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140 Cards in this Set

  • Front
  • Back
axon synapse with dendrite
axon synapse with cell body
axon synapse with axon
dendrite synapse with axon
dendrite synapse with dendrite
dendrite synapse with cell body
cell body synapse with axon
cell body synapse with cell body –uncommon, between efferent nuclei
Proprioception – internal joint and tendon neurons in the dorsal horn
skin sensory neurons in the dorsal horn
GI related, taste, smell neurons in the dorsal horn
GI, bladder, heart, vessels neurons in the dorsal horn
preganglion of ANS vetranl horn motor neurons (output assoc. OA and LMN)
– branched arch of skeletal m. – chew, pharynx, larynx ventral horn motor neurons (output assoc. OA and LMN)
somite-derived muscles of head and body, motor activity ventral horn motor neurons (OA and LMN)
higher levels of the brain that allow conscious interpretation and memory
Central Procession
distorted map of head and body surface proportional to density of cortical neurons that process sensory afferents from periphery
Sensory Homunculus
the process of sensing pain, receptors are called nociceptors
Receptors are activated in response to active or impending tissue injury.
Nociceptive Pain
Pain that arises from direct injury to nerves.
Neuropathic Pain
afferent nociceptor fibers that sense fast pain, mechanical stimuli
A? fibers
afferent nociceptor fibers that sense slow-wave pain – slower onset or longer duration; chemical , persistent mechanical, persistent thermal
C fibers
extreme sensitivity to pain
time of endurance (or maximum intensity) before the person wants to do something about the pain
influenced by: psychological, cultural, familial, environmental factors
pain tolerance
the point at which noxious stimulus is perceived as pain
pain threshold
pain that is perceived to be at a different point than the point of origin
referred pain
superficial structures; skin and subcutaneous; sharp, bright, burning; slow or fast onset
periosteum, muscles, tendons, joints, blood vessels; diffues; radiation of pain sometimes
deep somatic
visceral organs; transmitted by small unmyelinated fibers; ANS nervous responses of nausea, vomit, sweat, pallor, sometimes shock
Visceral (splanchnic)
less than 6 months. Anxiety and secondary reflex musculoskeletal spasms; intermittent or persistent.
disease or injury to peripheral nerves. Intractable sensory disturbances. Numbness, parasthesias, pain. Persistent or intermittent. Stabbing, jabbing, burning, shooting
severe, brief, sometimes repetitive attacks of sharp shooting or throbbing pain. Along the spinal or cranial nerve. Trigeminal nerve. Postherpetic nerve.
reflex sympathetic dystrophy
trauma to a nerve, soft tissue, broken bone
Complex Regional Pain Syndrome I
– reflex sympathetic causalgia
trauma to a nerve, soft tissue, broken bone
Complex Regional Pain Syndrome II
a type of neurologic pain
Phantom Limb
unicellular organisms that have an outer coating or cell wall in addition to a plasma membrane but no or few intracellular organelles.
n Possess DNA but lack nucleus, mitochondria, etc.
fragments of the bacterial cell membrane (lipopolysaccharides) are responsible for temperature increase
exogenous pyrogens
1. Damage tissues at their sites of replication
2. release toxins that enter the blood which result in systemic symptoms
3. toxins that cause damage – food poisoning
Ways bacteria cause illness
rod bacteria that are spiral in shape
Lyme disease, syphilis
very small self replicating organisms less than 1/3 the size of bacteria
– Possess a cell membrane but not a cell wall thus immune to cell-wall inhibiting antibiotics such as penicillin and the cephalosporins
– Possess a small DNA genome
intracellular pathogens similar to viruses, but produce a rigid cell wall like bacteria
– Contain RNA and DNA like bacteria, but reproduce by asexual division
– Scavenge essential nutrients and ATP from the host
Rickettsia, chlamydiae, Ehrlichieae and coxiella
Consist of nucleic acid (either DNA or RNA) surrounded by protein coat.
DNA is inserted into the host’s DNA
lack both the enzymatic machinery for metabolism and the ribosomes essential for protein synthesis.
Viruses that have the ability to transform normal hosts cells into malignant cells during the replication cycle.

cervical cancer, kaposi's sarcoma
oncogenic viruses
These insert into the host’s DNA and remain dormant for years.

herpes, mono, cytomegalovirus
latent viruses
1. replicate, kill host cell and lyse it, releasing more.
2. lie dormant, and begin replication much later.
3. transform normal cells into malignant cells.
ways viruses cause illness
Which infections predominate in US?
viral, bacterial
Which infections predominate globally?
1. responsible for Creutzfeld-Jakob disease and Kuru in humans and bovine spongiform encephalopathy or mad cow disease in animals
2. an infectious agent that lacks DNA or RNA, lacks a cell membrane or wall, possesses no cellular organelles
3. a normal structural protein that is found in most cells but has an abnormal shape
These infections are usually self limiting; limited to skin or subcutaneous tissues.
Serious infections are initiated through puncture or inhalation.
protozoa, helminths and arthropods
worm-like parasites including roundworms, tapeworm, and flukes
– Acquired by ingestion of eggs
vectors of infectious diseases (such as mosquitoes, lice and fleas) as well as ectoparasites including mites (scabies), and lice (head, body, pubic)
unicellular animals with well defined cell membrane, nucleus and organelles – responsible for diseases such as malaria, amebic dysentery, giardiasis, cryptosporidiosis
the study of factors, events and circumstances that influence the transmission of infectious diseases among humans
incidence, portal of entry, source, symptoms, disease course, site of infection and virulence factors
how infectious diseases are classified
the number of new cases that occur in a defined population (eg., per 100000) over a period of time (yearly)
the number of active cases of an infectious disease at any given time
if the incidence and prevalence of an infectious disease are expected and stable
an abrupt and unexpected increase in the incidence of disease over endemic rates
spread of disease beyond borders
process by which a pathogen enters the body, gains access to succeptible tissues, and causes disease
Portal of entry
direct entry through a defect in skin or mucous membranes
Classic example include the STD’s
– can also include vertical transmission from mother to child
direct contact
entry through the oral cavity - classic examples include food poisoning (bacterial), fecal-oral ingestion of viral particles (hepatitis, Norwalk and Rotavirus)
bacterial, viral and fungal
location, host, object, or substance from which the infectious agent was acquired
an infection acquired from the host itself
opportunistic infection
infections that develop while hospitalized
nosocomial infections
infections acquired outside the hospital setting
community acquired
the signs and symptoms expressed by the host
n Also referred to as the clinical picture or disease presentation
Can be specific or nonspecific
an infectious disease can be divided into distinguishable stages after entry of the pathogen
Course of Infectious Disease
the pathogen begins active replication – may be short (hours) or prolonged (6 months – hepatitis)
the pathogen begins active replication – may be short (hours) or prolonged (6 months – hepatitis)
– the initial appearance of symptoms which may be quite vague
period when the patient experiences the maximum symptoms
characterized by containment of the pathogen and elimination – may last for days, weeks or months
– total elimination of the pathogen without residual signs or symptoms of the disease
– Notable exceptions include chronic infection, subclinical or subacute illness, fulminant illness
protracted illness continuously or sporadically over months or years – hepatitis C is a classic example of a chronic infection
chronic infection
diseases that progress from infection to resolution without symptoms
subclinical or subacute
diseases that have a protracted prodromal stage (chronic pyelonephritis) – patients are usually unaware they have a disease until very advanced
abrupt onset of severe symptoms with little or no prodromal stage – death frequently ensues
fulminant illness
a general term used to describe inflammation of a particular tissue without respect to bacterial, viral infection, or noninfectious causes
denotes substances in the blood
the presence of microbial toxin in the blood
sepsis, septicemia
substances or products that are generated by infectious agents that enhance their ability to cause disease
– These include toxins, adhesion factors, evasive factors and invasive factors
virulence factors
proteins released from bacteria that affect cell function
– Classically these include diptheria toxin which inhibits protein synthesis and botulism toxin that inhibits neurotransmitter release
- can induce bleeding and clotting by damaging endothelial cells – the cells that line all vessels
fragments of bacterial cell wall and thus classified as lipopolysaccharides
– contribute to the inflammatory process by acting as chemotactic factors, causing fever
process by which a pathogen attaches to the host
adhesion factors
pathogens employ extracellular polysaccharides, slime, and mucous to discourage phagocytosis
evasive factors
in order to do this, you need to recover the pathogen or find evidence of its presence from the infected site and document of the clinical signs and symptoms
antigen detection via antibodies
DNA/RNA detection
PCR polymerize chain reaction
ways to diagnose
antibacterial agents
anitiviral agents
antifungal agents
ways to treat infectious diseases
condyloma acuminata caused by HPV, associated with cervical cancer
genital warts
caused by HSH II; neurotrophic, highly-cantagious. Produce single or multiple vesicles that rupture.
Genital Herpes
Most frequently reported STD
causative agent: Neisseria gonorrhoeae
in men, purulent urethritis usually develops
Most commonly transmitted STD
difference here is because chlamydia frequently produce asymptomatic urithritis epididymitis, and prostatitis
People have the disease without knowing
causative agent: spirochete Treponema pallidum
3 stages of the infection: primary (lesions), secondary (general malaise, fever), tertiary (gummas, dementia)
Material of very low density that must be enclosed to keep together.No definite shape. No definite volume, but they completely fill a container. The volume of the container is the volume of the gas in it. A gas exerts a pressure on all sides of the container that holds it. Gas can be compressed by pressures greater than the pressure the gas on its container.
1 mol of gas at STP =
22.4 L
Pt = P1 + P2, ...Pn
daltons law of partial pressures
where, P - pressure, V volume, n #of mols, R universal gas constant (STP), T temp
ideal gas law
has less O2 and more CO2 than the environment
at this stage, a cell may leave the cell cycle and either remain in an inactive state or reeneter the cell cycle at another time.
most variable time 8 hrs. to a year
G0 phase
at this stage the cell is post mitosis.
DNA synthesis ends
RNA and protein synthesis
Cell growth
8 hours to a year
at this stage, DNA replication occurs and yields 2 sets of chromosomes
10 - 20 hours
S - Main Phase I
G1, S, G2
premitotic phase
DNA stops
RNA and protein synthesis - yes
2-10 hours
cell division
0.5 to 1 hour
Mitosis - (Main Phase II)
these control the entry and progression through the cell cycle, they are synthesized at specific phases and then degrade
these regulate cyclin-CDK complexes
CDK inhibitor proteins
programmed cell death
cell division for reproduction and to replace dying cells. The number is regulated so that the number of dying = number replaced.
cellular proliferation
ovum and sperm
these have 1/2 the normal number of chromosomes (haploid)
all cells except gametes
have both sets of chromosomes (diploid)
somatic cells
cells that cannot divide and reproduce
neurons, cardiac and skeletal muscle cells
well-differentiated cells
cells that continue to divide and reproduce
blood, skin, liver
progenitor or parent cells
naive cells that can be stimulated to enter a cell cycle and differentiate
undifferentiated stem cells
preset and programmed expression of genes at certain part of cell growth to “turn on” specific new genes for discrete cell types
cell differentiation
one differentiated cell per stem
fertilized egg
small number of differentiated cell types per stem
many differentiated cell types per stem
new, uncoordinated growth; relatively autonomous; lacks normal regulatory controls of cell growth and division. Tends to keep growing. Growths serve no useful purpose, do not occur in response to an appropriate stimulus, and continue to grow at the expense of the host.
neoplasm; neoplasia
cancerous; undifferentiated (do not resemble tissue of origin), invading, can’t break off – metastasize
noncancerous; well differentiated (resemble tissue of origin), usually non-invading, non-metastasizing (not breaking off into pieces, not spreading).
swelling caused by many things including inflammation, trauma, neoplasms
malignant tumor of epithelial tissue
malignant tumor of mesenchymal origin
benign microscopic or macro finger-like projections on surface
marked neopplastic changes in cells that are found localized to tissue of origin before invasion
cancer in situ
grow by expansion
infiltrate and invade surrounding tissue; synthezise and secrete enzymes that breakdown proteins
cancer cells get into body spaces - peritoneal, pleural, pericardial, joint
secondary tumor in a different location; lymphatic spread; hematogenic spread; some types of preferential spread (like prostate to bone)
length of time for total mass to double in cell number
doubling time
process by which a normal cell is transformed to a malignant cell following exposure to carcinogenic agents
a term to describe how a normal cell becomes a cancer cell
1. DNA damage (mutation) from exposure
2. unregulated growth promoters
3. development of malignant tumor
initiator - promotion - progression model
process by which a normal cell is transformed to a malignant cell from dysfunction of genes that control cellular growth (mutated from proto-oncogenes) or that suppress tumors (inhibit cell proliferation)
oncogene and tumor supression gene model
1. viruses
2. environmental factors (carcinogens)
3. inheritance of defective gene
4. in vivo conversion of proto-oncogene to oncogene
Methods of triggering cancer