FINAL CONTENT MEMORIZE

Question 1

Compare and contrast the pathology and symptoms of benign prostatic hyperplasia with prostate cancer

Answer 1

Benign Prostatic Hyperplasia (BPH): enlarged prostate gland → associated with urethral compression
● Mechanical obstruction: excessive growth of epithelial cells
● Dynamic obstruction: excessive growth of smooth muscle cells
○ S/S: urinary hesitancy, urinary urgency, increased urinary frequency, dysuria, nocturia, dribbling,
incomplete bladder emptying, straining when voiding

Prostate cancer: 2nd most common non-skin cancer in men → good prognosis
● Asymptomatic until advanced
● Risk factors: diet, hormones (androgen), vasectomy, chronic inflammation
● More than 95% are adenocarcinomas
● S/S: nocturia, increased void frequency, straining when voiding, weak urine flow

Question 2

What are the three systems of pain perception

Answer 2

Sensory/Discriminative System

Motivational/Affective System

Cognitive/Evaluative System

Question 3

Describe the Sensory/Discriminative System of pain perception

Answer 3

Identifies presence, character, location &

intensity of pain
Ex: OLD CARTS = description

Question 4

Describe the Motivational/Affective System of pain perception

Answer 4

Determines individual’s conditioned
avoidance behaviors & emotional responses to
pain
Ex: condition a child (teach first, to avoid
dangerous things) → “NO, don’t touch, HOT”

Question 5

Describe the Cognitive/Evaluative System of pain perception

Answer 5

Overlies individual’s learned behavior
concerning experience of pain → can
modulate perception of pain.

Ex: person tolerates injection despite knowing
it may hurt

Question 6

What is there difference between pain threshold, dominance, and tolerance

Answer 6

Pain Threshold: Lowest amount of stimuli perceived as pain

Perceptual Dominance: Pain at one location may cause an increase in
threshold in another location
Ex: Chronic back pain < twisted ankle

Pain Tolerance: The greatest intensity of pain a person can endure

Question 7

Describe how a person’s level of consciousness reflects their neurological function

Answer 7

Level of Consciousness: alert & oriented (person, place, time, & event)

○ Most critical clinical index of nervous system function
○ “Red flag” when LOC has been altered

Question 8

Describe how a person’s pattern of breathing reflects their neurological function

Answer 8

Pattern of Breathing: (rate, rhythm, pattern)
○ Post-hyperventilation apnea (PHVA) – ↓ LOC, brainstem centers regulate the breathing
pattern by responding only to changes in PaCO2, no apnea
○ Cheyne-Stokes respirations (CSR) – abnormal rhythm of ventilation w/ alternating periods of
tachypnea and apnea; ↑ PaCO2 = tachypnea; ↓ PaCO2 = apnea; cycles

Question 9

Describe how a person’s pupillary reaction reflects their neurological function

Answer 9

Pupillary reaction: ‘PERRL’ – measure pupillary size/reaction; Abnormal Findings: 1st assessment
→ size 3, reassess → size 5 = swelling + edema ⇒ potential TBI
○ Indicates presence & level of brainstem dysfunction
○ Brainstem – controls homeostatic functions (vitals)

Question 10

Describe how a person’s motor responses reflects their neurological function

Answer 10

Motor Responses: evaluates level of brain dysfunction/location of brain damage
■ Normal Findings: 5/5 → symmetrical movement & strength
■ Abnormal Findings: stroke on RT side of brain → LT weakness/paralysis
● Coma pt → pinch to observe for reflex/movement

Question 11

Describe how a person’s oculomotor responses reflects their neurological function

Answer 11

Oculomotor Responses:
○ Resting, spontaneous, and reflexive eye movements that change at various levels of brain
dysfunction in comatose individuals
■ Fixed, dilated pupils = bad
■ For coma pt: can move head (manually) side to side and open eyes
● CANNOT MOVE pt’s head w/ spinal cord or cervical injury = DANGEROUS!

Question 12

Describe how a person’s Vomiting, yawning, and hiccups reflects their neurological function

Answer 12

Vomiting, yawning, hiccups: complex reflex-life motor responses
○ Ex: brain injury → projectile vomiting w/ no pre-warning S/S (no fast heartbeat or salivation)
○ Hiccups/Yawning → not intentional; natural reflex/response

Question 13

Describe the 2 types of brain injury manifestations:

Answer 13

Contusions: mechanical shear stress to nerves & tearing of blood vessels (bruise in brain) → leads to
infarction, necrosis, hemorrhage, brain edema (involves frontal, temporal, or base of brain) → always
expect them to get bigger/worse

Hematomas: arterial bleeding → can happen anywhere: 3 types
○ Extradural: bleeding b/w dura & skull w/i 48 hr → edema, LOC changes, hemorrhage
○ Subdural: bleeding b/w dura and brain (varying onset times)
○ Intracerebral: bleeding w/i brain → ↑ ICP d/t expanding mass in brain

Question 14

Describe Extradural Brain Hematomas

Answer 14

bleeding b/w dura & skull w/i 48 hr → edema, LOC changes, hemorrhage

Question 15

Describe Subdural brain hematomas

Answer 15

Subdural: bleeding b/w dura and brain (varying onset times)

Question 16

Describe Intracerebral brain hematomas

Answer 16

Intracerebral: bleeding within brain → ↑ ICP d/t expanding mass in brain

Question 17

Describe “primary injury” to the brain

Answer 17

direct result of blunt/penetrating insult to brain (2 types: focal and diffuse)

Question 18

Describe the two types of primary injury

Answer 18

Focal brain injury
○ Force that impacts the skull → transmits to underlying tissues (ex: head hits dashboard in crash)

Diffuse brain injury –
physiologic & neurological dysfunction w/o substantial anatomic disruption → hallmark S/S:
amnesia
AND axonal damage Ex: Shaken baby syndrome: brain bounces in skull & breaks axon pathways

Question 19

Describe the 2 types of focal brain injuries

Answer 19

1. Coup injuries: something strikes the head → directly beneath point of impact (head hits
   dashboard & damages frontal lobe)
2. Contrecoup injuries: injury that occurs opposite from the site of impact (head
   ricochets back after hitting dashboard & causes damage to back of brain)
   ● Results in brain contusions and hematomas

Question 20

Describe the 2 types of Diffuse brain injuries

Answer 20

Concussion: physiologic & neurological dysfunction w/o substantial anatomic disruption → hallmark S/S:
amnesia
● CT scan may not show contusions/hematoma → diagnosis based on patient h/x of events
1. Mild concussion (Grades I-III): temporary axonal disturbance → confusion, disorientation,
momentary amnesia → range from no loss OC to brief loss OC (few min.)
2. Classic cerebral concussion (Grade IV): loss of consciousness (up to 6 hours) →
amnesia/confusion lasts from hours to days

Diffuse axonal injury (DAI): axonal damage → disruption of nerve transmission
● Shear/tear/stretch of nerve axons → severity determined by degree of shearing force (expansive
damage)
○ Ex: Shaken baby syndrome: brain bounces in skull & breaks axon pathways
○ S/S: coma, cerebral vasodilation → edema → ↑ ICP
○ May lack physical S/S (no bruises) → appears to be “just sleeping” → may never wake
up/recover

Question 21

What are the 3 methods of classifying the anemias

Answer 21

Etiology (impaired RBC production, acute/chronic blood loss, ↑ RBC destruction, or combo of
all the above)

AND

Morphology (size of cell or hemoglobin content)

Question 22

Words ending in -cytic indicate an RBC’s ____.

Answer 22

Size: end w/ -cytic
● Macro cytic → RBC larger than normal
● Micro cytic → RBC smaller than normal
● Normo cytic → RBC normal in size (usually ↓ RBC quantity)

Question 23

Words ending in -chromic indicate an RBC’s ____.

Answer 23

Hemoglobin content: end w/ -chromic
● Normochromic: normal Hgb amount (usually ↓ RBC quantity)
● Hypochromic: low Hgb amount

Question 24

What is Anisocytosis:

Answer 24

Anisocytosis: RBCs in various sizes

Question 25

What is Poikilocytosis

Answer 25

RBCs in various shapes

Question 26

Name some moderate signs AND severe signs of anemia

Answer 26

Moderate:
Fatigue
Weakness
Dyspnea
Pallor

Severe:
fainting, chest pain, angina, heart attack

Question 27

What type of anemia is classified as “microcytic-hypochromic”

Answer 27

Iron deficiency anemia:

○ Most common type
○ Causes: nutritional iron deficiency or blood loss of 2-4 mL/day (depletes iron stores)
○ Hgb reaches 7-8 = S/S seen → fatigue, weakness, SOB, pallor
○ Can lead to brittle/thin/spoon-shaped concave nails ( koilonychia), red/sore tongue, dry/sore
corners of mouth ( angular stomatitis)

Question 28

What type of anemia is classified as “macrocytic-normochromic”

Answer 28

Folate deficiency anemia:

○ Causes: not enough folate in diet→ dependent on dietary intake
○ Not dependent on any other factor
○ Common in alcoholics and chronic malnutrition
○ S/S similar to pernicious anemia; except neurologic manifestations (paresthesia) →
weakness, fatigue, etc.

Question 29

What type of anemia is classified as “macrocytic-normochromic”

Answer 29

Pernicious anemia:
○ Most common macrocytic anemia
○ Causes: lack of intrinsic factor from gastric parietal cells (associated w/ type A autoimmune
gastritis) → results in vitamin B12 deficiency
○ Early S/S nonspecific/vague → develops slowly over 20-30 years d/t chronic blood loss
■ Hgb reaches 7-8: weakness, fatigue, anorexia, sore tongue, weight loss, difficulty
walking, abd pain → should resolve after correcting Hgb
● Nerve demyelination leads to irreversible S/S → paresthesia (tingling &
numbness)

■ Fatal if untreated → leads to heart failure

Question 30

Describe Polycythemia vera:

Answer 30

“too much of everything” → abnormal/uncontrolled proliferation of RBCs,
WBCs, platelets
○ Genetic (JAK2) mutation that results in overproduction of blood cells
○ Manifestations d/t ↑ red cell mass & hematocrit
■ Thickened blood (increased blood viscosity) & hyper-coagulopathy
■ S/S: Redness of face, hands, feet, ears, headache, drowsiness, chest pain (angina 
decreased blood flow)
○ Treatment: therapeutic phlebotomy

Question 31

What does “leukocytosis, neutrophilia, eosinophilia, basophilia” all mean

Answer 31

WBC increase

Question 32

What does “leukopenia, neutropenia, eosinopenia, basopenia” all mean

Answer 32

Decrease in WBC amount

Question 34

Neutrophilia means

Answer 34

phagocytes, infection or inflammation

Question 35

Eosinophilia means

Answer 35

allergen or parasitic invasion

Question 36

Basophilia means

Answer 36

hypersensitivity rxn, inflammation

Question 37

Neutropenia means

Answer 37

↓ prolonged severe infection

Question 38

Eosinopenia means

Answer 38

surgery, shock, trauma, burns, mental distress

Question 39

Basopenia means

Answer 39

acute infections, hyperthyroidism, long-term steroid therapy

Question 40

What are the Types of Splenomegaly:

Answer 40

● Hypersplenism – normal function of spleen become overactive where splenomegaly is present

● Congestive Splenomegaly – accompanied by ascites (r/t liver disorders → cirrhosis), portal
hypertension, & esophageal varices

● Infiltrative Splenomegaly – engorgement by macrophages w/ indigestible materials; tumors & cysts

Question 41

Common causes of splenomegaly

Answer 41

● Hepatitis
● Mononucleosis – aka “kissing disease or Epstein-Barr virus”
● Salmonella
● Tuberculosis

Question 42

Describe the clinical manifestations of Alterations of Platelet Function:

Answer 42

an increased bleeding
time in the presence of a normal platelet count (takes longer to stop bleeding)
● Manifestations:
○ Petechiae
○ Purpura
○ Mucosal bleeding
○ Gingival bleeding

Disorders can be congenital or acquired

Question 43

Describe the clinical manifestations of Alterations of Coagulation

Answer 43

liver issues → important to our ability to make vitamin K
● Vitamin K Deficiency: vitamin K necessary for synthesis & regulation of prothrombin → procoagulant
factors (VII, XI, X) & proteins C & S (anticoagulants)
● Liver Disease causes broad range of hemostasis disorders:
○ Defects in coagulation (ability to stop bleeding)
○ Fibrinolysis (clot formation & breaking down clot)
○ Platelet # & function

Question 44

What is Essential (primary) thrombocythemia (thrombocytosis):

Answer 44

characterized by platelet counts >400,000/mm3

● Myeloproliferative disorder of platelet precursor cells
● Megakaryocytes in the bone marrow (cells are stimulated – send out what we need) are produced in
excess
● Microvasculature thrombosis (clotting) or hemorrhage occurs; or both
○ Clot formed → mechanism for breaking clot down → constantly try to be broken down when it’s not needed → clots occlude vessels vasculature = lead to ischemic changes or hemorrhaging

Question 46

What is Thrombocytopenia:

Answer 46

low platelet level (in blood); Platelet count < 150,000/mm3
As platelet count drops → can cause more severe bleeding from minor trauma/injury or does not occur
from any type of trauma associated. Should be able to stop the bleeding
● Issues w/ hemostasis

Question 47

What is a Normal Platelet count

Answer 47

> 150,000 – 400,000/mm3

Reference Range:
● < 50,000/mm3

: hemorrhage from minor trauma ( d/t minor trauma/injury ⇒ bleeding longer or

develop bruises)
● < 15,000/mm3

: spontaneous bleeding (does not need to be from any trauma associated)

● < 10,000/mm3

: severe bleeding

Question 48

What are the causes of Thrombocytopenia

Answer 48

● Hypersplenism (normal function of spleen but is enlarged d/t overactivity)
● Autoimmune disease (at risk)
● Hypothermia (body too low ⇒ cause issues w/ platelets such as coagulopathy)
● Viral or bacterial infections that cause DIC (clot, clot, clot ⇒ bleed, bleed, bleed; utilizing all of the
clotting factors early on and then unable to clot later on)
● HIT (changes in platelet level)

Question 49

What is Disseminated Intravascular Coagulation (DIC)

Answer 49

Complex, acquired disorder in which clotting and hemorrhage simultaneously occur (clotting &
bleeding occur at the same time)
Possible cause: result of increased protease activity in the blood caused by unregulated release of thrombin w/
subsequent fibrin formation & accelerated fibrinolysis
Clot being formed + clot being broken down

Question 50

What causes Disseminated Intravascular Coagulation (DIC)

Answer 50

D/t some type of injury that precipitates this → endothelial damage/tissue factor is the primary
initiator of DIC
● Sepsis (major infection – complicate multiple system) is the most common condition associated with
DIC → usually gram negative
● Results from abnormally widespread & ongoing activation of clotting in small & mid-sized vessels
that alter the microcirculation, leading to ischemic necrosis in various organs, particularly the
kidney and lung
● Caused by imbalance between coagulant system (clot) and fibrinolytic system (clot break down) =
clotting factors are depleted
● Widespread deposition of fibrin in the microcirculation that leads to ischemia (blocked vessels),
microvascular thrombotic obstruction, and organ failure (if not corrected)
● Involves both widespread clotting & bleeding because of simultaneous procoagulant activation,
fibrinolytic activation, & consumption of platelets and coagulation factors that results directly in
serious bleeding

Question 51

What are signs/sx of Disseminated Intravascular Coagulation (DIC)

Answer 51

● Bleeding from venipuncture sites
● Bleeding from arterial lines
● Purpura, petechiae, & hematomas (bleeding profusely)
● Symmetric cyanosis of the fingers & toes
This pt is very sick → usually do not make it

Question 52

What is Heparin-Induced Thrombocytopenia (HIT)

Answer 52

● Immune-mediated, adverse drug reaction caused by IgG antibodies against the heparin-platelet factor
4 complex leading to platelet activation
○ A rxn to heparin ⇒ causing body to initiates immune response; leading to platelet activation =
adverse drug rxn to heparin (allergy to heparin)

● Leads to increased platelet consumption & decrease in platelet count beginning 5 to 10 days after
the administration of heparin
○ Basically, taking platelets out of the system that you need → drastic reduction
○ May not be seen initially; most cases pts who are hospitalized, who go home may experience
complications r/t to this type of thrombocytopenia

● Typically causes 50% drop in platelet count

Question 53

What is Immune Thrombocytopenic Purpura (ITP)

Answer 53

● Idiopathic – spontaneous
● Chronic form has IgG autoantibody that targets platelet glycoproteins (antibody destruction of plts)
○ Antibody-coated platelets are sequestered and removed from the circulation by macrophages
(help fight things & remove debris) in the spleen

○ “Spleen takes them out + gobbles them up”
○ Process: taken out of circulation by macrophages → platelets are seen as foreign source = house
them in spleen

● Acute form of ITP develops after a viral infection is one of the most common childhood bleeding
disorders (occur in children)

Question 54

Describe clinical manifestations of Immune Thrombocytopenic Purpura (ITP)

Answer 54

● Petechiae & purpura (minor bleeding problems; ex: bruising, little red/purple dots or rash-like
component)
● Progressing to major hemorrhage from mucosal sites (epistaxis, hematuria, menorrhagia, bleeding
gums; ex: nosebleeds, blood in urine, heavy menstrual cycles, bleeding from number of sources)

Question 55

What are the 3 types of Thrombotic Thrombocytopenic Purpura (TTP)

Answer 55

● Thrombotic Microangiopathy → platelets aggregate (clump together), form microthrombi (little clots),
and cause occlusion of arterioles and capillaries (blockage – prevent blood flow & oxygen); may lead to
increased platelet consumption and organ ischemia
● Chronic Relapsing TTP → rare familial form observed in children and usually recognized &
successfully treated
● Acute Idiopathic TTP → more common & more severe form; early diagnosis & treatment is
essential; may prove fatal within 90 days

Question 56

Clinical manifestations of sickle cell disease

Answer 56

Sickle Cell Disease → disorders characterized by the presence of an abnormal hemoglobin → one amino acid
(valine) replaces another (glutamic acid)
● Deoxygenation & dehydration cause the red cells to solidify & stretch into an elongated sickle shape

● Very painful condition → go into crisis
● Can affect varying systems (brain all the way down to legs)
● Misconceptions of “drug-seeking behavior”
● Results in: stroke, paralysis, issues w/ eyes, etc.
Can result in:
● Vaso-occlusive crisis (thrombotic crisis) – clots = painful in nature
● Aplastic crisis
● Sequestration crisis
● Hyperhemolytic crisis

Question 57

Describe Sickle cell trait →

Answer 57

child inherits Hb S from one parent and Hb A from another (carry the trait but not the
disease)
Other forms:
● Sickle cell–thalassemia disease
● Sickle cell–Hb C disease

Question 58

Differentiate between the 3 different types of hemophilia

Answer 58

Hemophilia → serious bleeding disorders
● Involve gene deletions or point mutations
● First signs by age 3 to 4 years include episodes of persistent bleeding from minor injuries (falls,
etc. – take longer to stop bleeding)

● Hemophilia A (factor VIII deficiency)
○ von Willebrand disease
● Hemophilia B (factor IX deficiency)
● Hemophilia C (factor XI deficiency)

Treatment: replete the factor = can better control in cases of surgery (provide deficient factor to keep pt safe –
prevent hemorrhaging)

Question 59

Treatment for Anemia:

Answer 59

Pernicious Anemia: provide Vitamin B12 (Cobalamin) → weekly injections initially until deficiency
is corrected; followed by monthly injections for remainder of individual’s life (lifelong treatment)
○ Or higher PO doses of Vitamin B12
○ If left untreated it can be fatal causing heart failure

Folate Deficiency Anemia: provide daily PO folate → can be easily corrected

Question 60

Treatment for Platelet Disorders:

Answer 60

● HIT: withdraw heparin & use alternative anticoagulant

Question 61

Name some malignant tumors

Answer 61

● Carcinoma → epithelial tissue
● Adenocarcinoma → from ductal or glandular tissue (ex: breast)
● Sarcoma → mesenchymal tissue (ex: skeletal muscle)
● Lymphoma → lymphatic tissue (ex: lymphatic system)
● Leukemia → blood-forming cells (ex: Hodgkin’s disease)

Question 62

Name some benign tumors

Answer 62

○ Lipoma (benign tumor of fat cells)
○ Leiomyoma
○ Meningioma (benign tumor originate in brain, meninges, or skull)

Question 63

What is Carcinoma in situ (CIS):

Answer 63

preinvasive epithelial tumors of glandular or epithelial origin that have
not broken through the basement membrane or invaded the surrounding stroma
● Has not spread beyond borders
● No metastases
● Ex: in situ lesions → found in stomach, endometrium, breast, large bowel
● Depends on size, location, if it warrants removal, monitor progression (small, stable, etc)

Question 64

Differentiate between proto-oncogene, oncogene, and tumor suppressor gene

Nature of cancer cells & what they can do

Answer 64

Proto-Oncogenes → normal genes that direct protein synthesis & cellular growth (designed to regulate normal
cellular proliferation)

Oncogenes → mutant genes (ex: cancer cells invade & take over → express themselves as oncogenes)

Question 65

Describe the 2 types of oncogenes

Answer 65

● Oncogene Activation – point mutation in RAS (“rat sarcoma”) gene converts from regulated to
unregulated
○ Normal cells: should be able to stop at a certain point; cancer cells have the ability to switch it
around & allow for mutation – can be expressed in a different manner = contribute to
development of cancer

● Translocations: portion of gene or chromosome that break off; relocate or attach itself on a different
chromosome → causes mutation
○ Burkitt lymphomas
○ Chronic myeloid leukemia
○ Gene amplification

Question 66

Describe the 2 general types of patho/phys of cancer

Answer 66

● Clonal proliferation or expansion
○ As a result of a mutation, a cell acquires characteristics that allow it to have selective advantage
over its neighbors
■ Increased growth rate or decreased apoptosis

● Transformation of normal cells
○ Decreased need for growth factors to multiply
○ Lack contact inhibition
○ Anchorage independence
○ Immortality

Uncontrolled cancer cell proliferation r/t inactivation of tumor suppressor genes – switching from a gene that
would normally regulate the cell cycle; in a normal state – regulate cell cycle and stop the ability of cells to
continue to have those growth signals, cell division, especially damaged cells, mutations

Question 67

Describe the role of Tumor-Suppressor Genes (also referred to as anti-oncogenes) in the proliferation of some cancers

Answer 67

→ encode proteins that in their normal state
negatively regulate proliferation; important role in unregulated process
● Mutation (inactivation) of tumor-suppressor genes
○ Allows unregulated cellular growth

Cancer cells will take over → inactivates genes (“protective genes”) = unregulated cellular growth
(problematic – d/t uncontrolled, mutated cells/genes)

Question 68

Describe the 2 protective genes against cancer

Answer 68

“Protective genes” – help regulate growth → to reduce mutation

■ Retinoblastoma (RB) gene – prototypical tumor suppressor gene; help w/ anti-growth
signals in a normal environment
● Monitor antigrowth cellular signals and block activation of the growth/division
phase in the cell cycle
● Mutations in RB lead to persistent cell growth

■ Tumor protein p53 (TP53)
● Called the guardian of the genome
● Monitors intracellular signals related to stress and activates the caretaker genes
that are responsible for the maintenance of genomic integrity (how its supposed to
work)
● Cancer cell → activate gene → not able to maintain integrity = allow for
mutation

Question 69

Describe the function of telomeres and immortality

Answer 69

● Telomeres – aids in the life cycle of cells (caps communicate to cells
– reach the end of the cycle → time to allow for self-destruction)
● Hallmark of cancer cells is their immortality – d/t
telomeres/telomerase (has a huge role)
● Body cells are not immortal and can only divide a limited number
of times
● Telomeres are protective caps on each chromosome & are held in
place by telomerase (enzyme) → block cell division and prevent
immortality
● Telomeres become smaller and smaller with each cell division
(chromosome becomes unstable + fragment → expected outcome as
cell dies)
● Cancer cells can activate telomerase → unlimited division &
proliferation (no longer can self-destruct; mutated cell will not die and begin to replicate → being
produced at a greater & faster rate = aids in malignant tumor being able to spread from one location
to the next)
○ Cancer cell now has a life of its own; w/o adequate treatment → cell can live forever

Question 70

Describe why smoking is a major risk factor for cancer and how it alters cellular structure and function.

Answer 70

Tobacco: multipotent carcinogenic mixture
● Leading cause of preventable death in the United States
● Linked to cancers of the lung, lower urinary tract, upper aerodigestive tract, liver, kidney,
pancreas, cervix, uterus
● Linked to myeloid leukemia
● Secondhand smoke (ETS) contains many toxic chemicals → at risk for developing cancer
● Cigar & pipe smoking equally harmful
● Educate importance of smoking/tobacco cessation can prevent development of cancers

Question 71

Describe why exposure to radiation is a major risk factor for cancer and how it alters cellular structure and function.

Answer 71

Ionizing Radiation: emission from x-rays, radioisotopes, radon, and other radioactive sources
● Exposure causes cell death, gene mutations, and chromosome aberrations (translocation)
● Mutations in germ cells are heritable
● Increased use of diagnostic testing of concern → ex: cough does not warrant a chest x-ray (only
purpose is to rule out only when necessary – outweigh risks vs benefits)
● Wear protective attire → lead vest
Electromagnetic Radiation (EMR): energy in the form of magnetic and electronic waves
● Non-ionizing, low-frequency radiation
○ Ex: microwaves, radar, cell phones, and power frequency radiation associated with electricity
and radio waves, fluorescent lights, computers, and other electric equipment

● May or may not be carcinogenic = debate (research still being done)

Question 72

Discuss the effects of alcohol consumption on cancer risk.

Answer 72

● Alcohol consumption ⇒ classified as human carcinogen
○ Excessive drinking plays a part in the development of several common cancers
● Risk factor for oral cavity, pharynx, larynx, esophagus, liver, colorectum, and breast cancers = at
higher risk w/ alcohol consumption
● Genetic factors involved
● No “safe limit” of intake!

Question 73

Describe the effects of ultraviolet radiation on the skin.

Answer 73

● Causes basal cell carcinoma, squamous cell carcinoma, and melanoma (increased incidence in the
particular type of skin cancer)
○ Sunlight is essential for vitamin D but is only dangerous w/ repeated exposure for a long period
of time (significant amount time & skin is exposed = chronic inflammation)

● Principal source is sunlight
● Ultraviolet A (UVA) and ultraviolet B (UVB)
● Released TNF-α in epidermis
● Produces ROS
● Promotes skin inflammation and release of free radicals

Question 74

Identify risk factors for HPV

Answer 74

Human Papillomavirus (HPV): one of the top cancer-causing infections & most common sexually transmitted
virus (multiple sexual partners)
● Commonly in women but can occur in men
● Routine Pap test q3-5 years for screening
● HPV vaccine (Gardasil) reduces cervical cancer
● Exclusively causes cervical cancer → precancerous & cancerous cervical lesions

Question 75

Identify risk factors for Cervical Cancer

Answer 75

Cervical Cancer: persistence of infection w/ high-risk HPV is a precursor to the development of cervical
intraepithelial neoplasia, lesions, and invasive cervical cancers
● HPV infection has been identified as a definite carcinogen for several types of cancer: cervical, penis,
vulvar, vaginal, anal, and some oropharyngeal (OPCs – include: base of tongue, tonsils, & pharynx)
○ OPCs – increased & common in men
● Linked to HPV-16 or HPV-18
● Contributing factors: vaginal douches → alteration in cervicovaginal microbiome
Risk Factors:
● Smoking
● Persistent infection
● Decreased immunity/immunosuppression
○ Immunosuppressant medications
○ Chronic stress
● Chronic inflammation
● STD → gonorrhea, chlamydia (multiple sexual partners)
● Poor nutrition

● Multiple pregnancies (how many children?) → high parity having more than 5 pregnancies of more than
20 weeks gestations
● Long-term oral contraceptive use

Question 76

What is one of the reasons cancer often causes severe fatigue

Answer 76

Angiogenesis – growth of new vessels (ability for cancer
cells to form their own vessels in order to feed themselves
to receive adequate nutrients, blood supply & oxygen in
order for the tumor to grow & migrate to other places

Question 77

What is Syndrome of
Cachexia

Answer 77

Most severe form of MALNUTRITION
● Includes anorexia, early satiety (can easily feel full early on),
weight loss, anemia, asthenia, taste alterations, and altered
protein, lipid, and carbohydrate metabolism
○ Based of disease/cancer progression
● Changes associated with this syndrome result in major
decrease in quality of life and indirectly result in death of
some individuals
● Commonly seen in later phases → r/t treatment & therapies = no
signs of progression

Question 78

Differentiate between the stages of cancer and TNM system