reduced blood supply
|C. Perfringens cause...||
|RNA synthesis happens here||
signs of disease subside
|What organ activates vitamin D?||
The breakdown of glucose
|what causes coagulative necrosis?||
ST Segmented: severe interruption of cardiac flow
Plaque is causing significant damage (large necrosis)
ST Segmented: severe interruption of cardiac flow
Nausea and vomiting
Fatigue and weakness
Congestive heart failure
Integrated communication system. CNS and PNS
one mutated gene in pair
tendency to develop unusual or recurrent infections = IMPAIRED IMMUNE SYSTEMcan be congenital or acquired
Use of drugs to treat disease.
|what type of disease is infarction?||
abnormal changes in a cell (deranged)
i.e. size, shape, organization
|destruction of alveolar walls and septa is typical of||
Circulate in plasma, loose association with albuminCannot cross blood-brain barrierStimulate two major classes of receptorsAlpha adrenergic receptors 1 & 2Beta adrenergic receptors 1 & 2
|dependent on the sensitivity and specificity||
|Malignant connective tissue tumors are referred to as?||
They are slow moving. They are extremely phagocytic and are long-lived. Therefore, in chronic inflammatory changes, we see these. They kill bacteria with oxygen free radicals plus they phagocytose foreign material and destroy it with their rich supply of lysosomal enzymes. One of the most important roles of _______is its involvement in the inflammatory response against parasites. A person with allergies has more of these than a normal person, because the body knows histamine is going to be released and we need to get it under control. The body fights it off by producing more of these. Name it.
|What organ is gonna be compromised with SLE?||
Evidence of a disease that is objective and can be seen, measured, or recorded.
|The longer the incubation period is, the more likely the disease is to be transmitted because the person doesn't know he/she has the disease. True or False?||
|Define respiratory alkalosis||
Alkalinity caused by excessive elimination of carbon dioxide resulting from increased respirations
occurs with decreased work load, pressure, uses, blood supply, nutrition, hormonal or nerve stimulation
type A - loss of clotting factor 8, 1 in 5000 males, more moderate
type B - loss or def. of clotting factor 9, 1 in 30000 males, more severe
cessation of breathing for 10 seconds or longer.
|contains a special enzyme that degrades peroxides. Helps control free radicals||
Fight or Flightstimulation of the sympathetic nervous system:CatecholaminesEpinephrine NorepinephrineCortisol
|When the bladder and urethra protrudes it is||
|Some cancers secrete growth factors that stimulate their own growth. This process is known as?||
Atherosclerosis is a good example of this. You dictate how this will progress. Blood vessels are supposed to be nice and open. If you eat McDonalds every day, the vessels start to close. The heart then has to work harder. Because of this, the heart will enlarge to get stronger, but the chambers of the heart get smaller. What kind of hypertrophy is this?
|This antibody is found in very small amounts in the body, unless you have allergies...||
A condition that is confined to one area.
|What are osteoblasts?||
The differentiated bone forming cells and secrete bone matrix on which Ca++ and PO precipitate
|What is the primary energy source for cells?||
|what is the primary choice of mood altering drugs?||
defects here are the usual cause of chromosomal defects.
meiosis - dipload (46) # of cells to start, end up with 4 daughter cells each w/ haploid (23) number of cells
|Which of the following is an attempt to localize and c ontain the foreign material during an inflammatory response||
Increase in cell size and functional tissue massResults of an increase workloadmuscle mass with exercise (physiological)myocardial hypertrophy valvular disease (pathological)
|Cells may adapt by||
1) increasing cellular concentration, 2) accumulating abnormal substances, 3) changing cell size or cell numbers, or, 4) undergoing a lethal change
|What type of antigenic variation is where a virus can turn off our cellular structure so it can stay hidden?||
|Stages of Cancer...What stage is when cancer is completely confined to the organ?||
cells are well differentiated and slow growing. Cohesive-stick together, centrifugal expansion. Encapsulated
mainly affects the CNS but may induce reversible hepatic and gastric changes
|Infectious Mono is caused by what virus||
epstein bar virus
|What are the complications associated with diverticulitis?||
Perforation with peritonitis, hemorrhage and bowel obstruction
|What is the pathogenesis of heat?||
cytokines dilate arterioles, increased bloodflow
|What is prodced by the anerobic, or first, stage of glycolysis?||
|x linked genes affect more _______ than ________||
males than females
|A tissue in which the cells vary in size and shap;e and show increased mitotic figures would be called what?||
|Reversible Cell Injury v. Cell Death||
Reversible cell injuryCellular swellingFatty changesCell deathApoptosis â programmed cell deathNecrosis â pathological form of cell injuryGangreneDry â impaired arterial system Moist â impaired venous systemGas â due to Clostridium
|who developed cell theory in mid 1830s?||
Schleiden and Schwann
|What type of tumor is named from the tissues from which they arise and also include the suffix "oma"?||
|When someone is have dark black tar, stool is is called ______ and likely from the _____||
|What two diseases are predominantly in the jewish culture?||
Tay-Sachs and Gauche Disease
|In what ways can HDV be acquired?||
Unprotected sex, sharing needles
|How is Calcitonin activated?||
- Calcitonin acts via increased cAMP concentrations to inhibit osteoclast motilty and cell shape and inactivates them
The major effect of calcitonin administration is a rapid fall in Ca+ caused by inhibition of bone resorption.
|example of physiologic atrophy||
shrinkage of the thymus gland with early development
|What is atrophy?||
cells are smaller, or are fewer in tissue
|Mean arterial pressure (MAP)||
and average blood pressure in an individual that is equal to diastolic pressure plus 1/3 of the pulse pressure and is considered the perfusion pressure of organs in the body.
|What type of immune deficiency is more common and is caused by another illness?||
Secondary (acquired) immunodeficiency
|mast cell synthesis||
activates new of these cells and other mediators including leukotrienes, prostoglandins and platele-activation factor
|Why does the spleen enlarge?||
shunting of blood into the splenic vein
|How does Estrogen affect your skeletal structure?||
Blocks PTH (parathyroid hormone) induced bone reabsorption
|How many chromosomes do somatic cells (all cells with the exception of sex cells) contain?||
46. Sex cells contain 23.
|What are the stages in Acute inflammation?||
Vascular response, cellular response, inflammatory mediators
|induces secretion of ACTH from anterior pituitary||
Secretion of ACTH from anterior pituitary activates
|stages of clinical course- acute||
short rapid onset, self limiting. can become chronic
|List the 4 major causes of jaundice:||
1. Excessive destruction of RBC's (sickle cell, hemolytic disease of newborn)2. Impaired Uptake of bilirubin by the liver cells (Hepatitis, Cirrhosis, Cancer of the Liver)3. Decreased conjugation of bilirubin4. Obstruction of bile flow in hepatic lobules or bile ducts
|How does estrogen cause myometrial excitability?||
In regards to the vagina, it stimulates growth and cornification of epithelium.
|what are possible causes for hypoxic injury? (7)||
decreased oxygen in air
loss of hemoglobin
decreased production of RBC
diseases of respiratory/cardiovascular
|which of the following statements does not apply to myashenia gravis||
dementia develops in the later stage
|If the therapeutic range is small how do we make sure we don't make a patient either toxic or untherapeutic?||
infuse the drugs, depot preperation, or reduce both the size of each dose and the dosing interval.
|How does PTH respond to changes in Ca+?||
PTH secretion responds to small alterations in plasma Ca+ within seconds.
This is because a unique calcium receptor within the parathyroid cell plasma membrane senses changes in the extracellular fluid concentration of Ca+.
|select the statement related to tuberculosis||
the microbe is an acid fast bacillus resisitant to many disenfectants
|Precocious puberty is defined as the appearance of secondary sexual development before age ___ in white girls, age ___ in African American girls and age ____ in boys of either race.||
6 in white girls, 7 in African American girls & 9 in boys of any race
|what are the 5 cancers that could cause hypercalcermia?||
1) squamous cell carcinoma of lung
2) breast carcinoma
3) renal carcinoma
4) adult T cell leukemia/lymphoma
5) ovarian carcinoma
|What would be the most likely cause of an iatrogenic disease?||
an unwanted effect of a prescribed drug
Fever Tachycardia Leukocytosis• Pain
fluid or drainage
craving non-food items
Cholesterol, calcium salts, or mixed
cells increase in size
change in cell type
produces, stores, secretes
When cells become smaller
|Signs of Hyponatremia||
IrritabilityConfusionAnorexiaSeizures (only with severe sodium deficit)Coma
Mean Corpuscle Hemoglobin Concentration
respiratory bronchiole, alveolar duct and alveolus
inflam. of common bile duct
Water Lipids and Carbohydrates Glycogen Proteins Pigments Calcium Urate
three copies of a chromosome
loss of differentiation and specialization of functions
dead/diseased tissue have calcium cells
When cells increase in number
Causes or reasons for phenomina
Levels over 5.6ml/dLVitamin D overdoseProlonged immobilizationBone TumorsChemotherapyWhen bone is demineralized and Ca is released. Also found in people who OD with Vit D. Immobilized pt's often have bone demineralization.
Above 2.1mEq/LCaused by increased intakeBone demineralizationMilk of Mag abuseRenal Disease
Under 4.5mg/dLCaused by pancreatic diseaseinsufficient dietary intakeLaxative abuse(big problem in elderly Milk of Mag causes diarrhea and removes Ca)MalabsorptionPresence of HypomagnesiaExcess phosphorus intakeRenal Disease
primary function of hemoglobin
|long arm of a chromosome||
abnormal detachment of primative foregut during embryogenesis
a communication between two hollow organs
|diseases of gallbladder||
Acute and chronic cholecystitis
cells increase in size-abnormal response; heart enlarged due to increased workload (hypertension).
collection of infected hair follicles that forms a draining abscess
cell injury caused by no oxygen
Decreased amount of urine production. Output of less that 30mL/hr. A minimum of 30mL/hr is normal.
|Classifications of Disease||
Inherited diseasesCongenital diseases or birth defectsMetabolic diseasesDegenerative diseasesNeoplastic diseasesImmunologic diseasesInfectious diseasesPhysical agent-induced diseasesNutritional deficiency diseasesIatrogenic diseasesPsychogenic diseasesIdiopathic diseases
(Intravascular and Interstitial) High in Sodium and low in Potassium. Composed of 15% soft tissue and 5% Blood vessels
When cells are damaged/injured and eventually die. It is specific to organ/tissue. The body will attempt to compensate and changes will be progressive.
Below 1.3 mEq/LCaused by chronic alcohol abuseLaxative abusepancreatic diseasemalnutrition
|clinical manifestations of b12 or folate deficiency||
fatigueparesthesiasdementia(megaloblastic madness)tacyhpneaarthralgia(joint pain)
differentiates dietary from pernicious anemiaradioactive dose of b12,3-4 hours later, injection of b12complete 24 hour urine collection and analysis
|which two valves are semilunar?||
aortic and pulmonary
hypersecretion of mucus into bronchi and trachea, mucous gland hypertrophy mucous results in airway obstruction with continued stimulus mucous gland hypertrophy with hypersecretion into small airways increases risk for pulmonary infections
part of the inflammation process is mucous prodcution
|hemodynamic pulmonary edema||
caused by increased hydrostatic pressure
-- left heart failure increases pulmonary vein pressure, transferred to pulmonary capillary beds edema is dependent, settles with gravity
|Asthma is also known as...||
reversible airway hyperreactivity
|Fetal Alcohol Syndrome||
Microcephaly- small brain Low birth weight Cardiovascular defects Developmental disabilities Physical- sm head and features Mental- decreased cognition speech problems, retardation at different levels.
cells are shrinking (not decreasing in #)
|carcinoma in situ||
pre-invasive epithelial tumor of glandular or squamous cellular origin
substances secreted by cancer cells that stimulates their own growth
bullous or ulcerative lesion caused by Staphylococcus or streptococcus
rapidly progressing malignant tumor of the melanocytes. Metastasis occurs through lymph nodes.
receives oxygen and nutrients from capillaries
|Hormones of ADRENAL CORTEX||
1.androgens & adrenal estrogen2.mineralocorticoids: aldosterone (in response to angiotensis II)-inc. activity of Na+ pump (conserve Na+ in nephron3.glucocorticoids: cortisol- metabolic, anti-inflammatory & growth suppresing effects (pg. 7)
Very specialized in response. Disposes of bacteria/virus and antigens.
When K levels are below 3.5mEq/L. Shows signs around 3.2 and is deadly around 2.5Caused by: Decreased IntakeExcess excretionExcess insulin intakeDiarrhea (More K is found in GI tract than anywhere else in the body)Gastric SuctionRenal Disease (Electrolytes are excreted through the renal system)
Excess sodium (over 140 mEq/L). May not show signs when slighly over but shows when majorly over.Caused by excess water loss or sodium gainSalt tabletsProcessed foodsIV fluidsDiabetes Insipidus
(signs and symptoms) Consequences of the alterations in cells or tissues that are characteristic of the disease or diagnostic of the process
Diseases caused by pathogens that damage the body in some way.
|carry oxygen to tissues||
primary function of RBC's
|normal value for platelets||
150,000-400,000 mm^3 per liter
|Myocytes account for ___% of cells and ____% of the volume of the heart||
|what does the LAD supply?||
apexleft anterior wallanterior septum
reduced lung weight, volume and acini for weight and gestational agefound in 10% of neonatal autopsies
cells are shrinking-no use of muscle (in a cast, paralysis)
presence of one copy of a given chromosome in diploid cell.
|Alopecia: Male & Female||
hair loss Male: inherited, irreversible, loss in central scalpFemale: thinning of central hair (onset 20-20years old)
|Type I Diabetes Mellitus||
-from cell mediated autoimmune destruction of beta islet cells(which relase insulin)-associated with certain HLA haplotypes (runs in family w/autoimune diesease)-presence of ICAs (islet cell antibodies) years inadvance-can't metabalize glucose- fasting blood glucose> 120mg/dL
Diseases caused by prenatal (period of time in utero life) influences
Tumors that grow and divide without respect to normal limits, invade and destroy adjacent tissues, and/or spread to other locations in the body
a mutation not inherited from either parent
|types of emboli||
blood clotfat(from bone marrow from fracture)airbacteriapowder(drug abuse)
fibrotic changes of the lung or pleura prevent full expansion of the lung (contract lung to a smaller volume)slow process, "extra" space will fill with fluid no tracheal deviation
|smooth muscle and connective tissue foregut cysts are filled with ...||
ciliated pseudostratified columnar epithelium w/ squamous metaplasia in areas of inflammation
oxygen restored to the cell, but not to function normally causing permanent injury.
|Nevi Origination Characteristics||
CAN TURN MALIGNANTO: skin C: pigmented or non-pigmented lesions that form from melanocytes beginnning at age 3-5.
|three causes of hypertrophy||
bring overused, requires more oxygen, muscles won't be flexible
(respond to TSH)- T4 & T3: metabolic processes-calcitonin: dec. serum calcium by inhibiting osteoclastic (break down of Ca) activity & inc. osteoblastic (growth promoting) activityhyperthyroidism= turn everything up (Grave's disease-autoimune- goiter, bulging eyes, heat intolerance, hypermetabolism)hypothyroidism=turn everything down (congenital defects-autosomal recesive, iodine deficiency, untreated= myxedema "mucinous"-slugish/overweight, respritory depression) IRREVERSABLE
a type of reversible cell injury that is an accumulation of water caused by a malfunction of the Sodium Potassium pump
|Reconstruction following Reconstruction||
Healing takes place in 1-6wks from onset. Protein and Vit.C is needed for the tissue regeneration process
|Signs of Hypokalemia||
Altered muscle function (pt can barely move)Weakness (so weak pt can barely get out of bed or walk)Cardiac dysrhythmia (look at Twave on EKG) Polyuria (min of 30mL output. 2000 mL is average. +2000mL is polyuria)Trauma to cellsBurns
When a person becomes stiff all over and has no pulse. Occurs progressively and begins within 4 hours of death. It is only temporary and lasts around 72 hours.
|restrictive pulmonary disease is characterized by:||
reduced expansion of lung parenchyma with decreased total lung capacity expiratory flow rate is normal or reduced proportionally to the lung capacity
|Cardiovascular Burn Response||
Fluid and protein move out of the vascular compartment Results: Decreased cardiac output elevated hematocrit elevated WBCs hypoproteinemia
things can go into parts of the body incorrectly
|Cell-mediated specific adaptive immunity||
Antibodies are developed by the t-cell lymphocytes
|Characteristics of Gas Gangrene||
Formation of bubbles in damaged muscle cells due to infection of necrotic tissue by anaerobic bacteria of the genus Clostridium. High temperature elevation. Moderate to sever pain. Can be fatal if not treated agressively.
|Basophils and Mast Cells||
WBC that contanes histomines. When the basophils are the main component in blood, expect signs such as water itchy eyes.
|4 types of exudates||
Serous - watery, clear to slightly yellowFibrinous - serous fluid with some fibrin. A little clear with pink and brownPurulent - puss = dead skin with WBC (Neutrophils)Hemorrhagic - Leakage of blood in vessels
|normal rbc count formales:females:||
males: 4.7 - 6.1 million cells/ mm^3females: 4.2 - 5.4 million cells/ mm^3
|semilunar valve's competency depends on what?||
the stretching and molding of their three cusps in presence of arterial backpressure
|Actinic keratosis Origination Characteristics||
CAN TURN MALIGNANT O: skin surface C: pigmented patch of rough, adherent scale
|Deficiency of ADH: Diabetes Insipidus||
-neurogenic DI: dec. synthesis of ADH -nephrogenic DI: failure of nephrone to respond to ADH-high thirst & urine volume, spec. gravity 1.001-1.005tx: vasopressin & DDAVP (used for bed wetting)
|FVE or Fluid Volume Excess||
Normally just an excess of fluids. Electrolytes are normally balanced. Caused by IV infusions, congestive heart failure, cirrhosis, renal disease etc.
|Partial Prothrombin Time uses||
-find a cause of abnormal bleeding or bruising-assess low levels of blood clotting factors-diagnose clotting factors-assess blood clotting time before surgery-regulate doses of heparin(anticoagulant)
|Hormones from hypothalamus via nerve axon to release at POSTERIOR pituitary||
ADH (controls serum osmolality by inc. water reabsorption in kidney) & oxytocin (love-mammory, uterine contractions, sperm motility?)
|With delayed wound healing you will experience||
Increased fragility or change in appearance of granulation tissueUnexpected pain/tendernessPocketing of epithelial tissueAbnormal smellPresence of exudateEdemaExtending margin or erythemaPyrexia (fever)Wound breakdown
|nursing interventions for prothrombin time||
-find a cause for abnormal bleeding or burising-monitor anti-coagulant therapy(Coumadin)-check for low levels of blood clotting factors-check for low levels of Vitamin K-monitor liver function-monitor systemic use of clotting factor
|When is healing complete in an injured area?||
When the scar/inijured area is no longer pink but is a normal color.
condensation of chromatin
Less than 7.35
examples: bone marrow, epithelia of skin, mucosa of GI tract
these can usually replace lost cells
healing by regeneration can usually occur
|Refer to cellular communication||
|Duchenne Muscular Dystrophy||
|Normal Serum Sodium||
condylomata-greek for..... HPV....mainly HPV 6 and 11. incubation 6wks to 8 months. enters mucous tears and infects basal cells of epithemlium. non-lytic virus. epithelial cells hypertrophy in virus presence. form soft fleshy tumor...pink
neutrophils forced to outermost lumen of blood vessels by RBC roleaux
tissue looks yellow-white, cheesy
this is coagulative with some liquefaction
some cells fall apart
typical of TB
|Look at cell-to cell adhesions||
Death of entire person
|Hydrostatic pressue pushes fluid (IN/OUT)||
fatty streak layer, fibrous plaque..developes by vessel injury and normal mechanisms of repair. vascular cells multiply.
abnormal localized arterial wall dilatation
work imposed on heart(a measure)
lysosomal enzymes cannot enter phagocytotic granules
Mitochondria: consists of outer and inner membranes, site of TCA and oxidative phosphorylation, leads to production of ATP
ER: meshwork of membranes continuous with plasma membrane, is differentiated into RER and SER
Golgi Apparatus: system of tubules and flattened cisterne, processes protein from RER, synthesizes glycoproteins and lipoproteins
Ribosomes: consist of RNA and protein, free/attached to RER, necessary for protein synthesis
Lysosomes: vesicles that break off of golgi apparatus, contain digestive/lytic enzymes
do not divide after birth
examples: neurons, cardiac muscle, skeletal muscle
healing by regeneration cannot occur
healing is by repair and fibrosis
Leukemias are primary malignant “tumors” of leukocyte precursors in bone marrow
The neoplastic leukocyte precursors are rapidly dividing, but do not produce a tumor mass – normal bone marrow is displaced and suppressed, and in most cases there is also an excessive number of “pre-leukocyte” cells in different stages of differentiation in the blood.
|what do the carbohydrates consist of?||
|If appropriate stimulation causes positive charges to flow into the cell, the line will deflect upward. this is called what?||
|what are amphipathic lipids?||
hydrophilic and hydrophobic
PaCO2 or HCO3 is normal
different between systolic and distolic pressure
An autoimmune or infectious disease characterized by inflammation fo the glomeruli tha may not product symptoms or may present with hematuria and proteinuria. Inflammation of the ? caused by caused by numerous factor, including immunologic abnormalities, ischemia, free radicals, drugs, toxins, vascular disorders, and systemic diseases, including diabetes mellitus and lupus erythematosus. The most common cause of chronic and end-stage renal failure.
|Possible outcomes of acute inflammation||
healing by fibrosis
most common type
cells die but outline of cell is maintained
no lysis of cell membrance
tissue appears like a solid mass of boiled meat
usually caused by anoxia in solid internal organs
Like Arthus phenomenon but chronic, same events occur, but since self Ag cannot be eliminated, there is continuing inflammation and tissue destruction.
a) early: inflammation leads to plasma protein infiltration and fibrinoid necrosis of blood vessel walls, which can lead to localized clotting in blood vessel walls
b) chronic: destruction of blood vessel walls, formation of microaneurysms, thrombosis and occlusion of these vessels, infarcts and ischemias results
Proteins made in liver with utilization of vitamin K, normally circulate in blood in inactive form, must be activated to contribute to clotting cascade
|what is neurohoromonal?||
hormones released from neurosecretory neurons into blood
|What does the eukaryotic cytoplasm consist of ?||
cytoplasmic matrix-cytosol-function-cytoplasmic organelles
Causes sodium and water reabsorption, potassium excretion (See notes for diagram)
volume of blood out per beat
HSV-1 oral...HSV-2 genital. HSV are neurotrophic, grow within neurons, latency. transmission through fluids. lytic. point of initail contact and move down nerve to skin. incubation period 2-10 days. primary infection is a smptomatic person but seronegative. virus is shead in month after lesion.
An abnormal formation in the body, usually formed of mineral salts and most commonly found in the gallbladder, kidney, or urinary bladder.
|Describe a granuloma||
Inflammatory lesion that is composed of macrophages, fibroblasts, epitheloid cells, giant cells, lymphocytes, and that forms microscopic aggregates or nodules
|Describe the pathogenesis of fever||
External triggers include trauma/ischemic injury, infection with endotoxin production, inflammation
Triggers lead to production of endogenous pyrogen (EP) by mononuclear phagocytes (macrophages)
1 hour later: EPs can be IL-1, TNF-a, INF-a, IL-6
EP travels to hypothalamus, cause production of prostaglandins, increase hypothalamus set point, triggers chills and warmth-seeking behaviors, increases corticosteroid release, decreases ADH release
|Define reversible cell injury||
Cellular response to adverse environmental stimulus within range of homeostasis caused by low level injury.
Cell will return to steady state with cessation of stimulus, usually mild and short-lived.
Cells can adapt by changing in size and number
|Which grandular tissue cannot heal by regeneration?||
|What are possible reasons for the following types of leukocytosis: excess of PMNs||
|List the leukocyte disorders||
Leukopenia – deficiency of leukocytes;
Leukocytosis –nonneoplastic elevation of WBC counts, due to normal, increased physiological demand;
leukemia – neoplastic elevation of WBCs in blood
|List other types of emboli besides thromboemboli||
foreign body emboli
|what types of chemical signaling exist?||
hormonal,neurohormonal, paracrine, autocrine autostimulation
|Is G2 phase longer or shorter than G1?||
|Single Gene Disorders (3 types)||
Autosomal dominant, Autosomal recessive, Sex-linked
Almost always associated with the X chromosome
Muscle stiffening (See notes for time period)
EDV determined, amount of blood that fills ventricle at rest
|Rapidly Progressive Glomerulonephritis (RPGN)||
(aka subacute, cresentic, or extracapillary glomerulonephritis), disease that develops over a period of days to weeks. o Disease affects primarily adults in theirs 50s and 60s and may be idiopathic or associated w/ proliferative glomerular disease (w/ diffuse proliferation of extracapillary cells), such as poststreptococcal glomerulonephritis and antineutrophil cytoplasmic antibodies.o By diagnosed, renal insufficiency is apparent. There is extensive proliferation of cells into the Bowman space w/ crescent formation. Typically, the glomerular injury is accompanied by a rapid decline in glomerular function, progressing to renal failure in a few weeks or months.o Hematuria is common and may/may not be accompanied by proteinuria, edema, or hypertension.
Also called an infection stone, this urinary stone develops when a urinary tract infection neutralizes the urine, enabling the bacteria to grow more rapidly and a jagged ammoniomagnesium phosphate stone to develop.
|Describe pathological findings of fibrinous inflammation||
exudate rich in albumin, immunoglobins, and fibrin
Exudate may organize to form fibrous tissue, which can then cause adhesion and scarring
|Chronic granulomatous disease||
absence of enzymes to make lysosomal free radicals
|Describe pathological findings in serous inflammation||
transduate is clear fluid
easy healing if causative factor is removed
serous fluid can be reabsorbed into tissue
|What is the difference between regeneration and repair||
Both are healing processes.
Regeneration: Uninjured parenchymal (functional) cells may replicate to replace injured cells if stroma (connective tissue and blood vessels) is not injured. Function is restored, no scarring, can occur if parenchymal cells can replicate.
Repair: When lost parenchymal cells cannot replicate and be replaced. Replacement by fibrous connective tissue called repair by fibrosis. Scar formation occurs with possible impairment of tissue function.
|What are the most common autoimmune diseases?||
|How does platelet plug become stabilized to form a clot?||
Platelet GPIIb/IIIa receptors bind fibrinogen (each end of fibrinogen binds to a platelet), so that platelets become linked together. But the fibrinogen must be converted to stable fibrin to stabilize the clot.
The coagulation cascade will convert the fibrinogen to fibrin. In order to assure that the coagulation cascade physically occurs near the fibrinogen so that fibrin is formed, platelets express a protein factor (platelet factor 3 (PF3) – NOT a circulating clotting factor) on their surfaces.
PF3 binds clotting factor V, which leads to binding of other clotting factors to platelet, so that coagulation cascade takes place where needed.
Keep in mind that the circulating clotting factors, made in liver, are always circulating in blood in inactive form – they are activated in coaguolation cascade
|List “anticoagulant” drugs used in therapy for thrombosis and thromboembolism and how do they work?||
Anticoagulant drugs include:
Heparin (given by IV or SC injection )
Low molecular weight heparins (LMWH) such as enoxaparin (Lovenox) (given by SC injection)
Warfarin (Coumadin) (given PO).
heparin and LMWH get rid or prevent thrombi and emboli by activating antithrombin III, a normal body enzyme that breaks down clotting factors. These drugs do not break down thrombus or embolus themselves, but prevent growth of thrombus or embolus so that normal body mechanisms can break down thrombus or embolus
warfarin – prevents thrombi and emboli by inhibition of vitamin K which is necessary to make clotting factors
|what are the types of signal transduction?||
extracellular messengers-channel regulation-second messengers
|Fat necrosis (3 parts)||
1. Caused by enzymes-lipases (that breakdown fat) 2. Examples: Breast, pancreas, abdominal structures 3. Opaque, chalk white appearances
|End Stage Renal Failure||
results from progressive chronic renal failure. There is less than 10% of remaining renal function and dialysis or kidney transplant is required to sustain life.
|Renal Cell Carcinoma||
A malignancy arising from the renal tubule that produces hematuria, flank pain, and an abdominal mass.
|Describe 3 pathogenic pathways leading to chronic inflammation||
a) extension of acute inflammation
b)prolonged healing of acute inflammation
c)persistence of cause of inflammation (microorganisms, prolonged exposure to toxins, autoimmune diseases, foreign bodies)
|What monitoring is done by means of the following measurements of electrical activity: ECG/EKG||
electrocardiogram: heart function
|List factors that may delay healing and repair||
large size of wound
poor blood flow
|Describe Progressive Systemic Sclerosis (PSS, Scleroderma) and what is its pathogenesis?||
This is an autoimmune disease that involves fibrosis of skin, GIT, kidneys, heart, muscles, lungs
Mainly occurs in women with peak incidence in 50-60 year age group.
Th cells respond to unknown antigen, release cytokines which attract other inflammatory cells, a Type IV hypersensitivity. These other cells release mediators that increase collagen production by fibroblasts, excessive fibrosis throughout body.
|Describe the basic features of antibodies/immunoglobins and their reaction with antigen||
Antibodies/Immunoglobins are Y shaped protein molecules produced by plasma cells (a type B cell).
Fab portion: "branches" of Y, each branch can bind to epitope of antigen, specificity is coded for by DNA of B cell, structure of this portion varies among antibodies according to specificity for a particular antigen.
Fc portion: "stem" of Y, fixed structure, the same in every antibody of same type in the same individual.
-can bind to macrophages, PMN's, eosinophils, allowing to phagocytize or kill antigen attached to branches of Y
-can bind to platelets, mast cells, causing release of mediators
-can bind to complement: causing activation of complement
|How are platelets formed from megakaryocyte progenitor cells?||
Membranes of megakaryocyte progenitor cells become discontinuous, cells extend portions of themselves through openings in marrow sinusoids
Fragments of these cells are shed into blood – à these fragments become platelets.
Platelets are fragments of cytoplasm and do not have a nucleus
(these include polymorphonuclear neutrophils /PMNs)
Lifespan is hours to few days, circulating granulocytes are mature, functional cells, can travel to tissues and carry out defensive function, PMNs are“first responders” and are predominant in acute inflammation.
|What is leukopoesis?||
This is the formation of WBCs which are called leukocytes in bone
Leukocytes include granulocytes, monocytes, and lymphocytes
|what is passive transport?||
net movement of molecules and ions across a membrane from higher to lower concentration( down a concentration gradient) does not require metabolic enery.
|Starling's Law of the Capillaries||
Hydrostatic pressure pushes fluid out, Osmotic pressure pulls fluid in
|before 20 weeks...of pregnancy induced hypertension||
PIH/GHTN, systolic pressure increases 30 mm Hg or greater. diastolic pressure increases 15 mm Hg
A condition i nwhic hteh flow of urine is blocked, frequently by ureteral or kidney stones, resulting in the reflux of urineand subsequent injury to the kidneys.
|Describe cellular events in acute inflammation||
In dilated capillaries, there is congestion of RBCs and rouleaux, causing margination of neutrophils and platelets.
There is adhesion of platelets to endothelial cells, platelets release mediators, mediates cause activation of endothelial cells to express sticky protein molecules.
Stickiness facilitates pavementing of neutrophils onto endothelial cell lining of capillaries.
Neutrophils develop pseudopods to emigrate between endothelial cells, through basement membrane, and out of blood vessels.
Neutrophils migrate by chemotaxis to site of injury
|Absence of LAD1, LAD2 adhesion molecules||
no binding of leukocytes to endothelial cells
|What is fever of undetermined origin (FUO)||
38.3c/101F continuing for 3 weeks
failure to determine cause
Usual causes: infection, malignant tumor, collagen-vascular diseases
In about 10-15% cases, cause is undetermined.
|List and categorize the most important causes of cell injury||
lack of oxygen, ischemia will decrease ATP formation
primary nutrient deficiency
secondary nutrient deficiency
viral infection: virus infected cells use up nutrients
exogenous: microbial toxins, drug OD, chemicals
endogenous: accumulation of a normal substance in body to toxic levels
hypothermia: ice in cytoplasm
radiation: production of free radicals
immunological injury: Ab, complement
|Which body cells can become infected by HIV?||
Th and some other cells:
microglia of nervous system
follicular dendritic cells in lymph nodes
|What is pathogenesis of contact dermatitis and give examples||
This is a Type IV hypersensitivity.
There are T cells and macrophages in skin lesions.
No granulomas are formed.
There is wheal formation and edema of affected skin
examples: poison ivy, latex allergy, gold allergy
|What is thrombocytopenia and what can cause this?||
a. Insufficient circulating platelets, that can lead to bleeding problems.
b. some possible causes -
bone marrow suppression
drugs (gold salts, thiazide diuretics, some antibiotics, heparin, others)
disseminated intravascular coagulation (DIC)
|Define infarction and infarct.||
a. infarction is the process by which an infarct is formed, infarction is most common and serious in arteries
b. infarct – region of necrosis caused by ischemia, most
often caused by thrombus that blocks a blood vessel. Other possible causes are tumor compressing a blood vessel and atherosclerosis in which there is blockage of a blood vessel.
|what is resting membrane potential?||
-inside of cell is negatively charged in comparison to the outside of cell (ex: in neurons usually is -70mv)
|what does the Golgi complex consist of ?||
flattended, smooth membranes-secretory vesicles-proteins from the ER are packaged in the Golgi complex-cisternae
|3 genetic defects in leukocyte function that result in recurrent bacterial infections in young children, with possibnle early death||
1. absence of LAD1, LAD2 adhesion molecules
2. Chediak-Higashi syndrome
3. Chronic granulomatous disease
|What is normal temperature and why must it be maintained||
Normal is 37C or 98.6F
Stable temperature is important for function of cells
|Describe 3 types of cell adaptations involving changes in size or number of cells in reversible cell injury||
Atrophy: decrease in size of cell
pathologic: muscle disuse/denervation
Hypertrophy: increase in size of cell
physiologic: muscle with exercise
pathologic: overwork of heart
Hyperplasia: increase in number of cells
physiologic: uterus in pregnancy
pathologic: callus on skin with excessive contact
|What is pathogenesis of rheumatoid arthritis||
Abs form against Ag of synovial tissues, AgAb complexes accumulate in joints, tissue damage, a chronic condition
Localized condition involving Type III hypersensitivity
|How can bone marrow function be restored in patients with leukemias and lymphomas||
Bone marrow Transplantation – to restore marrow function
750 ml from hip of donor
IV injection to recipient
donor cells become established in recipient bone marrow
|How may small blood vessel fragility occur and what can result?||
immune complex deposition in blood vessels - as with SLE, drugs, allergies
direct damage – bacterial toxins, snake venom
genetic problems causing defective blood vessels – such as hereditary hemorrhagic telangiectasia, Marfan’s syndrome
vitamin C deficiency (scurvy) – poor formation of blood vessels
Cushing’s disease – breakdown of blood vessels
senile purpura – age related – hands, wrists, upper arms, calves are mainly affected
Results include - bleeding from microvasculature, called vascular purpura – mainly seen in skin and GIT (petechiae and purpura) , kidneys (hematuria)
|What are the usual causes of arterial thromboemboli and how do they cause infarcts?||
Arterial thromboemboli usually break off from a cardiac mural thrombus, a cardiac valve thrombus, a thrombus in an aneurysm, or a thrombus at a site of atherosclerosis
These thromboemboli can easily cause infarcts, since in arteries, blood is traveling away from heart to smaller and smaller blood vessels.
The embolus easily lodges in small blood vessel à can cause infarct.
|What is amniotic fluid embolism, how does this occur, and what are possible consequences?||
Amniotic fluid embolus consists of amniotic fluid with infant’s cells – this reaches bloodstream
This occurs during delivery or C-section – entry of amniotic fluid with infant’s cells into uterine or cervical veins
1) less severe – embolus is carried to lungs and becomes trapped in small vessels à pulmonary function
2) more severe - injury to lung capillaries can occur, causing severe pulmonary edema
3) most severe - disseminated intravascular coagulation (DIC) – caused by substances in amniotic fluid that cause increased blood coagulation à obstruction of blood flow in lungs à circulatory collapse à tissue hypoxia, including brain à coma, seizures à 80% mortality rate
|Anti-gomerular Basement Membrane Disease||
a type of RPGN. Disease is rare and assoc. w/antibody formation against both pulmonary capillary and glomerular basement membranes, w/ activation of complement and neutrophils that damage the GBM
|What are the mechanisms of heat loss and how do they work to decrease body temperature||
Radiation: movement of heat away from warm surface
Evaporation: sweat is converted from liquid to gas, consumes energy
Conduction: transfer of heat to cooler surrounding medium
Convection: transfer of heat to air/water
|What type of tissue are cartilage and adipose tissue and how does healing occur in these tissues?||
Connective tissue and healing is prolonged due to limited blood supply.
cartilage: healing by fibrous repair, fibroblasts of perichondrium produces scar tissue, some loss of function
adipose tissue: cells cannot divide, but precursor cells produce new adipose cells, fibrosis does not occur
|List the main cells and organs that participate in specific immune reponse||
Primary lymphoid Organs: thymus, bone marrow
Secondary lymphoid Organs: lymph nodes, spleen, tonsils, Peyer's patches
Presence in other locations: MALT in GI, bronchial mucosa
T-cells develop in thymus
B-cells develop in bone marrow
plasma cells: differentiated B cells
T and B cells are stored in secondary lymphoid organs
|What are consequences and symptoms of lymphomas?||
There is loss of normal immune function with infections, also
|How do arterial thrombi and venous thrombi differ?||
In arterial thrombi there is more organization and smaller size. Lines of Zahn – more distinct layers seen in thrombus in arteries – swift blood flow then prevents further buildup of thrombus .
Venous thrombi are larger and less organized. They consist of a mixed region – less distinct layers are seen – slower blood flow then allows further buildup of thrombus; and also a red cap forms – this is accumulated coagulated blood on top of mixed region in veins or atria, builds up and lengthens in downstream direction
|How do most grandular tissues, such as liver and kidney heal with minor injury, more extensive injury and with even more sever, sustained injury?||
Most glands are made up of quiescent/stable cells, therefore can readily regenerate with minor injury.
More extensive injury: regeneration with some loss of normal structure and function
Severe, sustained injury:
-loss of parenchymal, stroma, ECM
-contracted scar tissue
-loss of function with irregular surface depressions
|What are the main differences between T cell and B lympohocytes?||
T cells: produced in bone marrow and thymus, mature in the thymus, many surface proteins, these proteins are T cell receptors which recognize surfaces of foreign antigen.
T cell DNA has hundreds of genes that can reaarange to form new populations of T cells, with receptors that can ever better recognize a specific foreign antigen
B cells: produced and mature in bone marrow, differentiate into plasma cells, which produce Ab and differentiate into memory B cells
B cells have many surface proteins/cell receptors, plasma cells also have coating of own antibodies which repsond to specific antigen, more production of Ab
|What is the difference between acute and chronic leukemias?||
a. acute – acute onset, more severe symptoms, immature, undifferentiated cell forms
b. chronic – gradual onset, less severe symptoms, differentiated cell forms
|What can happen if a vein is blocked by a thrombus||
Infarction due to venous obstruction is unlikely.
First of all, veins do not usually bring oxygen and nutrients to a tissue area. Also, there are usually collateral veins serving the same tissue area - if one is obstructed, blood can low through another vein.
However, reduced venous drainage can occur à leakage of fluid from veins à swelling, pain, ulceration of overlying skin in leg – this is called thrombophlebitis
|Describe healing of a wound by primary intention||
This occurs where wound is clean and edges are close together (e.g. surgical incision).
Healing by repair and fibrosis, angiogenesis and restoration occurs.
Additionally, granulation tissue appears in 2-3 days, fibroblasts in granulation tissue make procollagen organized into collagen fiber bundles outside of cell, ECM strengthens collagen, and there is realignment of collagen fibers after about 6th day, increasing strength.
Surface restoration is occurring. If a skin wound: keratinocytes of epidermis produce new keratin, which loosens scab, melanocytes of epidermis do not regenerate, scar area is pale
By 2nd week, changes in granulation tissue, fewer phagocytes, reabsorpion of blood vessels
Continued remodeling of collagen for about 3 months to maximal strength of scar, about 70-80% of normal.
|Why is ischemia is more serious than hypoxia?||
In ischemia there is a block of blood flow to the affected tissue so that NO oxygen or glucose (energy source) are delivered to the tissue.
Hypoxia is when a decreased amount of oxygen is delivered to the affected tissues, but tissues still receive glucose.
Glucose can still be broken down anaerobically (without oxygen) to produce some ATP (molecule providing energy to cell), although with less oxygen the process of oxidative phosphorylation cannot take place in mitochondria of cells, so that much less ATP is produced.