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179 Cards in this Set
- Front
- Back
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What is the function of the nucleus?
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It is the membrane enclosed organelle of eukaryotic cells. It contains most of the cell's genetic material (DNA)
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Explain the roles of the rough and smooth endoplasmic reticulum?
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ROUGH- resp. for production of proteins. Called rough due to ribosomes.
SMOOTH-processing of proteins, ldl metabolism. |
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What are the 8 specialized functions of the cell?
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Movement, conductivity, Metabolic Absorption, Secretion, Respiration, Reproduction, Communication.
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Explain the lipid bilayer?
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Amphipathic (Hydrophilic and Hydrophobic)
The barrier has a negative charge and ions are repelled by charged barrier. |
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What are ligands?
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Hormones that bind with cell receptors.
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What is the role of mitochondria?
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The "powerhouse" of the cell.
Resp. for ATP production, oxidative phosphorylation. |
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What is the role of lysosomes?
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The cell's waste disposal system. Contain digestive enzymes that break down waste materials and cellular debris.
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What is oxidative phosphorylation?
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Occurs in mitochondria. Mechanism by which energy is produced from carbs, fat, proteins, and transferred to ATP.
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PASSIVE VS. ACTIVE TRANSPORT?
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H20 and small elec. charged molecules move easily through pores in plasma membrane (passive)
Active transport requires movement against the concentration gradient (low to high) and requires the expenditure of ATP. |
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Explain the 3 types of cell junctions?
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desmosomes (adhering)
tight junctions (impermable) gap junctions (adhering/communicating) |
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How do cells communicate?
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They form protein channels (gap junctions)
they display the plasma membrane-bound signaling molecules and they secrete chemicals that signal to other cells (most common) |
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What is the difference between GTP VS GDP?
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GTP is guanosine triphosphate
think of it that with GTP the cell is "ON" and with GDP the cell is "OFF". When GTP is dephosphorylated, it becomes GDP (empty battery) |
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Explain the resting potential?
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All cells are electrically polarized with the inside more negatively charged than the outside. This Difference in charge is known as resting membrane potential and is -70 mv.
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What is action potential?
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When a nerve or muscle cell receives a stimulus that exceeds the membrane threshold value, there is a rapid change in rest. membrane potential. (carries signal along the nerve to convey info)
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Apoptosis VS Necrosis?
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APOPTOSIS- Programmed cell death. Keeps balance between cell proliferation and cell death. The capsases cleave and kill neatly.
NECROSIS- Messy! Cells burst and swell and spill contents causing inflammatory response. |
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HYPERTROPHY VS HYPERPLASIA?
DYSPLASIA VS METAPLASIA? |
Hypertrophy- Increase in SIZE of cell caused by increase work demands or hormonal stim. (heart/kidneys)
Hyperplasia- Increase in NUMBERS of cells, Increased rate of cellular division. (liver/uterus) Dysplasia- abnormal change in size and shape (cervix) Metaplasia- reversible replacement of one mature cell with another less differentiated cell type. (bronchioles/smoking) |
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Hydrostatic Pressure and Oncotic Pressure? What can effect them both?
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Hydrostatic pressure is the mechanical force of water pushing against cellular membranes.
Oncotic pressure- The amount of hydrostatic pressure required to oppose the osmotic mvmt of water . The overall osmotic effects of colloids, (plasma proteins) is called colloidal oncotic pressure. |
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ENDOCYTOSIS?
PHAGOCYTOSIS? PINOCYTOSIS? |
ENDOCYTOSIS- occurs when pits invaginate, internalizing ligand receptor complexes in coated vesicles.
PHAGOCYTOSIS- A type of endocytosis in which large particles such as bacteria are ingested through vacuoles. PINOCYTOSIS- type of endocytosis in which fluid and solute molecules are ingested through form. of small vesicles "cell drinking" |
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EXPLAIN THE CELL CYCLE?
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1.G1 PHASE- G=GAP, period between M phase and start of DNA Synthesis.
2.S PHASE- S= SYNTHESIS, (dna synthesized in nucleus) 3.G2 - RNA, protein synthesis 4.M PHASE- MITOSIS |
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What are the growth factors?
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cytokines-peptides that transmit signals within and between cells.
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TYPES OF NECROSIS?
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COAGULATIVE:
(kidneys/heart/adrenal) results from hypoxia/ischemia. protein changes from gelatinous to opaque state. LIQUEFACTIVE: results from ischemic injury to neurons and glial cells in brain. (cerebral infarct) CASEOUS- (t.b. infection) tissues appear soft and resemble cheese. FAT NECROSIS- (breast/pancreas/adbominal structures) caused by lipases. tissue appears opaque and white due to saponification. GANGRENOUS NECROSIS- (severe hypoxic injury, usually lower legs) tissue can be black and full of pus. |
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What is the danger of free radicals?
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They can cause membrane damage , difficult to control and initiate chain reactions. Can cause lipid peroxidation, alterations of protein, alterations of DNA.
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Signs of irreversible cell injury?
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Dense clumping and disruption of genetic material/plasma membrane/and organelle membrane.
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What are the effects of K and Na on membrane excitability?
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REMEMBER MORE K INSIDE CELL, AND MORE Na OUTSIDE CELL.
When extracellular K levels decrease rapidly, the intracellular K diffuses OUT of the cell and resting membrane potential becomes more NEGATIVE. The cell will become hyperpolarized, requiring a stronger stimulus to initiate an action potential, thereby decreasing excitability. If there is a disruption in the membrane, Ca wants to flood in the cell. Changes in extracellular Ca make the threshold potential less negative and decrease membrane excitability. *POTASSIUM AFFECTS RESTING MEMBRANE POTENTIAL *CALCIUM AFFECTS THE THRESHOLD POTENTIAL. |
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Effects of hypokalemia?
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Dysrhythmias, Skeletal muscle weakness, dep. of ventilation, paralysis, resp. arrest. Also it delays ventricular repolarization, (AV BLOCK, ATRIAL TACHYCARDIA)
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HYPERKALEMIA?
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Found in burns, massive crushing injuries.
symptoms: muscle weakness or paralysis, tingling of lips and fingers. |
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HOW IS POTASSIUM REGULATED?
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By kidneys, aldosterone, insulin, and changes in pH.
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What regulates the acid-base balance?
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The renal and respiratory systems, together with the body's buffer systems.
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What are the principal plasma buffers?
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Carbonic Acid-Bicarbonate,
protein (hemoglobin) and phosphate. |
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An abnormal change in bicarbonate causes?
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Metabolic Acidosis
or Metabolic Alkalosis |
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Causes of metabolic acidosis?
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Increase of noncarbonic acids or loss of bicarb from extracellular fluid.
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Causes of RESPIRATORY ACIDOSIS?
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Decrease of alveolar ventilation, and INCREASED CO2!!
(HYPERCAPNIA) |
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Causes of metabolic alkalosis?
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Increase in bicarb, caused by vomiting, GI suctioning, bicarb intake, and diuretic therapy.
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You have a patient with a pH of
7.45, a pCO2 of 21 and a HCO3 of 14. What is it? |
Compensated respiratory alkalosis.
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Causes of EDEMA?
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Accumulation of fluid in interstitial spaces, caused by arterial dilation, venous or lymphatic obstruction, loss of plasma proteins, increased capillary permeability, increased vascular volume.
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How is water balance regulated?
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by thirst and ADH, which is initiated by an increase in plasma osmolality or dec in circ. bld volume.
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Explain the renin-angiotensis-aldosterone system?
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Renin and angiotensin are enzymes that promote or inhibit the secretion of aldosterone and regulate sodium and water balance.
When circ. bld. volume is low, RENIN, is released from kidneys and stimulates ANGIOTENSIN 1, which is an inactive polypeptide, which is then converted into ANGIOTENSIN 2, which stimulates the secretion of aldosterone, and causes vasoconstriction. The vasoconstriction elevates the BP, and restores renal perfusion. |
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What is the difference between TRANSCRIPTION AND TRANSLATION?
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TRANSCRIPTION:
DNA specifies a sequence of RNA, (PROTEINS ARE SPECIFIED) TRANSLATION: single stranded RNA, directs the synthesis of polypeptides, and takes place in ribosomes. During translation, mRNA interacts with tRNA. |
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What is polyploidy?
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A euploid cell has some multiple of the normal chromosomes.
(triploidy or tetraploidy) both are lethal |
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ANEUPLOIDY?
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Somatic cells that do not have a multiple of 23 chromosomes. Usually a result of non-disjunction.
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TRISOMY?
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A type of aneuploidy in which one chromosome is present in three copies of somatic cells.
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DOWN SYNDROME?
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TRISOMY 21. Best known disease caused by chromosome alteration. Associated with increased maternal age.
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What are the most common aneuploidies of the sex chromosomes?
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47 XXX
45, X TURNER SYNDROME 47XXY KLEINFELTER'S SYNDROME AND 47 XYY |
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What is DOMINANCE?
RECESSIVE? |
DOMINANCE- the allele who's effects are observable
RECESSIVE- the allele who'e effects are hidden. |
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CHARACTERISITICS OF AUTOSOMAL DOMINANT INHERITANCE?
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RARE.
ON AVERAGE, HALF OF THE CHILDREN WILL BE HETEROZYGOUS AND HALF WILL BE BE NORMAL. EX:ACHONDROPLASIA, HUNTINGTON DISEASE. |
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WHAT IS A TUMOR SUPPRESOR GENE?
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Gene responsible for retinoblastoma, the normal function of its protein product is to regulate the cell cycle so that cells dont grow uncontrollably. When a mutation alters the protein, its tumor supressing capacity is lost and a tumor can form.
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AUTOSOMAL RECESSIVE?
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ALSO RARE, but carriers can be high.
most common lethal is cystic fibrosis. Cosanguinity is a factor. MALES AND FEMALES ARE AFFECTED IN EQUAL PROPORTIONS. COSANGUINUITY. SEEN IN SIBLINGS BUT NOT PARENTS. ONE FOURTH OF CARRIER OFFSPRING AFFECTED. EX: SICKLE CELL, CF, TAY-SACHS, HEMOCHROMATOSIS, AND GALACTOSEMIA. |
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X LINKED?
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(SEX LINKED)
TRAIT SEEN MUCH MORE OFTEN IN MALES THEN FEMALES. NEVER TRANSMITTED FROM FATHER TO SON. CARRIER FEMALES, "SKIPPED GENERATION" GENE PASSED FROM FATHER TO ALL DAUGHTERS, WHO IN TURN PASS TO HALF THEIR SONS. EX: DUCHENNE MUSCULAR DYSTROPHY |
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WHAT IS THE HALLMARK OF CANCER?
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ANAPLASIA-
loss of differentiation irregularities in size and shape of nucleus, and loss of normal tissue structure |
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CARCINOMAS?
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cancers arising in EPITHELIAL TISSUE.
IF ductal or glandular, adenocarcinoma. ex: mammary adenocarcinoma |
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SARCOMA?
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cancer of CONNECTIVE TISSUE.
EX: rhabdomyosarcoma |
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LYMPHOMA?
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Cancer of lymphatic tissue.
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LEUKEMIA?
ACUTE VS CHRONIC? |
cancers of blood forming cells.
acute=progenitor cells, immature cells function improperly chronic= mature cells, but unable to do the job. |
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WHAT ARE TUMOR MARKERS?
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Substances produced by cancer cells. Can be found in tumor, blood, urine, spinal fluid.
ex: AFP OR PSA |
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CANCER IS PREDOMINANTLY A DISEASE OF WHAT?
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AGING
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WHAT ARE TELOMERES?
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TELOMERES
are protective ends or caps, on each chromosome, and are placed and maintained by telomerase. Short telomres signal the cell to cease division. If telomeres are small the cells die. BUT CANCER CELLS ACTIVE TELOMERASE, and make it possible to divide and divide all over again. |
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WHAT IS CLONAL PROLIFERATION?
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A Mutant cell has a selective advantage over its neighbors, its progeny can accumulate faster.
(by increased growth rate and decreased apoptosis) |
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PROTO-ONCOGENES?
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Encode for growth factors.
ex: PDGF, growth factor receptors, signal transducers, (RAS), and nuclear growth promoting proteins. (only need ONE!!!) |
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TUMOR-SUPPRESOR GENES?
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encode proteins that in their normal state negatively regulate proliferation "put the brakes on"
(NEED TWO!!!) |
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SIX HALLMARKS OF CANCER?
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-SELF SUFFICIENCY IN GROWTH SIGNALS
-INSENSITIVITY TO ANTI-GROWTH SIGNALS -EVADING APOPTOSIS -LIMITLESS REPLICATIVE POTENTIAL -SUSTAINED ANGIOGENESIS -TISSUE INVASION AND METASTASIS |
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WHAT ENABLES METASTASIS?
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- Detachment and invasion.
-Survival and spread in circulation -selective adherence in favorable sites -recruit new blood vessel growth |
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HEMATOPOEISIS?
WHAT ARE THE TWO STAGES? |
Blood cell production.
Occurs in liver and spleen of fetus, and bone marrow after birth. 1-Proliferation 2-Maturation |
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WHAT IS THE DIFFERENTIATION OF THE MONOCYTES/MACROPHAGE LINE?
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1 HEMATOPOIETIC STEM CELL
2 COMMON MYELOID PROGENITOR 3 GRANULOCYTE 4 MONOCYTE PROGENITOR 5 MONOBLAST 6 MONOCYTE/MACROPHAGE |
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WHAT IS THE DIFFERENTIATION PATTERN OF THE RBC CELL LINE?
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1- HEMATOPOIETIC STEM CELL
2-COMMON MYELOID PROGENITOR 3-ERYTHROID PROGENITOR 4-PROERYTHROBLAST 5-ERYTHROCYTE |
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WHAT IS THE DIFFERENTIATION LINE OF THE NEUTROPHIL?
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1- HEMATOPOIETIC STEM CELL
2-COMMON MYELOID PROGENITOR 3-GRANULOCYTE/MONOCYTE PROGENITOR 4-GRANULOCYTE PROGENITOR 5-MYELOBLAST 6-NEUTROPHIL |
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ANEMIAS CAN BE CLASSIFIED ACCORDING TO WHAT?
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1- ERYTHROCYTE SIZE/CONCENTRATION OF HGB
2- THEIR CAUSE |
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MACROCYTIC-NORMOCHROMIC OR MEGALOBLASTIC-NORMOCHROMIC ANEMIAS ARE CAUSED BY?
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Deficiency of Vitamin B12.
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MOST COMMON ANEMIA?
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IDA
chronic poor, women if childbearing age, and children. |
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APLASTIC ANEMIA?
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-Characterized by pancytopenia.
a reduction of absence of all three blood cell types. -Results from failure or supression of bone marrow to produce blood cells -RARE |
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HEMOLYTIC ANEMIA?
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Premature accelerated destruction of erythrocytes.
-Can be congenital or acquired. |
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What are ANTIGENS AND ANTIBODIES?
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ANTIBODY-
immunoglobulin, a serum glycoprotein produced by plasma cells in response to a challenge by an immunogen. FIVE classes of immunoglobulins. ANTIGENS- A molecule that can react with antibodies, or antigen receptors on B AND T cells. |
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WHAT ARE THE TWO TYPES OF IMMUNITY?
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-INNATE RESISTANCE OR IMMUNITY BY NATURAL BARRIERS & INFLAMMATORY RESPONSE
AND ADAPTIVE (ACQUIRED) IMMUNE SYSTEM. |
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NAME SOME PHYSICAL AND MECHANICAL AND BIOCHEMICAL BARRIERS?
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first line of defense!!
skin and mucous membranes cathelicidins and defensins are antimicrobials prod. by epithelial cells. normal bacterial flora. |
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CHARCTERISTICS OF THE SECOND LINE OF DEFENSE(INFLAMMATORY RESPONSE) ?
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rapidly initiated, non-specific.
vascular vasodilation, increased capillary permeability, and white blood cell adherence to vessel walls. - The classical pathway, the alternative pathway, and the lectin pathway. Results in opsonization, activation of anaphylatoxins, cell lysis, leukocyte chemotaxis. |
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HOW DOES THE CLOTTING CASCADE HELP?
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Prevents spread of microrganisms, contains microorganisms and foreign bodies at the site of inflammation, provides framework for repair and healing.
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WHAT IS THE KININ SYSTEM?
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The kinin system proteins promote vasodilation and increased capillary permeability, and induce PAIN.
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H1 HISTAMINE RECEPTORS?
H2 HISTAMINE RECEPTORS? |
H1-PROMOTE INFLAMMATION
H2-INHIBIT INFLAMMATORY RESPONSE |
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STAGES OF PHAGOCYTOSIS?
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-RECOGNITION AND ADHERENCE
-ENGULFMENT -LYSOSOMAL FUSION -DESTRUCTION!! |
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WHAT ARE NEUTROPHILS?
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Predominant phagocyte of early inflammation. Attracted to inflamm. site by chemotactic factors.
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MONOCYTES AND MACROPHAGES?
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Arrive later. Remain longer to clean up debris and promote healing.
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EOSINOPHILS?
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help control mast cell vascular mediators and defend against
PARASITES |
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BASOPHILS?
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Granulocytes very similar to mast cells.
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NATURAL KILLER CELLS?
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Recognize and eliminate VIRUSES, cancer cells, and other abnormal cells.
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PLATELETS?
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Interact with coagulation cascade to stop bleeding, release mediators to control inflammation
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CYTOKINES?
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Soluble factors that regulate the inflammatory response and include interleukins, interferons, and tumor necrosis factor .
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LOCAL MANIFESTATIONS OF INFLAMMATION?
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Vasodilation, increased cap. permeability, redness, heat, swelling, and pain. Functions to dilute toxins and carry debris away from site.
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SYSTEMIC MANIFESTATIONS OF INFLAMMATION?
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Fever, leukocytosis, increased levels of circulating plasma proteins. (fibrinogen, C-reactive protein)
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CHARACTERISTICS OF CHRONIC INFLAMMATION?
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last two weeks or longer.
dense infiltration of lymphocytes and macrophages. To isolate infection and protect ag. tissue damage may form granuloma. |
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DESCRIBE ADAPTIVE IMMUNITY?
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Slower, specific, has MEMORY,
mediated by B AND T LYMPHOCYTES. B-humoral immunity, mediated by circulating antibodies. T-cell-mediated immunity, kills targets directly. B AND T lymphocytes bind antigen through cognate receptor complexes (BCR, TCR) |
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CD4 is a surface marker on what cell?
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HELPER T CELLS
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CD8 ?
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CYTOTOXIC T CELLS
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CD21 AND CD40?
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B CELLS
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WHAT IS CLONAL SELECTION?
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Process by which antigen selects lymphocytes with complementary TCRs and BCRs and induces an immune response with the production of specific antibody or cytotoxic T cells.
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WHAT IS THE ROLE OF MHC?
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Major histocompatability complex.
Antigen presentation is the primary role of molecules of the MHC. MHC molecules are gylcoproteins found on all cells except rbc's. divided into class 1 and class 2. |
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DESCRIBE MHC CLASS1?
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PRESENTS:" ENDOGENOUS"
antigens, derived from intracellular proteins. REACTS WITH: CD8 on Tc cells |
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DESCRIBE MHC CLASS 2?
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PRESENTS: "EXOGENOUS ANTIGENS", derived from extracellular organisms.
REACTS WITH: CD4 on Th cells |
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IgG?
IgE? |
IgG -Most prevalent
IgG- Most rare |
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IgD?
IgM? |
First and largest
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IgA?
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found in secretions, prevent infection on epithelial surfaces
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What are superantigens?
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Molecules produced by infectious agents, that can bind to Th cells TCR outside the normal antigen binding site. Results in excessive production of proinflammatory cytokines that can cause shock.
EX: Toxic shock syndrome and food poisoning. |
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What are hypersensitivity reactions?
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Allergy, autoimmunity, and alloimmunity.
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Alloimmunity vs Autoimmunity?
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ALLOIMMUNIY:Inappropriate immune response directed at beneifical foreign tissue (transfusion or transplants)
AUTOIMMUNITY: inapp. response directed at the host's own tissues. |
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TYPE 1 REACTIONS?
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IgE mediated.
Causes mast cell degradation and release of histamine. Histamine enhances the chemotaxis of eosinophils into sites of type 1 allergic reactions. |
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TYPE 2 REACTIONS?
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Tissue specific reactions, caused by 5 mechanisms:
complement-mediated lysis opsonization and phagocytosis, neutrophil mediated tissue damage, antibody dependent cell mediated cytotoxicity, and modulation of cellular function. |
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TYPE 3 REACTIONS?
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Immune-complex mediated reaction.Immune complexes are deposited in target tissues, where they activate the complement cascade, generating chemotactic fragments that attract NEUTROPHILS, that release lysosomal enzymes.
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TYPE 4 REACTIONS?
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Cell mediated reactions.
Caused by cytotoxic T lymphocytes or lymphokine producing T1 Cells. poison ivy |
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Describe SLE?
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Systemic Lupus Erythematosus
Chronic, multisystem, inflamm. disease and most serious of autoimmune disorders. Present with: arthralgias, arthritis, rash. renal disease, anemia. No cure, treat symptoms. More common in black women. |
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TYPES OF BACTERIA?
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"TRUE" Cocci, rod shaped, vibrios, spirilla. No nucleus, no mitochondria, no membrane bound organelles.
FILAMENTOUS: mycobacteria (TB) SPROCHETES: flexible, anaerobic, (syphillis) MYCOPLASMA: lack cell wall, small. (pneumonia) RICKSETTIA: parasites spread by vectors (lyme disease) CHLAMYDIA: parasites. |
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GRAM NEGATIVE AND EXAMPLES?
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Do NOT retain crystal violet dye in membrane.
RESP EX: hemophilus influenzae,klebsiella, bordetella, pseudomonas, GI: e. coli IMPORTANT: GRAM NEG. HAVE A LIPID POLYSACCHARIDE COAT KNOWN AS ENDOTOXIN. HAVE A THIN PEPTIDOGLYCAN LAYER. |
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GRAM POSITIVE?
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DO retain the violet dye.
staph and strep most common. HAVE A THICK PEPTIDOGLYCAN LAYER. MRSA, Strep Pyogenes, C. diff. GRAM + are facultative anaerobic, and everywhere! |
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PROCESS OF INFECTION?
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COLONIZATION, INVASION, MULTIPICATION, AND SPREAD.
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WHAT ARE THE FOUR STAGES OF INFECTIOUS DISEASE?
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1-Incubation period
2-Prodromal State 3-Invasion period 4-Convalescence period |
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ENDOTOXINS?
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Contained in cell wall of GRAM NEGATIVE BACTERIA.
The lipidpolysaccharide layer is responsible for toxic effects. Called "pyrogenic" because they prompt inflamm. response and produce fever. |
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WHAT ARE EXOTOXINS?
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Proteins released during bacterial growth.
They can damage cell membranes, inhibit protein synthesis, activate second messengers. ex:N. MENINGITIDIS Vaccines are available for many exotoxins: Tetanus, Diptheria, Pertussis. |
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TRUE OR FALSE
The virus life cycle includes the following: Attachment, Penetration, Uncoating, Replication, Assembly, and Release. |
TRUE
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TRUE OR FALSE?
A retrovirus uses REVERSE TRANSCRIPTASE to convert RNA into double stranded DNA. |
TRUE
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DESCRIBE MALARIA?
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Most common parasite is Plasmodium Falciparum.
A person is bit by an anopheles mosquito. The parasite enters the bloodstream, survives in the liver, and invades parenchymal cells. After several rounds of division, the liver cell ruptures and the parasites enter the blood, infecting RBC'S. Symptoms can be severe chills, fever, vomiting, sweating, pulmonary edema and severe anemia. |
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TRUE OR FALSE?
The major lab finding in patients with HIV is decreased CD8 cells? |
FALSE!!!
It's a decrease in CD4 Th cells. |
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TRUE OR FALSE?
Under ischemia, the loss of ATP causes the cells to SHRINK due to the influx of NaCl. |
TRUE!!!!!!
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WHICH ION IS RESPONSIBLE FOR CAUSING A RAPID CHANGE IN THE RESTING POTENTIAL AND INITIATES AN ACTION POTENTIAL?
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SODIUM.
The gates open and Na rushes into the cell, changing the membrane potential from negative to postive. |
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WHEN HOMOLOGOUS CHROMOSOMES FAIL TO SEPARATE DURING MITOSIS OR MEIOSIS THIS IS CALLED?
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NONDISJUNCTION
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WHAT LAB VALUES ARE ASSOCIATED WITH DIC?
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Decreased platelets and fibrinogen, prolonged PT, PTT, Thrombin time and increased Fibrin Degradation Products and elevated D Dimer.
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The PHILADELPHIA chromosome is a marker for which LEUKEMIA?
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CHRONIC
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NATURAL KILLER CELLS ASSOCIATE WITH?
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MHC 1
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HOW is the mitochondria affected by Ca ions?
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INFLUX of Ca ion into cell halts ATP PRODUCTION!
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COPD, sedative overdose, severe pneumonia, Guillain-Barre, mechanical hypoventilation, can all cause which acid base imbalance?
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RESPIRATORY ACIDOSIS
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Hyperventilation, hypoxia, pulmonary emboli, brain injuries, mechanical hyperventilation, can all cause which acid base imbalance?
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RESPIRATORY ALKALOSIS
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Diabetic Ketoacidosis, lactic acidosis, renal failure, GI fistulas, and shock cause which acid-base imbalance?
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METABOLIC ACIDOSIS
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Severe vomiting, excessive gastric suctioning, diuretic therapy, K deficits, excessive use of mineralcorticoids can all cause which acid-base disturbance?
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METABOLIC ALKALOSIS
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Which acid-base disorder presents with the following symptoms:
Drowsiness, dizziness, coma, LOW BP, V FIBB, Seizures, and hypoventilation. |
RESPIRATORY ACIDOSIS
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GENES whose protein products can directly or indirectly prevent cell division or lead to apoptosis...
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TUMOR SUPPRESSOR GENES
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VIRUSES ALMOST ALWAYS CAUSE A_________ MUTATION?
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PROTO-CONCOGEN
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TRUE OR FALSE:
IF A MUTATION OCCURS IN SOMATIC CELLS, IT IS NOT PASSED ON TO CHILDREN. |
TRUE
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SIGNS OF HYPOCALCEMIA?
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ANXIETY, IRRITABILITY, TETANY
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ECF IS CONTROLLED BY?
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THE SERUM SODIUM CONCENTRATION
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WHICH IMMUNOGLOBULIN IS MOST RESPONSIBLE FOR ANAPHYLAXIS?
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IgE?
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CYTOTOXIC CELLS THAT ATTACH TO VIRALLY INFECTED CELLS OR TUMORS TO MEDIATE THE DESTRUCTION OF THESE INJURIOUS CELLS IS AN EXAMPLE OF???
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CELL-MEDIATED IMMUNITY
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Which of the following is a low molecular weight protein released by the host cell that helps prevents viruses from infecting healthy cells?
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INTERFERON
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THE ABILITY OF AN AGENT TO PRODUCE DISEASE IS TERMED?
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PATHOGENICITY
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PASSING MATERNAL ANTIBODIES TO A FETUS IS AN EXAMPLE OF WHICH TYPE OF IMMUNITY?
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PASSIVE ACQUIRED IMMUNITY
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WHAT IS THE ACTION OF INTERLEUKIN?
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ATTRACTS WHITE BLOOD CELLS TO THE SITE OF INJURY AND BACTERIAL INVASION.
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PURPOSE OF NK CELLS?
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Recognize surface changes on body cells infected with a virus.
It then binds to, and kills the infected cell. |
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WHAT CAUSES ERYTHROBLASTOSIS FATALIS?
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RH NEGATIVE MOM HAS AN RH POSITIVE FIRST CHILD AND DEVELOPS ANTIBODIES. WHEN PREGNANT WITH SECOND CHILD, THE RBC'S ARE ATTACKED BY MOM'S ANTOBODIES. GIVE RHOGAM TO PREVENT THIS
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DESCRIBE A TYPE 1 HYPERSENSITIVITY REACTION?
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An immediate reaction that occurs in response to an interaction between an antigen and an IgE antibody.
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MAST CELLS AND BASOPHILS CONTAIN WHAT VASODILATORY SUBSTANCE?
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HISTAMINE
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THE MHC is a group of genes on a single chromosome that does what?
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Permits an immune response to distinguish SELF from what is FOREIGN.
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A vaccination is a form of what kind of immunity?
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Active Acquired Immunity.
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What is opsonization?
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When an antibody coats an antigen to facilitate its recognition by the immune system.
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B-CELLS are responsible for which type of immunity?
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HUMORAL IMMUNITY
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WHICH LEUKOCYTE WOULD DEFEND AGAINST A PARASITE?
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EOSINOPHIL
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WHAT IS THE ORDER OF CELLS? (HINT MONKEYS)
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NEVER
LET MONKEYS EAT BANANAS |
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MACROPHAGES AND NEUTROPHILS USE WHAT TO
PHAGOCYTOSE BACTERIA? |
NON HOST EPITOPES
(LPS) (MANOS) |
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STAGES OF INFLAMMATORY RESPONSE?
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INITIATE-acute inflamm., vessel leakage, swelling, redness/warmth, stop neutrophils
RECRUITMENT- induce adherence, chemokines, leukocytes REMOVE DEBRIS-activate leukocytes, if linger long enough, activate lymphocytes, and make antibodies PROMOTE REPAIR-macrophages, fibroblasts, collagen. |
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WHAT DOES HISTAMINE DO?
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Causes increased vascular permeability, allows more immune cells into affected tissue.
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WHAT IS FAB?
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ANTIGEN- BINDING FRAGMENT.
SPECIFICALLY RECOGNIZES ONE TYPE OF ANTIGEN!! |
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A BEE STING IS AN EXAMPLE OF WHICH IMMUNE RESPONSE?
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TYPE 1- IMMEDIATE
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HEMOLYTIC DISEASE OF NEWBORN IS WHICH TYPE OF IMMUNE RESPONSE?
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TYPE 2-CYTOTOXIC
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POISON IVY WILL CAUSE WHICH IMMUNE RESPONSE?
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TYPE 4
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WHAT IS THE PATHWAY OF THE RBC?
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In the bone marrow, erythroid progenitor cells proliferate and differentiate into large, nucleated proerythroblasts, which become normoblasts, which then become reticulocytes, which then finally become erythrocyte.
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EXPLAIN THE DIFFERENCE BETWEEN THE EXTRINSIC VS
INTRINSIC PATHWAY... |
*Both are part of coagulation cascade
EXTRINSIC PATHWAY= Activated by exposure of tissue factor (TF) during tissue damage. INTRINSIC= Activation of Hageman Factor VII to XIIa. THEY BOTH CONVERGE AT FACTOR X. FROM THAT POINT ON, A COMMON PATHWAY BEGINS A FORMATION OF A CLOT. |
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WHAT ARE OPSONINS?
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Molecules that "TAG" microorganisms for destruction by the neutrophils and macrophages.
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HODGKINS LYMPHOMA?
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Associated with highly distinctive cell, REED-STERNBERG, a malignant cell that arises from a B cell. LOCALIZED TO SINGLE GROUP OF NODES, (EX: CERVICAL) OFTEN LOCALIZED.
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NON-HODGKINS LYMPHOMA?
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MULTIPLE PERIPHERAL NODES, RARELY LOCALIZED.
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DESCRIBE B-CELL ACTIVATION (HUMORAL IMMUNE RESPONSE)
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NAIEVE (YET TO BE ACTIVATED)
BUT IMMUNOCOMPETENT, UPON POS. RECOGNITION OF FOREIGN EPITOPE, B CELLS WILL ENDOCYTOSE FOREIGN PATHOGEN, WILL BECOME ANTIGEN PRESENTING CELL,WITH MHC2, AND PRESENT IN ON OUTSIDE OF MEMBRANE, WAIT FOR HELPER T, WILL CONFIRM IT, ACTIVATE IT AND TURN ON MORE B CELLS TO CREATE ANTIBODIES AND MORE MEMORY B CELLS. THE PLASMA CELLS HAVE ANTIBODIES. |
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TRUE OR FALSE?
ANTIGEN PRESENTING CELLS ARE THE ONLY ONES THAT HAVE MHC 2 COMPLEXES AND CAN ENDOCYTOSE. |
TRUE
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HELPER T CELLS?
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AMPLIFY AND ACTIVATE HUMORAL RESPONSE
LOOKING FOR *MHC 2* CD4 POSITIVE |
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CYTOTOXIC T CELLS?
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ATTACK AND INFILTRATE CELLS COMPROMISED BY FOREIGN PATHOGEN.
*MHC 1* CD8 POSITIVE |
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TRUE OR FALSE?
ALL NUCLEATED CELLS HAVE MHC1 TO REPRESENT "SELF" AND BIND TO Tc (CD8) |
TRUE
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TRUE OR FALSE
IN GENERAL, B CELLS NEED Th to ACTIVATE |
TRUE
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TRUE OR FALSE
ALL ANTIBODIES START AS IgG? |
FALSE!!!!!!!!
ALL START AS IgM!! |
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HYPERSENSITIVITIES
TYPE 1 TYPE 2 TYPE 3 TYPE 4 |
1-ALLERGIES (MAST CELLS)
2-AUTOIMMUNE (TISSUE SPECIFIC) 3-SOLUBLE Ag, IMMUNOGLOBULIN (DEPOSITION IN CERTAIN AREAS OF BODY) 4- T CELL MEDIATED (TRANSPLANT) (POISON IVY) |
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SCID?
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BOTH B AND T CELLS PATHWAYS AFFECTED (USUALLY IN STEM CELLS)
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DIGEORGE'S SYNDROME?
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THYMUS MALFUNCTION, CAN'T MAKE T CELLS
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HIV?
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recognize CD4 cells, enter them by fusing with plasma membrane, inject genetic material.
hijack the host. TREAT: RT inhibitors block entry block integration |
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TRUE OR FALSE?
RNA VIRUS MUST CONTAIN REVERSE TRANSCRIPTASE |
TRUE
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WHICH CELLS ARE CAPABLE OF FORMING CLONES?
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T AND B CELLS
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TRUE OR FALSE
ICF IS 2/3 OF FLUID AND ECF IS 1/3 OF FLUID |
TRUE
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FOUR WAYS EDEMA OCCURS?
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-NOT ENOUGH ONCOTIC PRESSURE TO PULL FLUID BACK INTO CAPILLARY.
-LACK OF PLASMA PROTEINS (LIVER FAILURE, KIDNEY DAMAGE) -INCREASED TISSUE ONCOTIC PRESSURE. (INFLAMMATION) -LYMPH OBSTRUCTION |
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HOW DO WE MAINTAIN OUR BLOOD VOLUME? (WHICH SYSTEM)
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RENIN-ANGIOTENSIN SYSTEM
1- PRESSURE SENSOR IN KIDNEY SENSE DECREASED BP, KIDNEY RELEASES *RENIN* 2-RENIN CONVERTS ANGIOTENSINOGEN TO ANGIOTENSIN 1. 3-ANGIOTENSIN 1 CONVERTED TO ANGIOTENSIN 2 BY ACE IN LUNGS 4-ANGIOTENSIN 2 PROMOTES VASOCONSTRICTION, AND STIMULATES ALDOSTERONE (goes bk to kidney and increase sodium retention) 5-RENAL SODIUM AND WATER RETENTION AND AN INCREASE IN BP |
