead to fibrosis which is loss of function and smaller capillaries

71
Q

How long does chronic inflammation last?

A

Weeks to months to years

72
Q

What differs in chronic inflammation than in acute inflammation?

A

Chronic inflammation has macrophages, lymphocytes, and plasma cells

73
Q

How do we defend from pathogens?

A

Physical and chemical barriers , innate and adaptive immunity

74
Q

Microbiome is what?

A

all of the bacteria in the intestine

75
Q

How can pathogens get into the skin and cause infection?

A

Can enter through wounds, burns, cuts, foot sores ect

76
Q

How can the skin defend against pathogens?

A

It has a dense ketatinized outer layer of skin
The outside layer has a low oH of 5.5
It has contents of fatty acid which inhibit micrbial growth

77
Q

How does the respiratory tract defend against pathogens ?

A

Muscus, swallowing, cillia
Phagocytotic killing by alveolar macrophages
Secreted antibodies

78
Q

How can pathogens get in the respiratory tracts

A

Express molecules to adhere to the respiratory tract (flu vaccine)

79
Q

Defenses in the intentional tract

A

Acidic pH
Vicious mucus secretions
Lytic pancreatic enzymes and bile detergents
Antimicrobial peptides called defensins
IgA
Normal gut flora

80
Q

How can pathogens break the intestional tract defenses and cause diseases

A

Bacteria can release exotoxins to damage the mucosa
Viruses can be resistant to bile and digestive enzymes
Fungo in immunocompromised hosts
Intentional protozoan rely on cysts for transmission
Intestinal helminths such as ascaris typically cause abstraction for the gut

81
Q

The normal defenses in ingested pathogens include …..?

A

Frequent urination
Low pH in the vagina cause catabolism of glycogen in the normal epithelium by commensal lactobacilli

82
Q

What are the ways that pathogens can get into the urogenital tract?

A

Hard to get male UTI’s because its longer than girls
Antibiotics can kill helpful female bacteria and make it more susceptible
Intercorse can break down some layers make it more susceptible to pathogens

83
Q

What are the 4 ways microbes can evade the immune defense?

A
  1. Remaining inaccessible to the host immune system
  2. Constantly changing antigenic repertoires
  3. Can resist some antibodies and can resist phagocytosis
  4. inhibit the MHC expression which will ultimately keep the infected cells instead of getting rid of them
84
Q

What are the 3 mechanisms of viral entry into host cells?

A
  1. Host-cell receptors for a particular virus
    a) HIV : gp120 binds to CD4 and to the chemokine receptors CXCR4 or CCR5
    b) Rhinovirus : binds to ICAM-1
    c) SARS-CoV-2 : spike proteins/ACE2 receptor
  2. Cell-type specific transcription factors that recognize viral enhancer and promoter sequences
  3. Physical barriers
85
Q

What is the mechanism of viral injury?

A

Virus binds, viral genome replication and mRNA synthesis, viral protein synthesis, the viral proteins will then get expressed and is trying to assemble another particle that will spread to another cell

86
Q

What are the mechanisms of viral injury?

A
  1. Lyse of host cells
  2. Immune cell-mediated killing
  3. Alteration of apoptosis pathways (also they can inhibit apoptosis which will keep the virus alive longer)
  4. Introduction of cell proliferation which will result in cancer
  5. Inhibition of host cell DNA, RNA or protein synthesis
  6. Damage to the plasma membrane
  7. Damage to cells involved in the antimicrobial defense, leading to secondary infections
87
Q

Mechanisms of bacterial injury?

A
  1. The ability of bacteria to cause disease, depends on its ability to adhere to host cells, invade cells and tissues, deliver toxins to damage the cells
  2. Bacterial adherence to host cells
  3. Virulence of intracellular bacteria
  4. Bacterial endotoxin (has an LPS that is a major component of the outer cell wall of gram-negative bacteria
  5. Bacterial exotoxins, cause the damage themselves`
88
Q

How can diphtheria toxin inhibit protein synthesis?

A

The toxin AB goes into the cell and once in an endosome A gets released and catalyzes ADP-ribose from NAD to EF-2 (the elongation factor) which inactivates the protein synthesis thereby killing it

89
Q

What are parenchymal cells?

A

Functional cells of the organ (hepatocytes, myocytes, renal tubular cells)

90
Q

What are stomal cells?

A

Cells that support the structure of organs (ECM, blood vessels, connective tissue)

91
Q

Tissue regeneration is ?

A

Replacement of injured tissue with cells of the same type and function.

92
Q

What is tissue repair ?

A

occurs when the extent or nature of damage cannot be reversed by regeneration alone

93
Q

When theres acute injury what happens?

A

Regeneration of the tissue (normal function)
or
Repair, scar formation

94
Q

What happens when there is persistent tissue damage?

A

Fibrosis (wont act the same again)

95
Q

What are the 4 stages of healing after a tissue injury?

A

hemostasis (minutes)
inflammation (hours)
proliferation (days)
remodeling (weeks to months) still susceptible to injury but takes awhile

96
Q

What do macrophages secrete in the stages of healing during tissue injury?

A

EGF epidermal growth factors

97
Q

Complete injury healing require both ….?

A

proliferation and remodeling

98
Q

What are the determinants of regeneration versus repair?

A
  1. the nature of cells injured
  2. the extent of injury
  3. the presence or absence of ongoing inflammation
  4. underlying diseases
99
Q

What is primary intention wound management

A

A cut that gets a staple and heals up

100
Q

What is secondary intention? (wound management)

A

There is inflammation that they let heal naturally but pack with gause and takes time

101
Q

What is tertiary intention? (wound healing)

A

Over time after an infection they eventually close it up when the infection is gone

102
Q

What drives proliferation?

A

Growth factors

103
Q

Can you modulate EGF?

A

Yes, there are many potential drug targets for modulating EGF signaling, which leads to porliferation

104
Q

What type of drug enhancer will you give someone to start proliferation

A

A drug that enhances EGF activity

105
Q

What are some of the components and functions of the ECM (extracellular matrix)

A

ECM is a growth factor depot
ECM provides signals for proliferation
ECM is related to tissue shape as well as provides mechanical properties
ECM provides anchorage for cells through various interactions
ECM is related to adhesion and cell spreading

106
Q

What are the growth factors that regulate fibrosis

A

PDGF
TGFb
FGF-2

107
Q

What disease state can impair wound healing?

A

Diabetes

108
Q

What is edema?

A

When there is excess fluid in tissues that can cause excessive swelling

109
Q

What are the three key elements of shock?

A

Life threatening condition
circulatory failure
inadequate oxygenation

110
Q

What are the 4 types of shock?

A

Distributive shock (vasodilation)
Hypovolemic shock (lose vascular volume)
Cardiogenic shock (wrong with the heart)
Obstructive shock (passage blocked)

111
Q

What is the most common type of shock

A

Distributive shock (vasodilatory shock)

112
Q

What causes distributive shock?

A

Sepsis #1 cause
Anaphylaxis
Neurogenic

113
Q

What is septic shock?

A

An infection in the blood that results in organ disfunction / 25-50% mortality rate

114
Q

What gram-negative bacteria mediates septic shock?

A

Endotoxin

115
Q

What does adrenomedullin do?

A

Binds to receptor and tightens junctions causing less stuff to get through, it can induce vasodialation making the sepsis worse.
Intravasuclar space is good thing
Interstitial space is bad thing

116
Q

What happens when you give an antibody that attaches to adrenomoedullin?

A

It stays in the intravascular space making it not able to move across to the interstitial space thereby not causing the sepsis to get worse

117
Q

Causes of hypovolemic shock?

A

hemorrhage
sever burns
serve vomiting, diarrhea

118
Q

How does hypovolemic start?

A

A loss of plasma or blood volume

119
Q

What can cause a hemorrhage?

A

hypothermia
coagulopathy (losing coagulation factors)
acidosis

120
Q

What casues cardiogenic shock?

A

myocardial infraction
ventricular arrhthmia
cardia myopathy (muscle weakens)
valvular disease (leaky valves)

121
Q

What causes obstructive shock

A

Cardiac tamponade
pulmonary embolism
pnemothorax (air not in the heart causing pressure)

122
Q

What can you physically see when someone is going through one of the 4 shocks?

A

low blood pressure
high heart rate

123
Q

What is edema

A

edema is an accumulation of fluid in the interstitial space of body tissues (subcutaneous / legs, pulmonary, cerebral)

124
Q

What is hydrostatic pressure?

A

Pushes fluid out of vascular space

125
Q

What is colloid osmotic pressure?

A

Moves fluid in to vascular space and out of the interstitial space

126
Q

What is transudate?

A

Protein poor

127
Q

What is exudate?

A

Protein rich

128
Q

What are the 3 ways drugs can cause edema?

A

Lymphatic drainage disruption
Increased capillary hydrostatic pressure
Increased capillary permeability

PHRM824 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions