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JG > Pathophys block 1 > Flashcards

Pathophys block 1 Flashcards

1
Q

Epidemiology

A

is the study of causes, patterns and effects of diseases and health conditions in a given population.

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2
Q

Epidemiology importance

A

This scientific study allows for research of different conditions with the goal of developing preventative methods and identifying risk factors for the condition.

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3
Q

etiology:

A

cause of a disease

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4
Q

-pathogenesis:

A

mechanism that causes the disease

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5
Q

-patho=disease + physio= function + logy= study of—>

A

How disease processes work to cause dysfunction in the body.

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6
Q

congenital- cause of disease

A

something you are already born with and present when born
Ex: Down syndrome
Ex: birthmark

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7
Q

metabolic- cause of disease

A

our body processes. Partly impacted by the food we eat, genetics and ethnicity.

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8
Q

degenerative/drug induced

cause of disease

A
  • degenerative: changes as we age

- drug induced: could be recreational drugs or drugs taken under the provision of a provider.

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9
Q

neoplastic: Neoplasm

A

= “new growth” - uncontrolled growth of an abnormal cell line. May be benign or malignant (cancer) (SM,Ch. 1)

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10
Q

immunologic/autoimmune: cause of disease

A 
3 catergories of immunologic disease: 
over reaction (hypersensitivity), 
under reaction (immune deficiency as in AIDS) and autoimmune.
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11
Q

Autoimmune cause of disease

A

destruction of one’s own tissues by antibodies produced by one’s own immune system

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12
Q

infectious/inflammatory: cause of disease

A

diseases that are usually secondary to a primary disease, such as infection or autoimmune (SM, Ch.1)

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13
Q

nutritional: malnutrition – cause of disease

A

not enough resources for the body – can create disease. “Deficient protein means a decrease in osmotic pressure, a decrease in healing or formation of body tissue, or a decrease in antibody production. Vitamin or mineral deficiencies can lead to interference in tissue integrity or in biochemical reactions of metabolism” (SM: CH.1)

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14
Q

traumatic: cause of disease

A

physical force that mechanically disrupts the structure of the body which can disrupt function. Result is often called an injury

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15
Q

genetic: cause of disease

A

disease is due to transmission of defective genes or chromosomes from one or both parents

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16
Q

psychological/somatic: cause of disease

A

psychological factors are associated with and precede the condition. Physical symptoms are not intentionally produced or feigned, but are the result of psychological factors.

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17
Q

Iatrogenic: cause of disease

A

Illness caused by medical examination or treatment. Provider or treatment induced

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18
Q

Idiopathic: cause of disease

A

Disease or condition is one whose cause is unknown or arises spontaneously

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19
Q

Vascular: cause of disease

A

Includes any condition that has to do with your circulatory system

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20
Q

Organic: cause of disease

A

A disease resulting from recognizable anatomical changes in an organ or tissue of the body. It’s a manifestation of your own body, not caused by something external

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21
Q

signs:

A

objective findings, these are things the provider is able to see (swelling, cyanosis, heart rate)

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22
Q

symptoms/symptom complexes:

A

subjective findings, these are things the patient describes to the provider (nausea, abdominal pain, blurred vision).

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23
Q

syndrome:

A

is a set of symptoms that occur together and suggest a certain disease is present, or the patient has an increased chance of developing the disease.

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24
Q

asymptomatic:

A

No symptoms present

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25
Q

exogenous: stages of disease

A

Originating from outside the organism

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26
Q

endogenous: stages of disease

A

produced or originating within/inside and organism

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27
Q

complication: stages of disease

A

an unanticipated problem that arises after a procedure, treatmeant, or illness.

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28
Q

sequela (sequelae): stages of disease

A

a condition that is the consequence of a previous disease or injury eg.(chronic kidney disease can be a sequela of diabetes

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29
Q

convalescence: stages of disease

A

The time of recovery after a disease or procedure

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30
Q

recurrence: stages of disease

A

The return of signs and symptoms or a disease after a remission

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31
Q

remission: stages of disease

A

when the signs and symptoms of a disease disappear, remission can be temporary or permanent

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32
Q

exacerbation: stages of disease

A

when symptoms of the disease increase in severity and become worse

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33
Q

prodrome: stages of disease

A

an early symptom that may be indicative of the start of a disease.

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34
Q

acute: stages of disease

A

rapid onset, severe symptoms, and a short course.

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35
Q

subacute: stages of disease

A

between acute and chronic in character, less marked in severity or duration than the acute state.

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36
Q

subclinical: stages of disease

A

Having an disease that has yet to manifest into any clinical symptoms (diseases like diabetes and hypothyroidsm are often subclinical before they surface as clinical diseases)

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37
Q

chronic: stages of disease

A

opposite of acute, having a long duration with little changes and slow progression of the disease.

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38
Q

Equilibrium:

A

A process or reaction occurs at the same rate in forward and backward directions. There is no net change in the composition over time.

Eg, leak channels for water (aquaporins) would be considered at equilibrium if there is no movement of water in or out of cell (due to equal osmolarities in and out of cell).

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39
Q

Steady state:

A

Can be thought of homeostasis for a specific mechanism.

Eg, Na/K ATPase (aka Na/K pump) using energy from ATP hydrolysis to “exchange” sodium ions (3 for 2) for potassium ions. This maintains a constant internal concentration of potassium putting potassium in a steady state.

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40
Q

Diffusion:

A

Molecules will move from areas of high concentration to low concentration using a protein channel. No energy required.

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41
Q

Facilitated diffusion:

A

Molecules will bind to a transporter protein in the plasma membrane, the protein will change configuration (shape), the molecule will enter/exit cell based on the properties of diffusion (from high conc. to low conc.). No energy required.

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42
Q

Primary active transport:

A

Using energy to move molecules “upstream” against concentration gradients.

Eg, Na/K pump relies on hydrolysis of ATP to move potassium and sodium against concentration gradients. Requires energy.

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43
Q

Secondary active transport:

A

Uses concentration gradients enhanced by primary active transport to move other molecules against concentration gradient.

Eg, Na/Glucose symport, using the increased concentration of sodium, from Na/K pump, outside of the cell, sodium binds with a transporter protein that also requires glucose. This allows glucose to move into the cell as well - against its concentration gradient. Does not directly require energy; does require actions of primary active transport.

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44
Q
  • Countertransport or antiport,
A

is when the solute is moving opposite direction of Na+

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45
Q
  • Cotransport or Symport,
A

is when the solute is moving out of the cell or the same direction as Na+

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46
Q

metaplasia: RE: NEOPLASIA

A

change of one matured cell type to another cell type based on external stimuli: a reversible process.

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47
Q

carcinoma in situ: RE: NEOPLASIA

A

the progression of malignant growth is as follows: hyperplasia, atypia, carcinoma in suti, primary cancer, and metastisis. At the stage of carcinoma in situ, there is abnormal growth of atypical cells, but they are IN PLACE. They are still where they are supposed to be. The standard for this stage is whether or not the growth has broken through the basement membrane of whatever tissue it is.

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48
Q

invasive carcinoma: RE: NEOPLASIA

A

abnormal cells have increased in motility and have been able to cross the basement membrane into surrounding tissue. They are still in the same location in that they have not spread to a different organ, just a different type of tissue.

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49
Q

metastatic carcinoma: RE: NEOPLASIA

A

the hallmark of malignancy. A cancer that has metastasized has increased motility to the point where it has left the site of primary cancer, traveled through the lymphatic system, into the vessels, and has found a new home and continued to divide grow

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50
Q

hypertrophy: RE: NEOPLASIA

A

increase in the size of a tissue or organ based on the increase in the size of the cells

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51
Q

neoplasm/neoplasia: RE: NEOPLASIA

A

abnormal mass of cells that grows at the expense of the host and is caused at least in part by genetic abnormalities of the involved cells

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52
Q

anaplasia : RE: NEOPLASIA

A

loss of differentiation. This is a very worrisome sign in oncology. Cells that differentiate show that the normal pathway of development is at least partly intact. Anaplastic cells do not go through development and are frequently mitotic. Anaplastic tumors are always malignant

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53
Q

adjuvant: RE: NEOPLASIA

A

systemic treatment given after local measures were taken. For example, in breast cancer, a patient could have surgery (localized treatment), but still undergo chemotherapy (systemic) in order to kill any cells that were possibly missed and avoid the statistical relapse

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54
Q

neoadjuvant: RE: NEOPLASIA

A

a neoadjuvant is an adjuvant therapy administered before the main treatment. It could be chemotherapy or hormone therapy given the type of tumor in order to atrophy the growth, thus making surgery a possibility or one that is more likely to succeed.

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55
Q

remission: RE: NEOPLASIA

A

in terms of cancer, remission indicates that there is no measureable disease activity. However, it is not said to be cured as the return of the cancer is possible or even probable

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56
Q

cure RE: NEOPLASIA

A

A time without recurrence of a disease so that the risk of recurrence is small.

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57
Q

a. oncogene RE: NEOPLASIA

A

genes that code for a growth factor OR
genes that code for receptors of growth factor

derived from mutations

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58
Q

b. tumor suppressor genes RE: NEOPLASIA

A

regulate cell growth thru interaction of their products with the products of growth stimulating genes.

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59
Q

hyperplasia RE: NEOPLASIA

A

tissue size increases
increase in number of cells
increase in DNA replication

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60
Q

dysplasia RE: NEOPLASIA

A

abnormality of development.

in pathology, alteration in size, shape, and organization of adult

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61
Q

latent:

A

The disease is present, but lying dormant

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62
Q

incubation period:

A

This is the time between the initial exposure to the disease and when the first signs and symptoms appear.

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63
Q

Symptom complexes

A

symptoms that are grouped together and are characteristic of a certain disease or condition.

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64
Q

major pathways by which benign neoplasms spread throughout the body.

A

Remain localized and inflict damage by encroachment on adjacent structures.

usually mobile upon palpation

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65
Q

major pathways by which malignant neoplasms spread throughout the body.

Seeding of Body cavaties

A

typically in peritoneal cavity

cancer cells grow nodular implants on surrounding organs and walls

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66
Q

major pathways by which malignant neoplasms spread throughout the body.

lymphatic spread

A

most common

follows stepwise fashion following natural routes of lymphatic drainage

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67
Q

major pathways by which malignant neoplasms spread throughout the body.

hematogenous spread

A

common in sarcomas (connective tissue cancers)

spread through venous (most common) or arterial routes

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68
Q

angiogenesis

A

tumor making own blood supply.

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69
Q

Variations in Normal : genetics

A

especially phenotypically, many varieties of “normal”; genotypically, may be predisposed to conditions/diseases, family history

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70
Q

Variations in normal : culture

A

what is normal to one culture may not be normal to another: diet, number of children, rituals; these can also be potential predisposing factors to disease

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71
Q

Variations in Normal age

A

different challenges face different age groups based on immune function, growth, bone/muscle wear and tear, ability to get around, etc.

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72
Q

Variations in Normal : gender

A

self identify, doesn’t have much to do with our risk for disease

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73
Q

Variations in Normal : Sex

A

organs born with more often determine what at risk for

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74
Q

Variations : stress:

A

different groups face different physical, mental, emotion and psychosocial stresses; prolonged increased stress can suppress the immune system

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75
Q

Variations : environment:

A

housing, school, state, regional, national identification can change what’s considered normal; these can also potentially pose exposure concerns that can predispose an individual

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76
Q

Variations in Normal : lifestyle:

A

usually choices, kids don’t have as much power over lifestyle– behaviors such as exercise, sleep, recreation, substance use can vary in what’s normal and what puts an individual at risk for health concerns

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77
Q

Osmosis -

A

movement of WATER MOLECULES across a membrane

(remember - water follows solutes!)

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78
Q

Iso-osmotic -

A

solute concentration is equal inside and outside of the cell - net movement of water is zero = no change in cell volume

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79
Q

Hyperosmotic

A
  • cell volume will decrease due to water leaving the cell into the extracellular space
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80
Q

Hypoosmotic

A

cell volume will increase due to water entering the cell from the extracellular space

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81
Q

Endocytosis:

A

regions of the plasma membrane invaginate and pinch off to form vesicles, enclosing a small amount of extracellular material into the cell.

82
Q

Exocytosis:

A

intracellular vesicles fuse with the plasma membrane releasing the contents into the extracellular fluid.

83
Q

Importance of Endo/Exocytosis in a clinical application:

A

Between the combination of endo- and exocytosis, the plasma membrane is replaced every hour. This is important when prescribing drugs that affect the membrane proteins, as the membrane will have 100% turnover in 1 hour.

84
Q

general causes of cellular injury

A

Please Give Our Cells No Irreversible Injury

Physical Damage
Genetic
Oxygenation 
Chemical 
Nutritional
Infectious
Immunological
85
Q

Cellular injury from Free radicals Examples

A

Lipid peroxide in membranes - Damage to membrane
oxidative modification in proteins - disconfigured proteins in almost anyway possible
lesions in DNA - Breaks in DNA or cross linking

86
Q

hypoxia-

A

less than normal amount of oxygen reaching cells/ hypoxemia- less than normal amount of oxygen in blood

87
Q

anoxia-

A

complete deprivation of oxygen due to no blood supply to tissue- leads to infarct.

88
Q

ischemia-

A

diminished blood supply to cell or tissue-

89
Q

phagocytic-

A

cells that take particles and substances into self for destruction(WBC- macrophage and neutrophils)

90
Q

degeneration

A
  • Mild or reversible structural changes of a cell. Breakdown that leaves some loss of function
91
Q

regeneration-

A

replacement of lost cells and tissue whose function is so similar to original lost cells that replacements are considered identical. Reproduction of same tissue as lost.

92
Q

induction

(of cell injury):

A

Plasma membrane loses permeability. Sodium and water into cell. Potassium out of cell. Cell swells-> calcium enters cell.

93
Q

effector

A

molecules which selectively bind to cells in process of apoptosis to induce degradation by phagocytosis for macrophages

94
Q

degradation

A

The break down of unnecessary or dysfunctional cellular components by lysosymes. In cell death it is an adaptive response to stress which promotes survival of surrounding cells

95
Q

Reversible Cell Injury:

A

Damage to the cell that results in dysfunction of normal cellular homeostasis, If the stress on the cell is abated, the cell can return to normal physiologic function.

96
Q

Examples of Reversible Cell Injury

A 
decrease in ATP production, 
increased membrane permeability, 
loss of membrane selectivity, 
osmotic pressure imbalance, 
ionic imbalance, 
defects in protein synthesis, 
cytoskeletal and DNA damage
97
Q

Irreversible Cell Injury:

A

“The point of no return” When a cell is no longer able to withstand stress. Usually an inability to reverse 1.) mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation) and 2.) profound disturbances in membrane function. Results in cell death from apoptosis or necrosis.

98
Q

Induction:

Of cell death

A

Influx of calcium -> membrane disruption leads to hydrolyzing of proteins and DNA cleavage. Feedback mechanism leads to death.

99
Q

Functions of Extracellular Receptors

A
  • binds chemical messengers endowing specificity
    - may have multiple binding sites
    - binding of the outside causes changes in enzymatic activity inside
100
Q

Functions of Transmembrane receptor domain

A

-contains hydrophobic portions of the receptor

101
Q

Functions of Intracellular receptors

A

-contains amino acid segments where the receptor can be phosphorylated, and thereby regulated, by intracellular substances

102
Q

Arachidonic acid (AA):

A

second messenger derived from polyunsaturated fatty acid of plasma membrane phospholipids; eicosanoid precursor

103
Q

Eicosanoids:

A

local mediators in cell damage and inflammation; metabolites of arachidonic acid

104
Q
  • Cyclooxygenase (COX)

-

A

enzyme mediates formation of prostaglandins and thromboxane (involved in pathogenesis of pain and fever)

105
Q

Lipoxygenase

A

(LOX) enzyme mediates formation leukotrienes and lipoxins (potent chemotactic agents involved in intense vasoconstriction, bronchospasm and vascular permeability)

106
Q

COX inhibitors:

A

Asprin and nonsteroidal anti-inflammatory drugs (NSAIDs); blocks production of endoperoxides, prostaglandins (PGE, PGA) and thromboxanes

107
Q

Phospholipase A2 inhibitor:

A

steroids; blocks all eicosanoid production

108
Q

LOX and leukotriene inhibitors:

A

used to prevent production and/or actions of leukotriene in

treating asthma

109
Q

general causes of cellular injury PHYSICAL

A

injury from exposure to electricity, radiation, barotrauma, mechanical stress, burns, excessive cold

110
Q

general causes of cellular injury GENETIC

A

DNA alterations that result in cellular defects can be inherited or acquired (de novo – new) genetic mutations

111
Q

general causes of cellular injury OXYGENATION

A

too little oxygen (hypoxia), total O2 deprivation (anoxia) or excess O2 can cause cell damage

112
Q

general causes of cellular injury CHEMICAL

A

drugs and toxins can disrupt biochemical cell function or physical cellular structure

113
Q

general causes of cellular injury NUTRITIONAL

A

either deficiency or excess of vitamins, minerals, or proteins can cause cell injury.

114
Q

general causes of cellular injury INFECTIOUS

A

damage to cells can result from infectious pathogens. An organism, its toxins or the body’s immune response to the infectious agent can cause cell injury.

115
Q

general causes of cellular injury IMMUNOLOGIC

A

deficient or exuberant immune response, autoimmune response (inability to recognize self from non-self

116
Q

Apoptosis

A

aka Programmed Cell Death (PCD) aka suicide genes: implicated in both normal and pathologic tissue changes. Apoptosis is much “cleaner” and chronological than necrosis.

117
Q

Necrosis

A

is premature cell death. When necrosis occurs it’s not tidy and the cells that die swell, burst and spill their contents all over their neighbors causing a likely damaging inflammatory response

118
Q

Coagulative tissue necrosis

A

· Well-defined, firm and pale; tissue maintains its architecture
· Seen in cells that have undergone hypoxia (except in the brain); indicates an infarct
Ex: embolus in renal artery

119
Q

Liquefactive necrosis

A

· Tissue has liquefied by enzymes from white cells (granulocytes), while surrounding tissue is fairly intact
· Seen in bacterial infections, some fungal infections and brain hypoxia
Ex: lung abscess

120
Q

Caseous necrosis

A

· “Cheese-like,” soft, yellow and crumbly
· Seen in Tuberculosis lung infections or fungus infections.
Ex: lung and lymph node with caseous necrosis

121
Q

d. Fat: necrosis

A

· Flecks or spotting of yellow gritty material
· Indicates pancreatitis
Ex: abdomen of patient with acute pancreatitis

122
Q

Gummatous necrosis

A

· Pink and dusty-red nodules or plaques that vary in size; accumulation of necrotic tissue develops gummy consistency; most commonly affects skin and mucus membranes
· Associated with tertiary syphilis
Ex: destructive lesion on forehead; some ulcers and abscesses present

123
Q

Hemorrhagic necrosis

·

A

dying tissue leasing to bleeding; Tumor Necrosis Factor
breaking down tissue and causing bleeding
Ex: malaria, brain, deceased colon with hemorrhagic
spots (pictured)

124
Q

Fibrinoid necrosis

·

A

cell loses outline and becomes homogenous and pink; fibrin-like appearance
· Seen in blood vessels of people with autoimmune diseases such as systemic lupus erythematosus, polyarteritis nodosa and rheumatic fever
Ex: blood vessel with polyarteritis nodosa

125
Q

Fat saponification necrosis

·

A

Chalky white areas within fat due to breakdown of fat into fatty acids and precipitation of calcium (see fat necrosis)
Ex: X-ray of precipitated calcium mass in breast tissue

126
Q

Wet gangrene necrosis

A

· Appears swollen, dark red and liquefied; foul odor and obscured
border between dead and viable tissue
· Seen in bacterial infection involving the necrotic area

127
Q

Dry gangrene necrosis

A

· Appears black, dry and shriveled with sharp demarcation from viable tissue
· Occurs in a necrotic tissue (usually a limb) that has undergone coagulation necrosis

128
Q

a. atrophy CELLULAR –

A

Decrease in size or number of cells due to aging, disuse or reduced/absent blood supply, hormonal stimulation or neural stimulation

129
Q

b. hypertrophy – CELLULAR

A

Enlargement due to an increase in the SIZE of cells (trophy for biggest cell) caused by increased work demands or hormonal stimulation

130
Q

c. hyperplasia – CELLULAR

A

Enlargement due to an increased NUMBER of cells caused by an increased rate of cellular division

131
Q

metaplasia – CELLULAR

A

Reversible replacement of one mature cell type by another less mature cell type

132
Q

dysplasia (atypical hyperplasia) – CELLULAR

A

abnormal change in size, shape and organization of mature tissue cells

133
Q

anaplasia – CELLULAR

A

loss of structural differentiation within cell or group of cells, microscopic hallmark of cancer

134
Q

Most common Parasites in world

A 
Helminths and Protozoa
Ascaris 
Hookworms 
Trichuris 
Entamoeba 
Plasmodia 
Enterobius
135
Q

Least common Parasites in world - but still prevalent

A 
Filarias 
Schistosoma 
Giardia 
Trypanosoma 
Leishmania
136
Q

Protozoa kingdom/type (and kingdom drawbacks)

A

Eukaryote/Unicellular

Bc they are Eukaryotic - Antiprotozoal drugs are also toxic to human host - making them hard to treat

137
Q

Protozoa Pathogenesis (2)

A

i. Intestinal and urogenital tracts

ii. Blood cells and tissues

138
Q

Protozoan traits

A

Only a few are pathogenic out of tens of thousands
Can be intracelluar or extracellular parasites
Dormant immotile cyst stage (survival of hostile environments)

Motile, actively feeding and reproducing vegetative stage

139
Q

Clinically relevant protozoa and how they move (in general)

Amebas

A

Extend cytoplasmic projections (pseudopodia, “fake feet”)

SOME have flagella

140
Q

Clinically relevant protozoa and how they move (in general)

Flagellates

A

Rotating whip-like flagella

Thus, liquid environment

141
Q

Clinically relevant protozoa and how they move (in general)

Ciliates

A

Synchronus beating of hair-like cilia

“Row-boat” motion, cilia arranged methodically like oars

142
Q

Clinically relevant protozoa and how they move (in general)

Sporozoa

A

Non-motile

143
Q

Helminths Kingdom/Type

A

Multicellular/Eukaryotic

144
Q

helminths preferred home in body

A

Have preferred sites of infestation, often the intestines with little damage
Can disseminate to vital organs (e.g. brain, lungs, or liver) with severe damage

145
Q

Helminth - global prevalence

A

Estimated at least 70% of the world’s population is infected with a parasitic helminth
In North America, helminth diseases becoming rare
Endemic in regions of world with poor sanitation and human fecal material is used in fertilizer

146
Q

helminth Infection starts with…

A

larvae in raw or undercooked pork, beef, fish
eggs in feces
transmission by insect bite
direct skin penetration

147
Q

helminth categories

A

cestodes (tapeworms)
nematodes (roundworms)
trematatodes (flukes)

148
Q

Cestode traits (3)

A

Ribbon-like, segmented worms primarily intestinal parasites

Absorb soluble nutrients from host (lack own digestive system)

Can grow up to 15 meters (yes, meters) in intestine

149
Q

Reason for clinical injury: cestodes (3)

A

Sequesters host nutrients
Excrete toxic waste
Mechanical blockage of intestine (large number in intestine)

150
Q

Trematodes (flukes) Traits (3)

A

Small, approx 1 cm, leaf-like worms
Infest various organs of human host
All parasitic trematodes use freshwater snails as an intermediate host

151
Q

Categorized as one of two kinds of flukes:

A 
Sexual flukes (schistosomes)
Hermaphroditic flukes
152
Q

Hermaphroditic flukes

A

Reproduce asexually in snail before maturing in seconday host

153
Q

Sexual flukes (schistosomes)

A

Schitosomes have separate distinct sexes unlike hermaphroditic flukes
Mating occurs in human liver

154
Q

Nematodes (roundworms) Traits and tissue invasion

A

Elongated, nonsegmented worms tapered at both ends
Distinguishing characteristic: have own digestive system, including mouth, intestine, and anus
Can invade almost any human tissue type

155
Q

Nematodes Categorized by

A

Infect intestine or non-intestine

Infectious at either the egg-stage or larval-stage

156
Q

Most common nematode infection in US:

A

Enterobiasis (Pinworm disease)

157
Q

helminth: ascarias lifecyle

A 
Eggs expelled in fecal matter. 
Mature in soil for 2-3 weeks before infections. 
Eggs ingested. 
Hatch in small intestine. 
Worms migrate to blood stream 
travel to lungs, 
up trachea 
swallowed.
158
Q

Helminth: Ascarias

Human Acquisition

A

Oral ingestion of eggs.

159
Q

Helminth: Hookworm lifecylce

A

Larvae excreted in feces.
Penetrate skin.
Travel via circulatory system to lungs.
Crawl up trachea and re-swallowed.

160
Q

Helminth: Hookworm

Human Acquisition

A

Skin penetration.

161
Q

Helminth: Pinworm lifecycle

A

Eggs deposited perianaly.
Ingestion of eggs.
Matures in colon.

162
Q

Helminth: Pinworm

human acquisition

A

Oral ingestion of eggs. (fecal - oral)

163
Q

Helminth: Trichinosis Lifecycle

A

Ingestion of meat containing cysts. Pigs contract from eating scraps of meat of other infected animals.

164
Q

Helminth: trichinosis

human acquisition

A

Ingestion of contaminated pork.

165
Q 
Helminth Filariasis (elephantiasis) 
lifecycle
A

Mosquito bite introduces larvae.
Larvae mature in lymphatics.
Can migrate to blood where are taken up by another mosquito.
Develop further larvae in mosquito and reinfect human.

166
Q

Hleminth: Filariasis

human acquisition

A

Mosquito Bite

167
Q

Helminth: Onchocerciasis, (river blindness)

Lifecyle

A

larvae - threadlike worms (microfilaria) develop into adults.
hang out in sub-cute tissue
Ingested by Blackfly.

168
Q

Helminth: Onchocerciasis, (river blindness)

human acquisition

A

Bite of Blackfly

169
Q

Protozoa ; Malaria (any Plasmodium sp)

lifecycle - phases

A

Exoerythrocytic (Hepatic) Phase

Erythrocytic Phase

170
Q

Protozoa ; Malaria (any Plasmodium sp)

lifecycle - Hepatic (exo-RBC) Phase

A

During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host

Sporozoites infect liver cells
mature into schizonts
which rupture and release merozoites

After this initial replication in the liver, the parasites undergo asexual multiplication in the erythrocytes.

171
Q

Protozoa ; Malaria (any Plasmodium sp)

lifecycle - Erythrocytic (RBC) Phase

A

Merozoites infect red blood cells

The ring stage trophozoites mature into schizonts, which rupture releasing merozoites (rings evident in RBCs for dianosis)

Some parasites differentiate into sexual erythrocytic stages

Blood stage parasites are responsible for the clinical manifestations of the disease.

172
Q

Protozoa: Giardia

Lifecycle

A

Ingestion of cysts. Multiplication within colon wall. Expelled in fecal matter.

173
Q

Protozoa: Malaria (plasmodium sp)

human acquisition

A

mosquito bite by anapholes mosquito

174
Q

Protozoa: Giardia

Human Acquisition

A

Contaminated H2O

175
Q

Protozoa: Leishmania

Life cycle

A

Bite of sandfly. Invade macrophages, reproduce, kill host cell. Re-ingested by sandfly.

176
Q

Protozoa: Leishmania

Human Acquisition

A

via sandfly

177
Q

Giardia lamblia
Signs/Symptoms:
Most commonly diagnosed intestinal disease in the U.S.

A 
Often asymptomatic. 
GI distress, 
greasy, fatty diarrhea, 
abdominal pain, 
nausea and vomiting.
178
Q

Giardia lamblia

Pathogenesis:

A

Infection usually results from drinking contaminated water. Infects duodenum.

179
Q

Giardia lamblia

Diagnosis

A

: Presence of cysts or trophozoites in stools or ELISA test to measure Giardia antigen.

180
Q

Giardia lamblia

Treatment:

A

Metronidazole (flagyl).

181
Q

Trichomonas vaginalis
Signs/Symptoms:
Most common protozoal urogenital infection in humans.

A

Females: yellow, malodorous discharge.

Males (infects less commonly): white discharge.

182
Q

Trichomonas vaginalis

Diagnosis:

A

Detection of trophozoites in vaginal or urethral secretions.

183
Q

Trichomonas vaginalis

Treatment:

A

Metronidazole (flagyl).

184
Q

Trichomonas vaginalis

Pathogenesis:

A

Sexually transmitted.

185
Q

Cutaneous leishmaniasis

Signs/symptoms:

A

Ulcerating skin sores.

186
Q

Cutaneous leishmaniasis

Pathogenesis

A

: Infection via sandflies.

187
Q

Cutaneous leishmaniasis

Diagnosis:

A

Tissue samples taken from ulcers examined in lab.

188
Q

Cutaneous leishmaniasis

Treatment:

A

Most cases heal spontaneously.

Pharmacological treatment difficult because of drug toxicity. Pentavalent antimonial first choice.

189
Q

Mucocutaneous leishmaniasis

Signs/symptoms:

A

lesions at mucosal-dermal junctions of nose and mouth.
Can spread into mucosal tissue, “obliterating” nasal septum and oral cavity.
High incidence of secondary infection, sometimes leading to death.

190
Q

Mucocutaneous leishmaniasis

Pathogenesis:

A

Sandflies

191
Q

Mucocutaneous leishmaniasis

Diagnosis:

A

Tissue samples taken from ulcers examined in lab.

192
Q

Mucocutaneous leishmaniasis

Treatment

A

: Pharmacological treatment difficult because of drug toxicity. Pentavalent antimonials first choice.

193
Q

Visceral leishmaniasis

Signs/symptoms:

A

Enlarged spleen and liver; jaundice. Most have minor symptoms.

194
Q

Visceral leishmaniasis

Pathogenesis:

A

Sandflies. Initially infects macrophages, which migrate to spleen, liver and bone marrow where parasite multiples.

195
Q

Visceral leishmaniasis

Diagnosis

A

Liver, spleen or bone marrow biopsy needed for definitive diagnosis, but serological tests can be suggestive.

196
Q

Visceral leishmaniasis

Treatment

A

: Pharmacological treatment difficult because of drug toxicity. Pentavalent antimonials first choice.

197
Q

Trypanosoma brucii species

Signs/symptoms:

A

Causes African Sleeping Sickness

Flu-like symptoms. Lethargy. Sleepiness.

198
Q

Trypanosoma brucii species

Pathogenesis:

A

Transmitted by the bite of the tsetse fly. Ultimately infects central nervous system causing inflammation. Fatal without treatment.

199
Q

Trypanosoma brucii species

Diagnosis:

A

Microscopic examination of blood, cerebrospinal fluid, or lymph aspirates for protozoa.

200
Q

Trypanosoma brucii species

Treatment:

A

Early: Suramin or pentamidine.

Late (with CNS involvement): Melarsoprol (HIGHLY toxic. 5-15% of people die from treatment alone).

JG (6 decks)

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