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Mechanisms of Disease BLD 204 > Exam 4 Objectives > Flashcards

Exam 4 Objectives Flashcards

1
Q

Define environmental disease

A

Disorders caused by exposures to chemicals or physical agents like radiation in the ambient, workplace, or personal environments

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2
Q

Define toxicology

A 
The science of positions
Distribution 
Effects 
Mechanisms
Physical agents
Medications can be positions if too much is taken
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3
Q

Define dosage

A

The amount of exposure to a substance.

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4
Q

Discuss the possible results of exposure to environmental toxins

A

Skin, lung, or GI absorption -> blood stream transport to tissues -> stored or excreted

Want excreted; stored can be a problem

Cell toxicity, repair, excretion

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5
Q

Discuss the sources and clinical symptoms to lead

A

Comes from contaminated air, food, and soil contamination; flaking paint

Everyone who is exposed is at risk; especially children

Children absorb more from food, have a more permeable blood brain barrier, taken up into developing bones and teeth because its in competition with calcium.

It interferes with enzymes involved in heme synthesis; causes anemia
Inhibits NA and K dependent ATPases = fragile RBCs
Inhibits bone healing

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6
Q

Discuss the sources and clinical symptoms to mercury

A

Sources of exposure: fish and dental amalgams (fillings)

Symptoms: tremor, gingivitis, bizarre behavior (“mad as a hatter”), birth defects from in utero exposure

Concerned with methyl mercury not ethyl mercury. Methyl mercury stays in the body. Ethyl mercury can be excreted.

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7
Q

Discuss the sources and clinical symptoms to arsenic

A

Naturally occurring in soil and water (mining), wood preservatives, herbicides

Large amounts cause GI, cardio, and CNS disturbances due to interference with oxidative phosphorylation - messes up the electron transport chain

Chronic exposure increases risk of basal and squamous cell carcinomas

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8
Q

Define pneumoconiosis and list the etiologic agents which most commonly cause these disorders

A

Fibrotic changes in the lungs that is not neoplastic or metaplastic due to chronic inflammation

Mineral dust: coal, asbestos, beryllium, smoking tobacco

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9
Q

List the types of cancer linked to cigarette smoking

A

90% of lung cancers are linked to smoking

Cancer of the mouth, esophagus, larynx, lung, pancreas, and bladder

Other problems: chronic bronchitis, emphysema, MI, peptic ulcer, atherosrerlosis

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10
Q

Explain how emphysema and smoking are linked

A

1

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11
Q

Describe the mechanisms of ethanol toxicity

A

Increases in NADH/NAD+ ratio
Leads to fat accumulation in the liver which causes lactic acidosis in smaller amounts

Acetaldehyde increases causes tachycardia and hyperventilation

Metabolism of ethanol releases ROS which causes lipid per oxidation in the liver

Release of endotoxin by GNB in intestine

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12
Q

Define adverse drug reaction

A

Untoward effects of therapeutic drugs given in proper settings

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13
Q

Explain the effects of cocaine on neurotransmission

A

Cardiovascular: vasoconstriction, tachycardia, fetal arrhythmias

CNS: seizures

Pregnancy: fetal hypoxia, spontaneous abortion

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14
Q

Contrast primary and secondary malnutrition

A

Primary: components are missing form the diet, not eating something that you should be

Secondary: malabsorption, impaired utilization of storage or too much is lost. Too high a dietary need
Bowel diseases that won’t let you absorb things correctly.

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15
Q

Compare and contrast Marasmus and Kwashiorkor

A

Both are protein-energy malnutrition

Marasmus; somatic protein depletion; loss of muscle mass. Visceral protein is protected. Albumin is normal. Emaciation, anemia, vitamin deficiencies, immune deficiency (T -cell deficient)

Kwashiorkor: lack of protein > total caloric reaction. Loss of protein is in the visceral protein. Hypoalbuminemia leads to edema, which masks weight loss. Not enough albumin to maintain fluid balance. Lesions, hair changes, fatty liver, vitamin deficiency, immune defects.

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16
Q

Discuss the function, metabolism and clinical symptoms of deficiency of vitamin A

A

Functions:
Normal vision at low light (human vision) - night blindness
Differentiation of cells into mucus secretors - end up with metaplasia
Immunity (resistance to infection, diarrhea)
Light protective
Antioxidants

Metabolism:
Ingested in food -> absorbed in small intestine -> transported and stored in the liver -> transported to tissue RBP -> oxidized to retinoid acid in peripheral tissues

Deficiency: 
Night blindness
Xerophthalmia
Squamous metaplasia of URT
Immune deficiency

Toxicity
Acute: hedge, vomiting, dizziness, blurred vision, stupor
Chronic: weight loss, anorexia, nausea, bone pain, joint pain, risk of fracture

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17
Q

Discuss the function, metabolism and clinical symptoms of deficiency of vitamin D

A 
Function: maintaining normal plasma levels of Ca and P - important for bone maintenance
Stimulates intestinal absorption of Ca
Stimulates Ca resorption in the kidney
Works with PTH to regulate blood Ca
Promotes mineralization of bone

Metabolism:
Absorption or production -> alpha1 globulin binding and transport to liver -> conversation to 25-OH-D in liver -> conversion to 1,25-(OH)-D in kidney -> functions

Deficiency: 
Rickets (in children)
Osteomalacia (in adults)
Weakens nones
More cartilage at the epiphysis - in children 
Masses of cartilage in marrow cavity 
Disrupted cartilage placement 
Too many capillaries and fibroblasts trying to heal weak and injured zones
Deformation fo skeleton
18
Q

Discuss the function, metabolism and clinical symptoms of deficiency of vitamin C

A

Functions: biosynthesis
Activation of enzymes that hydroxylated pro collagen, making for strong collagen
Antioxidant

Metabolism: Absorption

Deficiency:
Scurry - poor vessel support; bleeding from gums, skin, and joints
Impaired healing and adequate bone matrix formation

19
Q

Define obesity

A

Increased body weight due to adipose tissue accumulation that is of sufficient magnitude to produce adverse health effects

20
Q

List factors that may affect weight

A 
Genetics
Environment
Psychologic
Microbiome
Biochemistry 
Location of fat stores
21
Q

Discuss the function of leptin

A

Linked to fat stored being enough
Induces signals to reduce food intake and increase energy expenditure
Mutations can cause massive obesity

22
Q

List clinical conditions that are linked to obesity

A 
Insulin resistance
High triglycerides and low HDL
Certain cancers: esophagus, endometrium, gallbladder, kidney
NASH (non-alcoholic steatohepatitis)
Gallbladder stone increase
Respiratory problems
Osteoarthritis
Inflammation (chronic)
23
Q

List two essential roles of the microbiota in healthy individuals

A

Crowding out pathogens

Extracting energy and nutrients from food

24
Q

Discuss ways that human micro biome research may eventually influence clinical practice

A

Clinical monitoring and maybe management of your microbiome

25
Q

Briefly state the routes of entry microbes use to initiate infection

A 
Opportunists take advantage of suppressed immune system 
Breaks in the skin 
Inhalation 
Ingestion 
Sexual transmission
26
Q

List three ways microbes cause damage

A

Release enzymes that destroy tissue and allow spread of proteases in cancer cells
Release visions
Transport within nerves
Inflammation

27
Q

Describe three characteristics of bacterial virulence

A

Virulence - how infectious it is; what amount will make you sick
Adherence to host cells
Invasion of host cells
Delivery of toxins

28
Q

Explain how quorum sensing and biofilm formation can make bacteria more virulent

A

How bacteria communicate with each other. Bacterial communication regulates biofilm formation, swarming, toxin production
Biofilms are especially resistant to the immune system and antibiotic treatment: EPS

29
Q

Give two examples of bacterial adherence which contributes to virulence

A

Wide groups of proteins called adherions.
Pili: E.coli N. gonorrheae
Protein F: strep. pyogenes

30
Q

Describe how bacteria invade a cell

A

Take a ride on the immune system
Use complement/opsonization
Type III secretion system
Manipulates the cytoskeleton

31
Q

Describe and give examples of five types of bacterial toxins

A

Bacterial endotoxins: LPS
Found on the outer-membrane of gram negative bacterial. Too much LPS sets of a cytokine storm - inflammation

Exotoxins: enzymes/proteases. Toxins that alter a signal or regulation of a pathway. Super antigens. Neurotoxins. Enterotoxins

32
Q

Describe three situations when the host response to bacterial or viral infection causes damage

A

Granulomatous inflammation: TB
Liver damage in HBV, HCV
Post-streptococcal glomerulonephritis - immune complexes; causes kidney issues

33
Q

Describe how microbes avoid detection by the host immune system

A 
Antigen variation 
Manipulating the immune response (down regulating MHC and up regulating homologues)
MHC-1 deletion causes escape from CD8+
Lack of MHC-1 causes NK cells to kill 
Resistance to innate defenses
Resistance to AMPs
Resistance to phagocytosis
Viral fighting of interferons, blocking apoptosis
34
Q

State two major groupings of viruses based on nucleic acid content.

A

RNA and DNA

35
Q

Explain how a virus enters a cell

A
  1. Virus attaches tot he cell membrane through protein invaded in tropism
  2. Virus enters the cell
  3. Virus moves to the site of replication within the host cell. Virus genome is released
  4. Viral replication
  5. Viral assembly and maturation
  6. Viral release from the host cells (virions)
36
Q

State the effects of a viral infection on a cell or tissue

A

Direct effects of virus on host cell:
Damage or kill
Persist without injuring (persistent infection)
Transform the cell (cancer)

Host tissue reactions to above changes
Lots of necrosis and inflammation

Responses of the immune system - acute phase response from the liver (systemic effect)

37
Q

State one main outcome from an acute productive viral infection and the effects on the cell and host

A

Active replication is happening
New viruses are being released by lysis or apoptosis
Acute illness/fever/cell death
Clear or die

38
Q

State the 4 situations that can results from the failure to eliminate a virus and what the effect is on the host

A
  1. Latency
  2. Chronic infection
  3. Persistent and slow infection
  4. Oncogenic outcomes
39
Q

State the 3 types of interferons and their sources

A

INF-alpha (leukocytes) Type I
IFN-beta (fibroblasts) Type I
IFN-gamma (T lymphocytes) Type II

40
Q

State the facts of interferons on a virus/virally infected cell

A

Interferons are specific.
Appear after infection
Inhibit viral replication
Triggers kinase activity which leads to transcription of genes that block viral infections
Does not inhibit viral attachment or entrance to the cell
Block mRNA translation by increases adenine trinucleotide which activates ribonuclease to cleave mRNA
Inactivates a protein initiation factor, inhibiting protein synthesis

41
Q

Define and recognize tropism

A

Binding or viral surface proteins to specific host cells proteins
HIV and CD4+ cells
In HIV there is a lack of CD4+ cells due to the infection killing them

Mechanisms of Disease BLD 204 (9 decks)

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