FINAL CONTENT MEMORIZE Flashcards
Compare and contrast the pathology and symptoms of benign prostatic hyperplasia with prostate cancer
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
What are the three systems of pain perception
Sensory/Discriminative System
Motivational/Affective System
Cognitive/Evaluative System
Describe the Sensory/Discriminative System of pain perception
Identifies presence, character, location &
intensity of pain
Ex: OLD CARTS = description
Describe the Motivational/Affective System of pain perception
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”
Describe the Cognitive/Evaluative System of pain perception
Overlies individual’s learned behavior
concerning experience of pain → can
modulate perception of pain.
Ex: person tolerates injection despite knowing
it may hurt
What is there difference between pain threshold, dominance, and tolerance
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
Describe how a person’s level of consciousness reflects their neurological function
Level of Consciousness: alert & oriented (person, place, time, & event)
○ Most critical clinical index of nervous system function
○ “Red flag” when LOC has been altered
Describe how a person’s pattern of breathing reflects their neurological function
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
Describe how a person’s pupillary reaction reflects their neurological function
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)
Describe how a person’s motor responses reflects their neurological function
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
Describe how a person’s oculomotor responses reflects their neurological function
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!
Describe how a person’s Vomiting, yawning, and hiccups reflects their neurological function
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
Describe the 2 types of brain injury manifestations:
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
Describe Extradural Brain Hematomas
bleeding b/w dura & skull w/i 48 hr → edema, LOC changes, hemorrhage
Describe Subdural brain hematomas
Subdural: bleeding b/w dura and brain (varying onset times)
Describe Intracerebral brain hematomas
Intracerebral: bleeding within brain → ↑ ICP d/t expanding mass in brain
Describe “primary injury” to the brain
direct result of blunt/penetrating insult to brain (2 types: focal and diffuse)
Describe the two types of primary injury
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
Describe the 2 types of focal brain injuries
- Coup injuries: something strikes the head → directly beneath point of impact (head hits
dashboard & damages frontal lobe) - 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
Describe the 2 types of Diffuse brain injuries
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
What are the 3 methods of classifying the anemias
Etiology (impaired RBC production, acute/chronic blood loss, ↑ RBC destruction, or combo of
all the above)
AND
Morphology (size of cell or hemoglobin content)
Words ending in -cytic indicate an RBC’s ____.
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)
Words ending in -chromic indicate an RBC’s ____.
Hemoglobin content: end w/ -chromic
● Normochromic: normal Hgb amount (usually ↓ RBC quantity)
● Hypochromic: low Hgb amount
What is Anisocytosis:
Anisocytosis: RBCs in various sizes
What is Poikilocytosis
RBCs in various shapes
Name some moderate signs AND severe signs of anemia
Moderate:
Fatigue
Weakness
Dyspnea
Pallor
Severe:
fainting, chest pain, angina, heart attack
What type of anemia is classified as “microcytic-hypochromic”
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)
What type of anemia is classified as “macrocytic-normochromic”
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.
What type of anemia is classified as “macrocytic-normochromic”
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
Describe Polycythemia vera:
“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
What does “leukocytosis, neutrophilia, eosinophilia, basophilia” all mean
WBC increase
What does “leukopenia, neutropenia, eosinopenia, basopenia” all mean
Decrease in WBC amount
Neutrophilia means
phagocytes, infection or inflammation
Eosinophilia means
allergen or parasitic invasion
Basophilia means
hypersensitivity rxn, inflammation
Neutropenia means
↓ prolonged severe infection
Eosinopenia means
surgery, shock, trauma, burns, mental distress
Basopenia means
acute infections, hyperthyroidism, long-term steroid therapy
What are the Types of Splenomegaly:
● 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
Common causes of splenomegaly
● Hepatitis
● Mononucleosis – aka “kissing disease or Epstein-Barr virus”
● Salmonella
● Tuberculosis
Describe the clinical manifestations of Alterations of Platelet Function:
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
Describe the clinical manifestations of Alterations of Coagulation
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
What is Essential (primary) thrombocythemia (thrombocytosis):
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
What is Thrombocytopenia:
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
What is a Normal Platelet count
> 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
What are the causes of Thrombocytopenia
● 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)
What is Disseminated Intravascular Coagulation (DIC)
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
What causes Disseminated Intravascular Coagulation (DIC)
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
What are signs/sx of Disseminated Intravascular Coagulation (DIC)
● 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
What is Heparin-Induced Thrombocytopenia (HIT)
● 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
What is Immune Thrombocytopenic Purpura (ITP)
● 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)
Describe clinical manifestations of Immune Thrombocytopenic Purpura (ITP)
● 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)
What are the 3 types of Thrombotic Thrombocytopenic Purpura (TTP)
● 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
Clinical manifestations of sickle cell disease
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
Describe Sickle cell trait →
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
Differentiate between the 3 different types of hemophilia
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)
Treatment for Anemia:
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
Treatment for Platelet Disorders:
● HIT: withdraw heparin & use alternative anticoagulant
Name some malignant tumors
● 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)
Name some benign tumors
○ Lipoma (benign tumor of fat cells)
○ Leiomyoma
○ Meningioma (benign tumor originate in brain, meninges, or skull)
What is Carcinoma in situ (CIS):
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)
Differentiate between proto-oncogene, oncogene, and tumor suppressor gene
Nature of cancer cells & what they can do
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)
Describe the 2 types of oncogenes
● 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
Describe the 2 general types of patho/phys of cancer
● 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
Describe the role of Tumor-Suppressor Genes (also referred to as anti-oncogenes) in the proliferation of some cancers
→ 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)
Describe the 2 protective genes against cancer
“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
Describe the function of telomeres and immortality
● 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
Describe why smoking is a major risk factor for cancer and how it alters cellular structure and function.
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
Describe why exposure to radiation is a major risk factor for cancer and how it alters cellular structure and function.
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)
Discuss the effects of alcohol consumption on cancer risk.
● 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!
Describe the effects of ultraviolet radiation on the skin.
● 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
Identify risk factors for HPV
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
Identify risk factors for Cervical Cancer
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
What is one of the reasons cancer often causes severe fatigue
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
What is Syndrome of
Cachexia
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
Differentiate between the stages of cancer and TNM system
