FINAL CONTENT MEMORIZE Flashcards

Question

What is Poikilocytosis

Answer 1

RBCs in various shapes

Answer 2

Moderate: Fatigue Weakness Dyspnea Pallor Severe: fainting, chest pain, angina, heart attack

Answer 3

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)

Answer 4

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.

Answer 5

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

Answer 6

“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

Answer 7

WBC increase

Answer 8

Decrease in WBC amount

Answer 9

phagocytes, infection or inflammation

Answer 10

allergen or parasitic invasion

Answer 11

hypersensitivity rxn, inflammation

Answer 12

↓ prolonged severe infection

Answer 13

surgery, shock, trauma, burns, mental distress

Answer 14

acute infections, hyperthyroidism, long-term steroid therapy

Answer 15

● 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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

> 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

Answer 22

● 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)

Answer 23

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*

Answer 24

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

Answer 25

● 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*

Answer 26

● 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

Answer 27

● 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)

Answer 28

● 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)

Answer 29

● 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

Answer 30

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

Answer 31

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

Answer 32

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)

Answer 33

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

Answer 34

● HIT: withdraw heparin & use alternative anticoagulant

Answer 35

● 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)

Answer 36

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

Answer 37

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)

Answer 38

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)

Answer 39

● 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

Answer 40

● 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*

Answer 41

→ 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)*

Answer 42

“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

Answer 43

● 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

Answer 44

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

Answer 45

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)

Answer 46

● 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!

Answer 47

● 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

Answer 48

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

Answer 49

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

Answer 50

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

Answer 51

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