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Patho Exam 1

cell regulation, cancer, fluid & electrolyte, skin & burns

TermDefinition
Mitosis (M phase) phase of cell cycle where division/replication occurs
labile, stable, permanent What are 3 types of cells in body?
G0 resting phase of cell cycle
S phase DNA replication phase of cell cycle
G0, G1, S, G2, M cell cycle stages
oncology study of cancer and their treatment
etiology original cause of cellular alteration or disease
homeostasis condition of equilibrium when various physiologic factors are within normal limits
allostasis body's way of adapting to acute stress to maintain homeostasis
cellular adaptation protective mechanism to prevent cellular and tissue harm because of stressors
pathognomic changes unique histological findings that represent distinct disease processes
histology microscopic study of tissues and cells for diagnostic purposes
biopsy extraction of cell samples from an organ or mass of tissue to allow for histological examination
labile cell cell type that divides rapidly
hair cells, epithelial cells examples of labile cells
stable cell type of cell that stays in the G0 phase until more cells are needed
liver cells example of stable cells
permanent cell type of cell that enters G0 phase and stays theres
nerve cells example of permanent cell
differentiation process of cell changing from simple form (stem cell) to a more specialized cell (progenitor cell)
Atrophy shrinkage of cells; can occur from decrease in work demands
Hypertrophy enlarging of cells; occurs from excessive use which cab be physiologic or pathologic
Hyperplasia increase in the number of abnormal cells in an area and occurs in response to a noxious stimulus (once stimulus is removed, cells can return back to normal)
excessive estrogen production that causes endometrial hyperplasia and leads to abnormal menstrual bleeding example of hyperplasia
Metaplasia reversible change where one cell type is replaced by another in reponse to chronic irritation; protective mechanism
cells in esophagus that are constantly exposed to stomach acid/gastric secretions as a result of GERD are replaced by stomach cells because the stomach cells are made to withstand very high acidity of gastric secretions example of metaplasia
Dysplasia characterized by deranged cell growth of specific tissue resulting in cells that vary in size, shape and organization (can be reversed if irritant is removed); considered precancerous
cervical cells found in abnormal PAP smear example of dysplasia
Anaplasia cells that divide rapidly and have little to no resemblance to normal cells; cancerous
Neoplasia new growth; cancerous
well-differentiated, well-defined border; progressive and slow growth; grows by expansion and does not invade surrounding tissues; does not metastasize characteristics of benign cells?
undifferentiated, atypical structure, poorly defined borders; growth rate dependent on differentiation: more undifferentiated the cells, more rapid rate of growth; invasive and infiltrates tissues; gains access to lymph and blood vessels to metastasize characteristics of malignant cells?
Apoptosis programmed cell death
ovaries become dysfunctional during menopause example of apoptosis as a physiologic protective mechanism
injury from physical agents, radiation injury, chemical injury; dysfunction of Na-K pump; loss of plasma membrane integrity; defects in protein synthesis; injury from biologic agents; genetics; intracellular accumulations; hypoxia; free radical injury causes of cell injury?
spinal muscular atrophy (increased apoptosis); prostate cancer (decreased apoptosis) examples of pathologic apoptosis?
Necrosis irreversible cell death due to injury/stressors, leads to membrane disintegration, lysosomal activation and autolysis; initiation of inflammatory reaction
Infarction ischemic necrosis
Gangrene prolonged ischemia, infarction and necrosis; occurs from bacteria that grow in dead tissue
wet & dry gangrene what are the 2 types of gangrene?
wet gangrene bacteria invades the tissue which causes it to swell, ooze and have distinct odor
dry gangrene lack of blood supply causing the tissue to dry, shrink and turn black
diabetic ulcer type of wet gangrene?
frostbite type of dry gangrene?
angiogenesis formation of new blood vessels
carcinogenesis initiation of cancer formation
aging cancer is a disease of?
viruses/chronic inflammation, radiation & chemicals which contain highly reactive oxygen species/free radicals, tobacco, diet, lifestyle, environment, genetics, age, sex, hormonal agents common causes of cancer
HPV, hepatitis examples of cancer-causing viruses
H. pylori example of cancer-causing bacteria
sun exposure/UV radiation, radiation from Xrays examples of cancer-causing physical agents
tobacco and alcohol, pesticides examples of cancer-causing chemical agents
sporadic mutations that lead to cancer are from exposure to carcinogens in environment
inherited mutations that lead to cancer from parent
tumor suppressor genes genes that guard against cancer formation
proto-oncogenes control normal cell growth and proliferation
oncogenes mutated proto-oncogenes that allow unrestrained cell division
1. Initiation 2. Promotion 3. Progression 3 step process to carcinogenesis
Initiation initial damage to DNA
Promotion altered cell divides and passes on abnormal DNA
Progression benign lesions proliferate & invade adjacent tissue or metastasize
Adenoma benign tumor, glandular tissue or organ
Lipoma tumor derived from fat cells
Hemangioma tumor made of collection of blood vessels in skin or internal organ
Desmoid tumor highly invasive, not metastasizing tumors
Nevi non-cancerous moles on skin
Myoma muscle tumor
Carcinoma malignant epithelial cells
Adenocarcinoma cancer of the glandular or ductal tissue
Sarcoma cancer of mesenchymal origin, such as connective tissue, cartilage and bone
leukemia cancerous changes in leukocytes
lymphoma cancerous lymphocytes in lymph tissue
system used to determine size of tumor and extent of disease What is TNM staging?
extent of primary tumor T (in TNM staging)
Tx primary tumor cannot be assessed
T0 no evidence of primary tumor
Tis (carcinoma in situ) cells are found only in area where formed
T1, T2, T3, T4 increasing size and/or local extent of primary tumor
absence or presence & extent of regional lymph node metastasis N (in TNM staging)
Nx regional lymph nodes cannot be assessed
N0 no regional lymph node metastasis
N1, N2, N3 increasing involvement in regional lymph nodes
absence or presence of distant metastasis M (in TNM staging)
Mx distant metastasis cannot be assessed
M0 no distant metastasis
M distant metastasis
C diagnosis through clinical staging (exhibits symptoms)
P pathological staging (biopsy)
B symptoms of fever and weight loss, etc. in a tumor
Tumor grading (G) Defines type of tissue from which the tumor originated and degree to which tumor cells retain functional & histological characteristics of the tissue of origin
Gx grade cannot be assessed
G1 well differentiated
G2 moderately differentiated
G3 poorly differentiated
G4 undifferentiated; poor prognosis
blood vessels, lymph vessels & surgery ways cancer cells metastasize?
wearing sunscreen, cessation of smoking, healthy diet & exercise primary prevention examples
screenings (i.e. PAP smear, mammogram, colonoscopy around age 50, dermatology screenings) secondary prevention examples
treatment (chemotherapy, radiation), palliative care tertiary prevention examples
Primary prevention prevention focuses on preventing or delaying onset of cancer
Secondary prevention prevention focuses on early detection through screening
Tertiary prevention prevention focuses on treatment, management or prevention of progression to later stages
anemia, leukopenia, thrombocytopenia, pain, cachexia, paraneoplastic syndrome, fatigue & sleep disorders, loss of tissue integrity, side effects from medication/treatment, decreased resistance to infections symptoms of cancer?
cachexia end-stage wasting of musces and tissues of body
anorexia no appetite
paraneoplastic syndrome unexpected pathology provoked by presence of cancer; symptoms unrelated to cancer iteself but because the body is not functioning like it's supposed to
bones, liver, brain, lymph nodes, adrenal glands common sites of lung cancer metastasis
brain, chest wall, liver, lung, bone, lymph nodes common sites of breast cancer metastasis
women & men (not as common) who is at risk of breast cancer?
prolonged reproductive life, family history & genetics (BRCA1&BRCA2 genes), age>50 years, hormone replacement therapy, overexpression of estrogen &progresterone receptors, obesity (estrogen stored in fat), late childbirth, no pregnancies, Ashkenazi Jewish risk factors for breast cancer?
clinical manifestations known risk factors and symptoms
biopsy most definitive way to diagnose cancer?
mamogram, ultrasound, fine needle or excisional biopsy, ductogram, PET scan, biopsy sample tests ways to diagnose breast cancer?
mammograms at age 40 when/how do we screen for breast cancer?
Luminal A breast cancer slow-growing breast cancer, 90% cure rate
Luminal B breast cancer aggressive breast cancers that invade blood vessels and lymph nodes
Basal (triple negative) very aggressive, rapidly growing breast cancer that lacks estrogen, progesterone and HER2 receptors
HER2-enriched breast cancer that overproduces HER2 stimulating cell growth
Carcinoma in situ proliferation of breast cancer cells within ducts or lobules, no invasion surrounding tissue
Lobular carcinoma in situ nonpalpable lesion, discovered via biopsy
Invasive carcinoma primarily adenocarcinoma
Paget's disease of the nipple ductal carcinoma in situ extends into area of nipple and areola causing redness and crusting of nipple
singular, nontender, firm mass; irregular borders; adherence to skin or chest wall; upper, outer quadrant of breast; nipple discharge; swelling in one breast; nipple or skin retraction; peau d'orange (thickening of skin); paget's disease of breast breast cancer signs and symptoms?
Prostate cancer adenocarcinoma only in males that is classified using Gleason system and TMN system
men aged 55+ who is at greatest risk of prostate cancer?
vertebral bones where does prostate cancer usually metastasize to?
Hematuria blood in urine
Azotemia blood urine nitrogen is high
hematuria, azotemia, anemia, anorexia, back pain late stage symptoms of prostate cancer?
family history; consumption of dietary fat, red meat, fried foods, dairy; high calcium intake; smoking; African American ethnicity; high alcohol intake; exposure to Agent Orange & cadmium risk factors for prostate cancer?
sometimes no symptoms; obstructed urine flow (decreased force of stream, incomplete bladder emptying, straining) early symptoms of prostate cancer?
digital rectal exam, PSA (prostate surface antigen) test, biopsy diagnostics for prostate cancer?
60% what percentage of total body weight is water?
intracellular fluid fluid inside cell
extracellular fluid Na+ and water in plasma, found in intravascular compartments (arteries, veins, capillaries)
interstitial fluid (space) space between cells or between cells & capillaries where extracellular fluid can be found, contains water and electrolytes, but not proteins
albumin protein responsible for movement of water into and out of the vessels
osmolarity measure of particles per L of solution
reciprocal (opposite) relationship of blood and urine osmolarity
isotonic solution that has equal distribution of sodium and water in both ICF and ECF
hypotonic solution has lower tonicity (sodium level) or solute concentration than what is found inside cell (ICF); causes cell to swell
dehydration when would a hypotonic solution be given to a patient?
increase volume in blood vessel when would isotonic solution be given to patient?
0.9% NaCL; lactated ringer's examples of isotonic IV fluid?
hypertonic solution that has higher tonicity (sodium level) or solute concentration than what is found inside cell
cerebral edema when would hypertonic solution be given to patient?
osmosis process by which solvent (water) passes through semipermeable membrane from lower concentration to higher concentration until equilibrium is reached
diffusion movement of ions and molecules across semi-permeable membrane from area of high concentration to area of lower concentration until equilibrium is reached; example is CO2 and O2 movement in the body
filtration process by which solid particles in a liquid or gaseous fluid are removed by filter medium that permits the fluid to pass through but retains solid particles (e.g. nephorns in kidney = renal filtration)
active transport process of moving molecules across cell membrane from area of lower to higher concentration requiring use of ATP; movemement occurs through ion channels (e.g. movement of electrons)
Na+/K+ Pump Na+ is main ECF cation, K+ is main ICF cation; assists in maintenance of neuromuscular excitabiity and acid-based balances; uses ATPase pump to maintain Na+ as extracellular cation and K+ as intracellular cation
hydrostatic pressure pushing force exerted by water in the bloodtream; source of pumping is the heart (arterial end); exerts outward force that pushes water through capillary membrane pores into ISF and ICF compartments
osmotic pressure pressure exerted by solutes (i.e. electrolytes, mainly sodium ions and plasma proteins) in bloodstream; force that pulls water into the bloodstream from the ICF and ISF on the venous side and opposes hydrostatic pressure at all capillary membranes
oncotic pressure type of osmotic pressure exerted specifically by albumin in the bloodstream
3.1-4.3 g/dL normal serum albumin level?
low albumin means low oncotic pressure, so the force exerted by hydrostatic pressure overwhelms oncotic pressure and this causes water in the bloodstream to be pushed outward from capillary membrane pores into ISF and ICF how does hypoalbuminemia (low albumin) alter the oncotic pressure?
275-295 milliosmoles/kg of water normal plasma osmolality
edema condition caused by excess fluid left in ISF and ICF compartments; could be due to elevated hydrostatic pressure, diminished osmotic pressure created by low amount of solutes in bloodstream, or as a result of inflammation or sodium retention
Renin angiotensin aldosterone system RAAS stands for
low circulation, low renal perfusion, or low blood pressure detected by kidneys what activates RAAS?
RAAS mechanism used to replenish blood volume and raise blood pressure
renin what is the initial enzyme secreted by kidneys when RAAS is activated?
cleaves angiotensinogen into angiotensin I What does renin do in the liver?
Angiotensin-converting enzyme (ACE) enzyme in the lungs that converts angiotensin I to angiotensin II
angiotensin II vasoconstrictor that raises BP and stimulates the adrenal gland to release aldosterone
aldosterone mineralcorticoid that increases sodium and water reabsorption into the bloodstream at the distal tubule of the nephrons and stimulates the excretion of potassium secretion into urine, which increases blood volume and blood pressure
natriuresis excretion of a large amount of both sodium and water by the kidneys in response to excess ECF volume
Atrial natriuretic peptide (ANP) hormone released when there is too much fluid sensed in the right atrium of the heart which stimulates diuresis
diuresis release of fluid in form of urine from kidneys
Antidiuretic hormone (ADH) hormone stimulated by posterior pituitary gland when the blood pressure is low and causes kidneys to retain water in the blood to help elevate BP
Brain Natiuretic peptide hormone released when blood vessels in brain and left ventricle of heart sense excess fluid in the vessels which stimulates diuresis; used to diagnose left-sided heart failure
dependent edema collection of venous blood in lower extremities; resulting from high hydrostatic pressure pushes fluid into ISF or venous insufficiency (veins can't take extra fluid or blood back to the heart so it pools)
pitting edema occurs when pressure is applied to small area and indentation persists after release of pressure; can indicate kidney disease or heart failure
sequestered fluids fluids accumulated in body cavities normally free of fluids
transudate serous filtrate of blood
fluid inside blister e.g. of transudate
exudate contains blood, lymph, proteins, pathogens, inflammatory cells
pus e.g. of exudate
pericardial sac, peritoneal cavity, pleural space (around lung) spaces where sequestered fluid may accumulate
young and elderly who is at the greatest risk for dehydration (hypovolemia)?
2.1-8.5 mg/dL BUN normal range?
prolonged diarrhea, massive burns, fever & sweating causes of dehydration/hypovolemia
thirst, dry mucous membranes, sunken eyes, poor skin turgor, hypotension, low urine output, dark colored urine, weight loss, tachycardia symptoms of dehydration/hypovolemia?
Sensible loss water loss that can be measured
urination, vomit, ostomy or wound drainage examples of sensible loss
Insensible loss water loss that can't be perceived or measured
lungs, sweat, feces, burns examples of insensible loss
sodium electrolyte imbalance related with hyper/hypovlemia
hypervolemia fluid volume overload
heart failure (activation of RAAS due to low perfusion of kidney) most common cause of hypervolemia
cancers that secrete ADH/SIADH (syndrome of inappropriate ADH), cirrhosis of liver due to hypoalbuminemia, polycystic kidney disease (interference with nephrons, no urine production); hypoalbuminemia caused by protein deficiency; some types of hypotension causes of hypervolemia
noticeable edema in arms, legs, face; edema in abdomen; rapid weight gain; cramping; headache; bloating; shortness of breath; high BP; bounding pulse; crackles in lungs; heart problems including CHF symptoms of hypervolemia
oliguria low urine output
anuria no urine output
135-145 mEq/L sodium normal range
Hypernatremia elevated sodium levels
>145 mEq/L hypernatremia range
water loss and water retention (excess secretion of aldosterone, high salt in diet, overproduction of RAAS system) causes of hypernatremia
dehydration,thirst, tachycardia, oliguria, decreased salivation, headache, seizures, decreased reflexes, poor skin turgor, flushed skin, weak, thready pulse signs & symptoms of hypovolemia hypernatremia
edema, weight gain, hypertension; mental changes and pulomary edema if severe signs & symptoms of hypervolemia hypernatremia
athlete outside in the sun sweating profusely and losing fluids rapidly; if not replinishing fluid as quickly as losing it, leads to dehydration -> less water = less blood volume, causes sodium concentration to rise example of hyovolemia hypernatremia
Hyponatremia decreased sodium levels
<135 mEq/L hyponatremia range
excess water, sodium diluted; syndrome of inappropriate ADH (SIADH) causes of hypervolemia hyponatremia
person with diarrhea and vomiting example of hypovolemia hyponatremia
Hypovolemic hyponatremia losing water and sodium at the same rate
Hypovolemic hypernatremia dehydration (loss of water leads to high sodium concentration)
renal causes: adrenal insufficiency, osmotic, diuresis, diuretic use nonrenal causes: diarrhea, vomiting, excessive sweating causes of hypovolemic hyponatremia
headache, lethargy, confusion, muscle cramps, cell swelling may leads to seizure and coma symptoms of hypervolemic hyponatremia
thirst, hypotension, tachycardia, neurologic deficits may develop symptoms of hypovolemic hyponatremia
Hypervolemic hypernatremia high sodium causes water retention
Hypervolemic hyponatremia excess fluid causes sodium to be diluted
3.5-5 mEq/L normal range for Potassium
Potassium what is considered the most important electrolyte?
electrical signaling potassium is needed for:
hypokalemia decreased potassium levels
<3.5 mEq/L hypokalemia range
cardiac arrhythmias including prolonged PR interval, flattened T wave and prominent U wave main distinguishing signs & symptoms of hypokalemia
diuretics most common cause of hypokalemia
dietary K+ deficiency, vomiting & diarrhea, NG suction, hyperaldosteronism, salt-wasting kidney disease, GI surgery, alkalosis, laxative abuse causes of hypokalemia
hyperkalemia elevated potassium levels
>5 mEq/L hyperkalemia range
>7 mEq/L severe hyperkalemia range
risk of cardiac arrest, tall & peaked T wave, wide QRS complexes, dizziness main distinguishing signs & symptoms of hyperkalemia
excessive intake of K+, aldosterone deficiency, Na+ depletion, acidosis, tissue trauma, burns, extreme exercise, renal failure, Addison's disease (lack of cortisol), hemolysis, potassium-sparing diuretics, ACE inhibitors causes of hyperkalemia
orange juice, bananas, dried fruits, meats foods high in potassium
8.5-10.5 mg/dL normal range of calcium
muscle contraction calcium is needed for:
<8.5 mg/dL hypocalcemia range
hypocalcemia decreased levels of calcium
arrhythmias (heart block & ventricular fibrillation), increased neuromuscular excitability, hyperactive reflexes, positive Chvostek's and Trousseau's sign, hypotension main distinguishing signs & symptoms of hypocalcemia
hypoparathyroidism, malabsorption syndrome, hypomagnesemia, hyperphosphatemia, renal failure, insufficient vitamin D, hypoalbuminemia, diuretic therapy, diarrhea, acute pancreatitis, gastric surgery, massive blood transfusions causes of hypocalcemia
>10 mg/dL hypercalcemia range
hypercalcemia elevated levels of calcium
kidney stones, hematuria, tongue fasciculations, decreased neuromuscular excitability (tetany), ataxia, loss of muscle tone, hypertension main distinguishing signs & symptoms of hypercalcemia
bone pain, bone fragility, dry skin & hair, cataracts, depression, dementia chronic signs & symptoms of hypocalcemia
hyperparathyroidism, cancer, excessve Ca2+ in diet, excessive vitamin D, prolonged immobility, hypophosphatemia, diuretics, ACE inhibitors, lithium therapy, malignancy of bone or blood causes of hypercalcemia
respiratory what system is magnesium important for?
1.8-3 mEq/L normal range for Magnesium
hypomagnesemia decreased levels of magnesium
<1.5 mEq/L hypomagnesemia range
respiratory muscle paralysis main distinguishing symptom of hypomagnesemia
prolonged diarrhea, malnutrition w/ malabsorption, alcoholism/cirrhosis, laxative abuse, increased renal excretion of magnesium, diabetic ketoacidosis (DKA), sepsis, burns & serious wounds requiring debridement causes of hypomagnesemia
hypermagnesemia elevated levels of magnesium
>2.5 mEq/L hypermagnesemia range
kidney failure most common cause of hypermagnesemia
excessive use of magnesium-containing laxatives & antacids, untreated diabetic ketoacidosis, excessive magnesium infusion causes of hypermagnesemia
inhibits acetylcholine release & can cause diminished neuromuscular function, muscle weakness, hyporeflexia, hypotension & arrhythmias, lethargy & confusion some signs & symptoms of hypermagnesemia
2.5-4.5 mg/dL phosphate normal range
hypophosphatemia decreased levels of phosphate
<2.5 mg/dL hypophosphatemia range
ingestion of excess antacids (aluminum), severe diarrhea, lack of vitamin D, hypercalcemia, alkalosis, hyperparathyroidism, diabetic ketoacidosis causes of hypophosphatemia
anorexia, confusion, ataxia (difficulty walking), joint stiffness main distinguishing signs & symptoms of hypophosphatemia
hyperphosphatemia elevated levels of phosphate
>4.5 mg/dL hyperphosphatemia range
kidney failure most common cause of hyperphosphatemia
usually associated with hypocalcemia & reflect those symptoms (paresthesia, muscle cramps, tetany, hypotension, cardiac arrhythmias) signs & symptoms of hyperphosphatemia
hem(o) or hemat(o) prefix for blood
erythr(o) prefix for red
leuk(o) prefix for white
an prefix for without
immun prefix for immunity
lymph prefix for clear water or fluid
thromb prefix for clot
necr prefix for death
ology suffix for study of
rrhage suffix for excessive flow
oma suffix for tumor
poiesis suffix for production
penia suffix for deficiency
cytes suffix for cells
emia suffix for condition of blood
globin suffix for protein
osis suffix for abnormal conditions
philia suffix for abnormal attraction or love of
itis suffix for inflammation
4000-10,000 cells/mcL WBC normal range
males: 4.5-5.5 million cells/mcL females: 4-4.9 million cells/mcL RBC normal range
male: 45-52% female: 37-48% HCT normal range
male:13-18 gm/dL female: 12-16 gm/dL HGB normal range
150,000-450,000 cells/mcL platelets normal range
10-13 seconds PT normal range
1.1 or below INR normal range
30-40 seconds aPTT normal range
albumin hydrophilic protein (helps pull water back into the cell) that is made in the liver; functions as carriers; controls plasma oncotic pressure
hematopoeisis process of blood cell production in adult bone marrow or in the liver & spleen of fetus
transport O2 and CO2 role of erythrocytes
defend body against infection and remove debris role of leukocytes
blood coagulation & control of bleeding role of thrombocytes
medullay hematopoeisis blood cell production that occurs in the bone marrow
extramedullary hematopoeisis blood cell production that occurs outside of the bone marrow in the liver & spleen
myeloid stem cells very immature cells that start differentiation of red blood cells, platelets and most white blood cells
erythroblasts before becoming a reticulocyte, these are slightly differentiated but still immature myeloid stem cells
reticulocyte immature red blood cell
red blood cells are being damaged too quickly and not enough time to replenish them what could an increase in reticulocyte count indicate?
megakaryoblasts very immature cells that will eventually become platelets; slighlty differentiated from myeloid stem cells
megakaryocytes immature cells that become platelets
myeloblasts slighlty differentiated from myeloid stem cells, these immature cells go on to become granulocytes
monoblasts slightly differentiated from myeloid stem cells, these immature cells go on to become monocytes
B cells & T cells (lymphocytes) lymphoid stem cells go on to eventually become?
yellow bone marrow after age 7, red bone marrow starts to become ?
fatty embolus what is the risk of breaking a long bone in an adult?
neutrophils, basophils, eosinophils what are the granulocytes?
inflammation role of basophils?
allergic & parasitic infections role of eosinophils?
segs what distinguishes mature neutrophils?
bands or stabs what distinguishes immature neutrophils?
innate immunity role of neutrophils?
phagocytosis, synthesize & secrete cytokines, mature into dendritic cells role of monocytes?
immune response cells role of lymphocytes?
leukocytosis abnormally high number of WBCs in blood circulation
>11,000 cells/mcL leukocytosis range
leukemoid reaction abnormally & extremely high number of WBCs in blood circulation
>50,000 cells/mcL leukemoid reaction range
leukopenia abnormally low number of WBCs in blood circulation
<4000 cells/mcL leukopenia range
thrombocytopenia abnormally low number of platelets, resulting from decrease in platelet production, increased sequestration of platelets in the spleen or decreased platelet survival
drug-induced thrombocytopenia-ASA patient presents with petechial hemorrhages and purpura, platelet counts <20,000 cells/mcL, no distinctly apparent cause, associated with drug (including herbal and OTC meds) that has been taken for about 1 week or intermittently over long period
idiopathic (immune) thrombocytopenia purpura (ITP) one of the most common autoimmune disorders, caused by autoantibodies that develop against platelets ; can be caused by acute infection ( virus) in kids; presents with petechiae, purpura, bleeding gums, epistaxis, abnormal menstrual bleeding, splenomegaly
thrombotic thrombocytopenia purpura (TTP) caused by deficiency of enzyme metalloprotease (destroyed by autoantibodies) that acts on vWF which leads to unmodified vWF, causing platelet adhesion & aggreagation, then leads to widespread micro-clot formation which uses up the platelets and RBCs
hemolytic anemia, thrombocytopenic purpura, neurological abnormalities, fever, renal disease 5 signs & symptoms of thrombotic thrombocytopenia purpura?
spleen site of platelet destruction?
Platelets activate when bound to collagen or vWF at site of vascular injury which causes them to secrete chemicals that cause vasoconstriction Step 1 of hemostasis (first step)
Formation of platelet plug (activated platelets are sticky and clump together) Step 2 of hemostasis
Tissue factor activates coagulation cascade (extrinsic vs intrinsic, common) -> platelet plug + fibrin = clot Step 3 of hemostasis
Clot retraction ( activated platelets transduce contractile forces using actin & myosin on the fibrin network of thrombus which squeezes the serum from the clot, over time increases clot density and decreases clot size) Step 4 of hemostasis
fibrinolysis (small cascade that use tPA and produces plasmin which cleaves fibrin and dissolves clot) Step 5 of hemostasis (last step)
thrombopoietin synthesized from liver & activates platelet formation
Adhesion, activation and aggregation 3 steps of platelet plug formation
Intrinsic pathway longer pathway, responsible for forming a clot when damage occurs through the wall of blood vessel
aPTT (activated partial thromboplastin time) determines how long the intrinsic pathway is
Extrinsic pathway shorter pathway, responsible for forming a clot when there is superficial damage occurring to epithelial tissue
tissue factor release of this factor stimulates the extrinsic pathway
von Willebrand factor release of this factor stimulates the intrinsic pathway
PT and INR determines how long it takes the extrinsic pathway to respond
Common pathway starts the actual production of fibrin, starts with factor X
Factor X -> Factor V -> Prothrombin becomes Thrombin -> Fibrinogen becomes Fibrin steps of common pathway
ischemia inadequate blood supply to part of body typically caused by a blocked vessel
embolus traveling thrombus
D-dimer checks blood for clots
erythropoeitin released by the kidney in states of hypoxia with stimulates the bone marrow to produce RBCs
Anemia abnormally low number of circulating RBCs or levels of hemoglobin or both
Gi tract blood loss, heavy menstrual periods, tachycardia, jaundice, fatigue, splenomegaly; nutritional anemias can cause glossitis, cheilitis, koilonychia or pica signs and symptoms of anemia
deficiencies (iron, vitamin B12, folic acid), blood loss (chronic and acute), hemoglobinopathies, medications, hemolysis causes of anemia
Iron deficiency anemia common worldwide cause of anemia resulting from dietary deficiency, loss of iron through bleeding or increased demands
Pernicious anemia deficiency in B12 caused by poor dietary intake of B12 or instrinsic factor in GI tract that cause poor or malabsorption of B12 (e.g autoimmune disease like ulcerative colitis and Crohn's disease)
Hemolytic anemia anemia caused by destruction of RBCs that outpaces synthesis of RBCsin bone marrow; can be acute or chronic; can occur because of various disorders including hemoglobinopathies, medication side effects, autoimmune disorders, blood transfusions
Anemia of acute blood loss drop in RBC population caused by hemorrhage (i.e. trauma), or significant acute internal blood loss into the thoracic and abdominal cavities caused by rupture of an artery or organ
Anemia of chronic blood loss patient endures slow, gradual blood loss via the GI tract or excessive monthly menstrual loss; usually subtle and asymptomatic
hemoglobinopathy, sickle cell anemia, thalassemia, hereditary spherocytosis, blood transfusion reactions types of hemolytic anemia
hemoglobinopathy inherited disorder of the structure of the hemoglobin molecule (causing it to not carry oxygen efficiently) that can lead to destruction of the RBC
because dehydration can cause sickle cells to swell, clump and cause ischemia (leads to stroke) important for person with sickle cell disease to stay hydrated, why?
thalassemia genetic disorder that causes defects in Hgb synthesis
Aplastic anemia occurs when bone marrow fails, resulting in hypocellular bone marrow and pancytopenia; very rare, most of the time acquired because of infections such as HIV, hepatitis or Epstein Barr
pancytopenia defiiciency of all blood cells
Hodgkin Disease more curable form of lymphoma that originates in a single node or chain of nodes, with Reed-Sternberg cells present
Non-hodgkin's disease more common lymphoma originating at extranodal sites that spreads to anatomically contiguous nodes, NO Reed-Sternberg cells present
Leukemia malignant neoplasms arising from transformation of single blood cell line derived from hematopoietic stem cells
leukostasis, tumor lysis syndrome, hyperuricemia, blast crisis complications of leukemia
Chronic Lymphocytic leukemia (CLL), Acute Lymphocytic Leukemia (ALL), Chronic Myelogenous Leukemia (CML), Acute Myelogenous Leukemia (AML) 4 types of leukemia:
erythema reddened skin
induration hardening or thickening of skin
bulla large blister
telangiectasia fine, irregular red lines produced by dilation of capillaries (spider veins)
pustule papule filled with pus (pimple)
scale fragment of dry skin
scar permanent replacement of normal skin with connective tissue
ulcer loss of epidermal and dermal tissue
lichenification hardening or thickening of skin with markings due to trauma
macule flat area of pigmentation (freckle)
nodule solid lump greater than 0.5 cm in diameter (bug bite or cystic acne)
plaque raised, flat-topped lesion greater than 2 cm (eczema or psoriasis)
vesicle small blister
wheals (urticaria) transient, pale elevated papules with pink margins
albinism genetic disorder, lack of pigmentation
vitligo abnormalities in melanin production leading to discolored skin patches
melasma appearance of dark macules on the face, more common in brown-skinned women
lentigos age spots
xerosis dry skin, more easily bruised/damaged
pruritis itching
telogen effluvium decreased growth vs rest cycle of hair (overall thinning)
alopecia sudden loss of hair in one area of scalp
pitting tiny dents in nails, sign of psoriasis
clubbing widened nails, bulging fingertips, soft nail bed, downward curving of nails (caused by chronic hypoxia)
koilnychia spooning of the nails (sign of liver and/or thyroid problem)
paronychia pain and swelling around paronychial fold
onychomycosis fungal or yeast infection of nail folds
onycholysis infection that causes nail plate to separate from nail bed
hyperhidrosis excessive sweat production
anhidrosis diminished sweat production, caused by hidradentitis supprativa (clogging of aprocine glands)
acne vulgaris multifactorial inflammation of sebaceous glands, most commonly seen in puberty due to hormones; there is a bacterial component
acne rosacea reddened cheek caused by inflammatory process
birthmarks present at birth or develop during infancy, may darken with age
hemangiomas benign tumor of a bundle of blood vessles, can be internal or external
port wine stains pemanent blood vessel abnormalities, causing red splotching on infants skin, may lighten/fade with age
UV wood's light use of UV light that causes bacteria or fungi to grow
Nevi moles, most common type of benign skin tumor
actinic keratosis premalignant lesion; rough, scaly, red plaques
lentigos premalignant skin lesion; brown spot (age spots)
malignant melanoma most lethal form of cancer, originates in melanocytes (beginning on surface but then becomes dysplastic, penetrates and metastasizes), considered deadliest form of skin cancer
asymmetry, border (flat, raised, irregular?), color (darker, variable?), diameter, evolving ABCDE of assessed nevi
basal cell carcinoma most common and least invasive form of skin cancer, begins as small, dome-shaped bump with shiny, translucent texture and grows slowly and deeply
squamous cell carcinoma may develop from actinic keratosis, risk increases with age/uv exposure, appears as red, crusted or scaly patch and may appear as non-healing ulcer or firm, red nodule; treatable if caught early
temperature control, barrier protection, secretion and absorption, vitamin D production, immunological surveillance, mirror for internal disease processes, indicator of general health functions of the skin?
superficial burn damage only to epidermal layer; vasodilation causes redness to skin, no blisters, heals in less than 1 week
superficial partial-thickness burns chars the epidermis and papillary dermis; edema & epidermal blisters; skin in wet, raw and pink or white; painful; heals in 3-6 weeks and may scar
deep partial-thickness injuries burns through epidermis & dermis; skin may be mottled; blistering
full-thickness injuries damage to epidermis, dermis, hair follices and all underlying structures; nerve endings destroyed so pain is rare; skin may be white, black, brown or red; significant edema in surrounding tissues
Rule of 9s and Lund & Browder method two methods of determining surface area of a burn?
Lund & Browder (more precise of estimating extent of burn and more accurate for children) which method of determing surface area of a burn is more accurate?
rapid, pre-hospital, emergent situations when is Rule of 9s used?
zone of coagulation deepest point of injury and most irreversible damage
zone of stasis decreased tissue perfusion; potentially reversible damage
zone of hyperemia outer zone, reddened due to vasodilation; minimal tissue damage; heals well
ABCDEF (airway, breathing, circulation, disability, exposure, fluid resuscitation) priority of burn care?
contracture deep thermal and full thickness burns that start to heal become constricted regions of tissue, especially around joints, which limits function
hypertrophic scarring aka keloids, hyperemic raised areas of firm skin
compartment syndrome full-thickness circumferential and near-circumferential skin burns become tough, dead tissue which compromises circulation and causes excessive fluid build up and this causes ischemia and blood flow to tissue is lost
burn and scald 2 common burn etiologies
thermal, chemical, electrical, radiation types of burns
cell damage and death release vasoactive substances which increases vascular permeability with fluid and protein shift from ICF to ECF, leak into ISF (increased risk for hypovolemia); cell damage (leak of potassium into ECF increases risk for hyperkalemia complications of burns
depth, how the injury occurred, causative agent, temperature of burning agent, duration of contact with burning agent, thickness of skin in area burned classifying burns
Minor burn partial-thickness burn of less than 15% TBSA in adults or full-thickness burn of less than 2% TBSA not involving special care areas
Moderate burn burn less than 10% of TBSA full-thickness and no special care areas or partial-thickness burn of 15-25% TBSA in adults
Major burns partial-thickness burn exceeding 25% TBSA in adults, full-thickness burn exceeding 10% TBSA, involves special carea areas, all burns involving inhalataion injury, electrical injury, concurrent trauma and poor-risk patients
Created by: blangen2
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