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209 Cards in this Set
- Front
- Back
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What are the combination therapies used for ALL?
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Prenisone + Vincristine
POMP Prednisone + Oncovin (Vincristine) + Methotrexate + Purimethol |
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Prednisone
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Steroid
Induces lymphocytopenia Used for ALL and lymphomas (chemotherapy) |
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Vincristine
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Chemotherapeutic
Mitotic inhibitor Binds to tubulin, blocking it from forming microtubules Adverse effects: Peripheral neuropathy Phlebitis Alopecia Multiple GI problems Used for ALL One DOC for Hodgkin's lymphoma |
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Purimethol
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Chemotherapeutic
Another name for 6-MP Adverse effects: Stomatitis Bone marrow suppression Alopecia Nausea/vomiting Renal and hepatic damage |
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What is the drug combination used to treat a Wilms' tumor?
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Dactinomycin + Vincristine
Congenital kidney tumor - manifests between 2-5 years of age |
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What are the treatment combinations for Hodgkin's Disease?
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Old - MOPP
Mechlorethamine + Oncovin (Vincristine) + Prednisone + Procarbazine New - ABVD Adriamycin + Bleomycin + Vinblastine + Dacarbazine |
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Dacarbazine
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Chemotherapeutic
Alkylating agent Kills neoplastic cells by adding alkyl group to their DNA Adverse effects: Highly emetogenic Extreme bone marrow suppression |
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Mechlorethamine
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Chemotherapeutic
Alkylating agent Alkylates guanines in DNA so that they cross link in pairs or are removed Adverse effects: Severe nausea/vomiting Extreme bone marrow suppression Herpes zoster (if VZV provirus is present) Extensive blisters if contact with skin or mucous membranes |
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Procarbazine
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Chemotherapeutic
Inhibits DNA and RNA synthesis Adverse effects: Bone marrow suppression Disulfiram reactions Neurotoxicity (drowsiness that progresses to hallucinations and paresthesias) |
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Cyclophosphamide
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Chemotherapeutic
Alkylating agent (most widely used) Used for any lymphoma or leukemia, ovarian and breast cancer, childhood malignancies of any kind, multiple myeloma Becomes active after biotransformation by P450 Adverse effects: Alopecia Bone marrow suppression Leukocytosis Amenorrhea Sterility Can cause secondary cancer *Hemorrhagic cystitis (may progress to bladder fibrosis) |
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Bleomycin
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Chemotherapeutic (formerly an antibiotic)
Mainly used for genitourinary cancers or lymphomas One DOC for testicular cancer Adverse effect: Pulmonary fibrosis (results in restrictive lung disease) |
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Cisplatin
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Chemotherapeutic
Platinum compound - extremely toxic Causes intra- and inter-strand cross linking between nucleotides to stop DNA and RNA synthesis Also binds many proteins (including enzymes) to render cell non-function (unable to survive) Used for solid tumors (metastatic testicular cancer, ovarian cancer, bladder cancer) DOC for testicular and bladder cancer Adverse effects: Persistent intractable vomiting (stimulates serotonin receptors in chemoreceptor trigger zone) Nephrotoxicity Ototoxicity Peripheral neuropathy (paresthesias, loss of proprioception) Related drugs - carboplatin (less renal toxicity but more bone marrow suppression), oxaliplatin (particularly neurotoxic - severe peripheral neuropathies when exposed to cold) |
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L-Asparaginase
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Chemotherapeutic
Causes asparagine to convert to aspartic acid Deprives neosplastic cells of external source of asparagine Mainly used for ALL, but not first line Adverse effects: Hypersensitivity reaction Decreased clotting factors Liver problems Pancreatitis Seizures Coma |
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6-MP
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Chemotherapeutic
DOC for ALL Adverse effects: Severe bone marrow suppression (due to interference with nucleic acid) Hepatotoxicity |
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What are the main side effects of all chemotherapeutic agents?
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GI side effects
Nausea/vomiting Stomatitis Bone marrow suppression Alopecia |
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Cytarabine
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Chemotherapeutic
DOC for AML Adverse effects: Stomatitis Nausea/vomiting |
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5-FU
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Chemotherapeutic
Used for solid tumors (breast, colorectal, gastric tumors) Most common use is colorectal cancers Adverse effects: GI problems Nausea/vomiting |
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Actinomycin
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Chemotherapeutic
Adverse effects: Stomatitis Alopecia Immunosuppression Severe bone marrow suppression (dose limiting) |
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Doxorubicin
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Chemotherapeutic
Used for AML, ALL, lymphomas, ovarian and breast cancers Adverse effects: Stomatitis Alopecia Immunosuppression Severe bone marrow depression Red urine Cardiac toxicity (dilated cardiomyopathy) |
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Vinblastine
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Chemotherapeutic
DOC for testicular cancer Can be used for lymphoma Adverse effect: Bone marrow suppression |
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Mechlorethamine
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Chemotherapeutic
Used for hematologic malignancies (leukemia, lymphoma) Adverse effects: Severe bone marrow suppression May induce secondary cancers |
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Chlorambucil
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Chemotherapeutic
Similar to mechlorethamine (alkylating agent) Adverse effects: Bone marrow suppression Potential for generating secondary cancer Related drugs - melphalan, lomustine, busulfan |
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Leuprolide
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Chemotherapeutic
Used for prostate cancer Synthetic analog of GnRH - causes suppresion of sex hormone synthesis Adverse effects: Hot flashes |
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Flutamide
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Chemotherapeutic
Used for prostate cancer Blocks activation of testosterone receptor, minimizing effects of testosterone Adverse effects: Gynecomastia |
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Hydroxyurea
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Chemotherapeutic
Inhibits ribonucleotide reductase (enzyme key to nucleotide synthesis in WBCs) Inhibits WBC proliferation Used to treat leukemias Adverse effects: Bone marrow toxicity (can be managed by careful titration) Also useful in sickle cell - induces synthesis of fetal hemoglobin |
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ATRA (All-Trans-Retinoic Acid)
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Chemotherapeutic
Version of vitamin A Binds to mutated retinoic acid receptor found only in cells of AML subtype 3 (15:17 translocation) Causes blasts to complete differentiation into mature myeloid cells Successful in inducing remission in 90% Adverse effect: Can induce DIC |
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Tamoxifen
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Chemotherapeutic
Estrogen receptor modulator Inhibits estrogen receptors in breast tissue Used in treatment and prophylaxis of breast cancer Adverse effects: Hot flashes Increased risk of DVT and PE Increased incidence of endometrial cancer |
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Taxanes
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Chemotherapeutic
Paclitaxel, Docetaxel Inhibit microtubule disassembly Cells cannot disassemble microtubules, causing apoptosis Used for breast, lung, ovarian cancers Adverse effects: Bone marrow suppression (dose limiting) |
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What are the main actions of NSAIDs?
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Anti inflammatory
Analgesia Anti-pyretic |
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What enzyme converts phospholipids to arachidonic acid?
What inhibits and increases this enzyme? |
Phospholipase A2
Inhibit: corticosteroids Increase: bradykinin, angiotensin II |
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What enzyme converts arachidonic acid to prostaglandins?
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Cyclooxygenase (COX)
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What do the prostaglandins do?
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Inflammatory response
Pain Vasodilation Fever |
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PGE2 (Prostaglandin E2)
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Mediates pain by sensitizing nerve endings to other pain mediators (bradykinin, histamine)
Elevates anterior hypothalamic thermoregulatory center set-point (causes fever) |
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PGI2 (Prostacyclin)
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Inhibits gastric secretions
When inhibited by NSAIDs, contributes to GI side effects |
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Is aspirin a reversible or irreversible COX inhibitor?
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Irreversible
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How does aspirin reduce coagulation?
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Acetylates COX in platelets to prevent thromboxane formation
Thromboxane enhances platelet aggregation Platelets have no nucleus or DNA, so cannot produce more COX Less thromboxane = less coagulation |
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What is aspirin used to treat?
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Rheumatoid arthritis (DOC)
Headache Arthralgia Angina PDA (patent ductus arteriosus) Topical for corns and calluses Prophylactic for MI, stroke, A fib |
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What results from aspirin overdose?
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Respiratory alkalosis
Metabolic acidosis Respiratory acidosis in severest cases Hyperventilation (at toxic levels central respiratory paralysis occurs, causing hypoventilation) Tinnitus |
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What makes acetominophen not a true NSAID?
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Has no peripheral anti-inflammatory action
Action limited to CNS COX - does reduce fever and pain |
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Phenylbutazone
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NSAID
No longer used in US due to severe side effects (use limited to dogs, horses, camels) Binds extensively to albumin, so can reach levels greater than desired if taken with other drugs Adverse effects: Agranulocytosis Fatal aplastic anemia |
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Indomethacin
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NSAID
Similar drugs - etodolac, sulindac Not generally used to lower fever Reserved for severe instances (anti-inflammatory for acute gouty arthritis, ankylosing spondylitis, osteoarthritis of the hip; pain control for uveitis, postoperative ophthalmic procedures; fever reducer for Hodgkin's disease) Adverse effects: GI disturbances Ulceration that may perforate and hemorrhage Pancreatitis Hepatitis (can be fatal) Aplastic anemia |
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COX-2 Inhibitors
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Selectively inhibit COX-2
Less GI side effects Celecoxib (cannot be used in sulfa allergic patients) |
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What are some of the adverse effects of all NSAIDS?
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May increase risk of miscarriage if used around time of conception
Exacerbate heart failure and hypertension Chronic use can promote serious GI disorders Non-selectives inhibit platelet function and can increase bleeding risk |
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What is responsible for most of the clinical symptoms of amino acid disorders?
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Accumulation of metabolites
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Albinism
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Amino acid disorder
Enzyme defect: Tyrosinase Symptoms: Unpigmented skin and eyes Tyrosine hydroxylase is intact - can still make dopa, epi, norepi |
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Phenylketonuria
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Amino acid disorder
Enzyme defect: Phenylalanine hydroxylase Symptoms: Mental retardation Hypopigmentation Musty odor |
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Alkaptonuria
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Amino acid disorder
Enzyme defect: Homogentisate oxidase Symptoms: Arthritis Ochronosis (bluish black discoloration of certain tissues due to deposition of HGA) Dark urine |
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Maple Syrup Urine Disease
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Amino acid disorder
Enzyme defect: branched chain decarboxylase Symptoms: Hyperreflexia Sweet odor to urine |
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Homocystinuria
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Amino acid disorder
Enzyme defect: cystathionine synthetase Symptoms: Mental retardation Lens dislocation |
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Cystinuria
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Amino acid disorder
Transporter disorder: dibasic amino acid transporter Symptoms: Urinary cystine stones |
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Hartnup Disease
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Amino acid disorder
Transporter disorder: neutral amino acid transporter Tryptophan deficiency leads to niacin deficiency leads to pellagra Symptoms: (3 D's) Dermatitis Dementia Diarrhea |
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Pyranose
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Ring with 5 carbons + 1 oxygen
Example: glucose |
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Furanose
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Ring with 4 carbons + 1 oxygen
Example: fructose |
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Anomeric Carbon
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C atom with 4 different ligands
For sugars this refers to C1 in ring form |
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Epimers
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Isomers that differ in only ONE carbon
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Enantiomers
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Mirror image
Flipped at all anomeric C atoms |
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Reducing Sugars
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Oxygen on C1 atom is available for redox reaction
Glucose, galactose, fructose (Sucrose is non-reducing sugar) |
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What do hexose kinases do?
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Enzymes that phosphorylate glucose to glucose-6-phosphate
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Hexokinase
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Hexose kinase
Organs: muscles Substrate specificity: many hexoses Affinity: high Vmax (capacity): low Inhibited by glucose-6-phosphate?: yes |
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Glucokinase
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Hexose kinase
Organ: liver Substrate specificity: many hexoses Affinity: low Vmax (capacity): high Inhibited by glucose-6-phosphate?: no |
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What are the two possible positions of carbon 1 in saccharides?
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Alpha-bond - carbon 1 in alpha position (down)
Beta-bond - carbon 1 in beta position (up) |
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Maltose
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Disaccharide
Found in beer Composition: glucose + glucose Bond: alpha1-4 |
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Lactose
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Disaccharide
Found in milk Composition: glucose + galactose Bond: beta1-4 |
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Sucrose
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Disaccharide
Table sugar Composition: glucose + fructose Bond: alpha1 - beta2 |
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Glycogen/Starch
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Polysaccharide
Composition: many glucoses Bond: alpha1-4 (chains), alpha1-6 (branch points) |
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Cellulose
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Polysaccharide
Composition: many glucoses Bond: beta1-4 Cannot be hydrolyzed by humans (indigestible) |
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Fructosuria
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Saccharide disorder
Enzyme defect: fructokinase Symptoms: Benign Asymptomatic |
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Fructose Intolerance
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Saccharide disorder
Enzyme defect: aldolase B Symptoms: Hypoglycemia Liver failure |
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Galactosemia
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Saccharide disorder
Enzyme defect: uridyltransferase Symptoms: Cataracts Mental retardation |
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Lactose Intolerance
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Saccharide disorder
Enzyme defect: lactase (usually acquired) Symptoms: Diarrhea Diarrhea of any cause can result in temporary lactase deficiency |
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What causes the symptoms associated with glycogen storage diseases?
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Glycogen accumulation in organs
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What does glycogen phosphorylase do?
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Cleaves alpha1-4 bond to release glucose-1-phosphate
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Von Gierke Disease
(Type I Glycogen Storage Disease) |
Enzyme defect: glucose-6-phosphatase
Organs affected: Liver Kidneys Symptoms: Fasting hypoglycemia Acidosis Failure to thrive |
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Pompe Disease
(Type II Glycogen Storage Disease) |
Enzyme defect: alpha-glucosidase (lysosomes)
Organs affected: All organs Symptoms: Muscle hypotonia Cardiac failure Death before age 2 |
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McArdle Disease
(Type V Glycogen Storage Disease) |
Enzyme defect: skeletal muscle glycogen phosphorylase
Symptoms: Muscle pain/cramps with exercise Progressive muscle weakness |
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What are glycosaminoglycans?
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Mucopolysaccharides - GAGs
Long, unbranched polysaccharides composed of repeating disaccharides One of the disaccharides is a hexoamine Can bind large amounts of water (become gel) and provide lubrication Hyaluronic acid Heparin Keratan sulfate Chondroitin sulfate Dermatan sulfate |
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Hurler Syndrome
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Mucopolysaccharidosis
Enzyme defect: alpha-L iduronidase Symptoms: Corneal clouding Mental retardation |
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Scheie Syndrome
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Mucopolysaccharideosis
Enzyme defect: alpha-L iduronidase Symptoms: Corneal clouding Normal intelligence |
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Hunter Syndrome
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Mucopolysaccharidosis
Enzyme defect: iduronate sulfatase Symptoms: No corneal clouding Mental retardation |
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What are proteoglycans?
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Have a protein core to which numerous side chains of glycosaminoglycans attach
Major functions: lubricants, extracellular matrix, molecular "sieve" |
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What are the essential fatty acids?
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Linoleic acid
Arachidonic acid |
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Palmitic Acid
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Saturated fatty acid
Structure: 16:0 Product of human fatty acid synthesis |
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Stearic Acid
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Saturated fatty acid
Structure: 18:0 |
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Palmitoleic Acid
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Monounsaturated fatty acid (one C=C double bond)
Structure: 16:1(9) |
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Oleic Acid
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Monounsaturated fatty acid (one C=C double bond)
Structure: 18:1(9) |
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Linoleic Acid
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Polyunsaturated fatty acid (many C=C double bonds)
Structure: 18:2(9,12) Plant oils |
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Linolenic Acid
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Polyunsaturated fatty acid (many C=C double bonds)
Structure: 18:3(9,12,15) Plant oils |
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Arachidonic Acid
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Polyunsaturated fatty acid (many C=C double bonds)
Structure: 20:4(5,8,11,14) Precursor of prostaglandins |
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What happens when bile contains more cholesterol than can be solublized?
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Crystallizes to form stones
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Primary Bile Acids
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Cholic acid
Chenodeoxycholic acid Derived from cholesterol |
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Secondary Bile Acids
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Deoxycholic acid
Lithocholic acid Produced from primary conjugated bile salts by intestinal bacteria Less soluble secondary bile acids are excreted |
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Conjugated Bile Acids
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Glycocholic acid (cholic acid + glycine)
Taurocholic acid (cholic acid + taurine) Ionized at physiologic pH Form micelles with dietary fats |
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Glycero-Phospholipids
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Spontaneously form lipid bilayers (cell membranes)
Phosphatidyl choline (lecithin) - phosphatidic acid + choline Phosphatidyl ethanolamine - posphatidic acid + ethanolamine Phosphatidyl serine - phosphatidic acid + serine Phosphatidyl inositol - phosphatidic acid + inositol Cardiolipin - 2 phosphatidic acid + glycerine |
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Sphingo-Phospholipids
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Ceramide - sphingosine + fatty acid
Sphingomyelin - ceramide + choline |
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Glycolipids
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Cerebroside - ceramide + monosaccharide
Globoside - ceramide + oligosaccharide Ganglioside - ceramide + oligosaccharide + NANA |
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Niemann-Pick Disease
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Sphingolipidosis
Autosomal recessive Accumulate: sphingomyelin Enzyme defect: sphingomyelinase Symptoms: Liver and spleen enlargement Foamy cells |
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Gaucher Disease
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Sphingolipidosis
Autosomal recessive Accumulate: glucocerebrosides Enzyme defect: beta-glucoside Symptoms: Liver and spleen enlargement Osteoporosis Usually seen in Ashkenazi Jews |
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Krabbe Disease
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Sphingolipidosis
Autosomal recessive Accumulate: galactocerebrosides Enzyme defect: beta-galactosidase Symptoms: Blindness Deafness Convulsions Globoid cells |
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Metachromatic Leukodystrophy
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Sphingolipidosis
Autosomal recessive Accumulate: sulfatides Enzyme defect: arylsulfatase Symptoms: Progressive paralysis |
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Fabry Disease
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Sphingolipidosis
X-linked recessive Accumulate: globosides Enzyme defect: alpha-galactosidase Symptoms: Reddish-purple skin rash Kidney failure Heart failure Angiokeratoma |
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Tay-Sachs Disease
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Sphingolipidosis
Autosomal recessive Accumulate: gangliosides Enzyme defect: hexosaminidase Symptoms: Blindness Cherry red macula More often found in Ashkenazi Jews |
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Acute Intermittent Porphyria
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Accumulate: porphobilinogen
Photosensitivity: no Symptoms: Abdominal pain |
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Cutanea Tarda
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Porphyria
Accumulate: uroporphyrinogen Photosensitivity: yes |
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Coproporphyria
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Accumulate: coproporphyrinogen
Photosensitivity: yes Symptoms: Abdominal pain |
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Lead Poisoning
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Porphyria
Accumulate: ALA protoporphyrin Photosensitivity: no Symptoms: Anemia (microcytic, hypochromic, with basophilic stippling) |
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Preferred Nutrients:
Brain |
Normal: glucose
Prolonged fast: ketone bodies, glucose |
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Preferred Nutrients:
Muscle |
Normal:
Rest - fatty acids Exercise - glucose Prolonged fast: fatty acids |
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Preferred Nutrients:
Heart |
Normal: fatty acids, ketone bodies, lactate, glucose
Prolonged fast: fatty acids, ketone bodies, lactate, glucose "Takes anything" |
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Preferred Nutrients:
Erythrocytes |
Normal: glucose
Prolonged fast: glucose |
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Vitamin A
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Function: part of rhodopsin
Signs of deficiency: Night blindness (retinal) Growth retardation (retinoic acid) |
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Vitamin D
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Function: calcium absorption in GI tract, supports PTH in bone
Signs of deficiency: Rickets Osteomalacia |
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Vitamin E
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Function: antioxidant
Signs of deficiency: Ataxia |
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Vitamin K
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Function: carboxylation of glutamate
Signs of deficiency: Bleeding disorder (factors II, VII, IX, X) |
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Vitamin C
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Function: hydroxylation of proline and lysine
Signs of deficiency: Scurvy |
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Vitamin B1
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Thiamin
Function: decarboxylation Signs of deficiency: Beriberi |
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Vitamin B2
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Riboflavin
Function: flavins Signs of deficiency: Glossitis Cheilosis |
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Vitamin B6
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Pyridoxine
Functions: transaminations, deaminations Signs of deficiency: Microcytic anemia Neuropathy |
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Vitamin B12
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Functions: methionine synthesis, odd carbon fatty acid degradation
Signs of deficiency: Macrocytic anemia Neuropathy D. latum (worm infestation) |
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Vitamin B3
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Niacin
Function: NAD+, NADP+ Signs of deficiency: Pellagra (diarrhea, dementia, dermatitis) |
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Vitamin B5
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Pantothenate (pantothenic acid)
Function: coenzyme A Signs of deficiency: Headache Nausea |
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Vitamin B7
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Biotin
Function: carboxylations Signs of deficiency: Seborrheic dermatitis Nervous disorders Avidin (raw egg white) binds biotin |
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Folic Acid
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Folate
Function: one carbon metabolism Signs of deficiency: Macrocytic anemia Glossitis Cholitis |
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Pneumonia
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Infectious pneumonitis - infection of lung parenchyma, including alveolar spaces and interstitial tissues
Risk factors: Alcoholism Institutionalism Smoking COPD Immune compromise Extremes of age (eldery, young children) |
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Bronchopneumonia
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Pneumonia confined to alveoli contiguous to bronchi
Rales (and possibly rhonchi) on auscultation Peribronchial infiltrates on chest Xray Primary etiologic agents: Hemophilus Pseudomonas Staphylococcus |
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Lobar Pneumonia
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Pneumonia confined to entire lobe
Dullness to percussion Consolidation ("white out") in affected lobe on chest Xray Primary etiologic agents: Pneumococcus (#1 cause of all pneumonia) - sudden onset with dyspnea, cough, fever, rigors Klebsiella pneumoniae (Friedlander's pneumonia) - prolonged onset, progressive dyspnea, cough, fever, currant jelly sputum Process: 1. Congestion - lobe fills with bacteria and mucus 2. Red hepatization - lobe fills with RBCs 3. Grey hepatization - lobe fills with fibrin 4. Resolution |
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Atypical Pneumonia
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Usually patchy pneumonia of lower lobes bilaterally
Rales on auscultation Patchy bilateral pulmonary infiltrates on chest Xray Primary etiologic agents: Viruses - RSV, adenovirus, influenza in children, influenza (A and B) in adults Mycoplasma pneumoniae (Eaton agent) - "walking pneumonia" |
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Mycoplasma pneumoniae
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Eaton agent
Most common lung pathogen age 5-35 Causes pharyngitis, bronchitis, bullous myringitis, pneumonia Atypical pneumonia - "walking pneumonia" Triad: malaise, sore throat, dry cough that evolves to productive cough of mucopurulent sputum (over weeks to months) |
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Legionnaire's Disease
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Unilateral patchy segmental or lobar alveolar infiltrate on chest Xray
Rales on auscultation High fever with relative bradycardia, diarrhea, productive cough Usually affects middle aged males 25% mortality without treatment Etiologic agent: Legionella pneumophila |
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Aspiration Pneumonia
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Due to aspiration of some substance or organism to produce acute inflammation +/- hypoxia +/- pulmonary infection
Causes: Gastric acid (chemical pneumonitis) - acute onset SOB, pink frothy sputum, broncho spasm, cyanosis - due to aspiration of vomitus during inebriation or drug overdose Anaerobic bacteria (from gingiva) - insidious onset cough, fever, purulent foul smelling sputum - due to aspiration of gingival organisms in saliva secondary to decreased consciousness or decreased pharyngeal space/airway control Mechanical obstruction - acute SOB, cyanosis - drowning, aspiration of objects |
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What cancer sites metastasize to the lung?
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Breast
Colon Prostate Kidney Thyroid Stomach Cervix Rectum Testes Bone Melanoma |
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Primary Lung Tumors
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Peak: 45-70 years of age
70-90% due to smoking |
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Lung Mass:
Hamartoma |
Benign
Anomalous development of tissue natural to lung - not a true tumor |
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Lung Mass:
Adenoma |
Benign
Tumor of glandular structure or origin |
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Lung Mass:
Leiomyoma |
Benign
Tumor of smooth muscle |
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Lung Mass:
Carcinoid TUmor |
Specialized serotonin and histamine producing tumor
May be benign or malignant Arises from GI mucosa (stomach, appendix) If metastasizes to liver, causes carcinoid syndrome - flushing, diarrhea, bronchospasm, right heart valve lesions, hypotension (diagnosed by urinary 5'-HIAA) |
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Lung Mass:
Lung Carcinoma |
Malignant
Epithelial origin First symptom is new onset cough or change in frequency or character of existing cough 4 types: Adenocarcinoma Squamous cell carcinoma Large cell carcinoma Small cell carcinoma (oat cell carcinoma) |
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Lung Carcinoma:
Lung Adenocarcinoma |
Malignant
Associated with pre-existing lung scar Occurs in peripheral lung fields |
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Lung Carcinoma:
Squamous Cell Carcinoma |
Malignant
Associated with smoking May paraneoplastically produce PTH-like peptide resulting in hypercalcemia Occurs in area central to mediastinum |
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Lung Carcinoma:
Large Cell Carcinoma |
Malignant
Associated with smoking Occurs in periphery of lung |
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Lung Carcinoma:
Small Cell Carcinoma |
Malignant
Also called oat cell carcinoma Associated with smoking Worst prognosis Occurs centrally near mediastinum May paraneoplastically produce: ADH - causes fluid overload ACTH - causes Cushing's syndrome May cause Eaton-Lambert Syndrome (autoimmune disease) - proximal muscle weakness, antibody to presynaptic calcium channels at neuromuscular junction |
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Pancoast Tumor
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Any mass in apex of lung
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What causes Horner's Syndrome? What is it?
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Pancoast tumor
Injury to lower neck/upper chest Due to compression or damage to cervical sympathetic ganglia Symptoms result from termination of sympathetic stimulus to side of head and face Symptoms: Sinking of eyeball Miosis Ptosis Vasodilation Anhidrosis |
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Nephritic Syndrome
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Due to inflammation of glomerulus
Associated with diffuse inflammatory changes Inflammation decreases filtering functions of glomerulus Acute onset and rapid progression Symptoms: Hematuria Red cell casts (pathognomonic) Hypertension Edema Increased BUN/creatinine (azotemia - accumulation of nitrogenous compounds in blood) Examples: Post-streptococcal glomerulonephritis Goodpasture's Syndrome Diffuse proliferative glomerulonephritis |
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Nephrotic Syndrome
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Due to changes in glomerular permeability (loss of size/charge selectivity)
Symptoms are result of massive protein loss Prolonged onset with severe prolonged increase in glomerular permeability to proteins Symptoms: Severe proteinuria Frothy urine (due to proteins) Hypoalbuminemia Hyperlipidemia Edema (secondary to decreased oncotic pressure from loss of albumin) Examples: Minimal change disease Membranous glomerulonephritis |
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Key Features:
Acute Nephritic Syndrome |
Hematuria and RBC casts
Azotemia Variable proteinuria (less than 3.5g/day) Oliguria Edema Hypertension |
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Key Features:
Rapidly Progressive Glomerulonephritis |
Severest form of nephritic syndrome
Proteinuria Acute renal failure Severe oliguria Severe edema Hypertension Marked azotemia |
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Key Features:
Nephrotic Syndrome |
Proteinuria >3.5g/day
Hypoalbuminemia Hyperlipidemia Lipiduria |
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Key Features:
Chronic Renal Failure |
Azotemia and uremia progressing for years
Uremia symptoms: Muscle cramps/twitches Fatigue Decreased mental acuity Nausea/vomiting Hypertension (secondary to hypervolemia) Pruritis Pericarditis Uremic frost (if severe enough) |
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Rapidly Progressive (Crescentic) Glomerulonephritis
(RPGN) |
Severe glomerular injury - severe form of nephritic syndrome
Without treatment, will cause death from renal failure (weeks to months) Crescents - proliferation of epithelium of Bowman's capsule surrounding glomerulus 3 types: Type I - antibody mediated toxicity - causes: idiopathic, Goodpasture's Type II - immune complex disease - causes: idiopathic, SLE, Henoch-Schonlein, post-infectious Type III - pseudo-immune - causes: idiopathic, Webener's, microscopic polyangiitis, advanced terminal polyarteritis nodosa |
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Minimal Change Disease
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Also called lipoid nephrosis, foot process disease
Nephrotic syndrome Risk: 1-30 years - most common childhood nephrotic disease (4/5th) Cause: idiopathic, 30% have history of recent URI Biopsy findings: loss of foot processes |
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Membranous Glomerulonephritis
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Nephrotic
Risk: 30-50s - most common adult nephrotic disorder Cause: idiopathic, can be associated with colon or lung carcinoma, chronic infection, heavy metal exposure, drugs Findings: microscopic hematuria, renal vein thrombosis (common complication), thickened basement membranes with subepithelial deposits of IgG and C3 ("spike and dome" pattern) Progresses to chronic renal failure and end-stage renal disease in several years |
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Focal Segmental Glomerulosclerosis
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Nephrotic
Risk: under 35 Cause: idiopathic, can be due to chronic ureteral reflux or heroin abuse Findings: hematuria, hypertension, renal insufficiency, sclerosis of glomerulus in focal and segmental pattern Progresses to diffuse and global sclerosis that causes chronic renal failure |
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Membranoproliferative Glomperulonephritis
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Also called mesangiocapillary glomerulonephritis
Temporarily nephritic, progresses to nephrotic Risk: 5-30 years, predilection for females Cause: immune complex deposition in glomerulus, associated with recent URI, chronic infection (esp. Hep C), heroin abuse, cancers, SLE and other autoimmune disorders Findings: mesangial cell proliferation with capillary basement membrane thickening and splitting, subendothelial C3 deposits, "tram tracking," decreased complement levels Usually progresses to chronic renal failure within 10 years |
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Acute Proliferative Glomerulonephritis
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Also called acute post-streptococcal glomerulonephritis, acute post-infectious glomerulonephritis
Nephritic Risk: 3-14 years, risk declines with age Cause: occurs after group A strep infection Findings: positive ASO titer, decreased C3 complement, mesangial proliferation with subepithelial deposits of IgG and C3 in coarsely granular pattern ("lumpy-bumpy," "hump-like") Usually self limited with excellent prognosis |
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Anti-Glomerular Basement Membrane Disease
(Goodpasture's Syndrome) |
Nephritic
Risk: 11-39 years, strong predilection for males Cause: anti-glomerular basement membrane antibodies, deposited antibodies activate complement Findings: hemoptysis, mesangial proliferation and linear deposition of IgG and C3, crescents (if progress to rapidly progressive glomerulonephritis) Most progress to rapidly progressive glomerulonephritis and end stage renal disease within months to years |
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IgA Nephropathy
(Berger's Disease) |
Nephritic
Most common primary glomerular disease Risk: 11-29 years, strong predilection for males Cause: immune complex deposition (mainly IgA) causes complement activation, usually follows viral URI, GI syndrome, or other acute pronounced infectious episode Findings: focal and segmental glomerular mesangial proliferation with IgA immune complex deposits, increased serum IgA Usually benign but 20% develop chronic renal failure |
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Diabetic Glomerulosclerosis
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Also called Kimmelstiel-Wilson Syndrome
Most common secondary glomerular disease Nephrotic and nephritic features Risk: any age, 20 years after onset of diabetes mellitus Findings: microalbuminuria, small kidneys, diffuse glomerulosclerosis that later becomes nodular (Kimmelstiel-Wilson nodules) Gradual progression to chronic renal failure and end stage renal disease |
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Acute Tubular Necrosis
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Characterized by death of cells lining renal tubules
Results in renal tubule dysfunction Most common cause is pre-acute renal failure (too little blood delivered to kidney, too little fluid to renal tubules) Muddy brown cases in urine (pathognomonic) If cause is promptly addressed, most fully recover within 7-21 days If not addressed, causes chronic renal failure |
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Toxic Acute Tubular Necrosis
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Acute tubular necrosis due to destruction of renal tubules secondary to toxins
Causes: Free hemoglobin (from massive hemolysis) Myoglobin (from rhabdomyolysis) Ethylene glycol Aminoglycosides Amphotericin B Cisplatin Contrast media If cause is promptly addressed, most fully recover within 7-21 days If not addressed, causes chronic renal failure |
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Types of Acute Renal Failure:
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Pre-renal
Intrinsic (renal) Post-renal |
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Pre-Renal Acute Renal Failure
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Due to hypoperfusion of kidneys and inadquate blood delivery to glomerulus
Causes: hypotension, dehydration, hemorrhage, severe CHF, shock Result: oliguria Labs: high BUN/creatinine with BUN:creatinine ratio over 20:1 TX: IV fluids If left untreated can evolve into acute tubular necrosis |
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Intrinsic (Renal) Acute Renal Failure
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Causes:
Acute tubular injury - drugs, heavy metals, contrast agents Acute glomerulonephritis Acute tubulointerstitial nephritis - inflammation ofparenchyma secondary to allergicreaction or infection Acute vascular nephropathy- pathology of renal vessels Infiltrative diseases - molecular infiltrate settles in kidney tissue (sarcoidosis, amyloidosis) Labs: high BUN/creatinine with BUN:creatinine ratio less than 10:1, elevated postassium, sodium, magnesium, chloride, decreased calcium TX: identify and treat cause May cause acute tubular necrosis Even with treatment mortality rate is 30% |
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Post-Renal Acute Renal Failure
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Due to obstruction of outflow of urine
Causes: BPH, bladder stone, urolithiasis of ureters, renal collecting system injury Features: oliguria (possibly anuria), pain, potassium levels rise Permanent kidney damage may result even after removal of obstruction (depnding on severity and duration) |
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Chronic Renal Failure
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Also called chronic kidney disease, chronic renal disease
Permanent reduction in renal function that progresses over weeks/months/years 75% secondary to diabetes, glomerulonephritis, hypertension 5 stages - stage 5 is end stage renal disease (ESRD) Presents with fatigue, malaise, nausea, general feeling of "unwell" |
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Urolithiasis
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Urinary calculi
Symptoms: Many are silent Back pain Renal colic (excruciating, intermittent, radiates down ureter) Nausea/vomiting Abdominal distention Chills/fever Hematuria Urinary frequency Costovertebral angle tenderness Restlessness Managment: oral and IV fluids, lithotripsy (ultrasound to break up stone) |
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Calcium Stones
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5% due to hyperparathyroidism, less due to acidosis or diffuse bone disease
Usually precipitated by dehydration Most common type of kidney stone Primary treatment is hydration Thiazides can reduce potential (cause calcium uptake from renal tubule) |
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Magnesium-Ammonium-Phosphate Stone
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Also called triple stone, staghorn calculus, struvite
Caused by urea splitting organsims (Proteus, Staph saprophyticus) Antibiotics help eradicate inciting organisms (TMX-SMP or nitrofurantoin) |
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Uric Acid Stone
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Uric acid crystal core with calcium oxalate crystal deposits
Causes: Excessive consumption of purines Gout Leukemia Tumor lysis syndrome (or other disorders of high cell turnover) |
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Cystine Stone
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Result of cystinuria (autosomal recessive disorder)
Impaired tubular resorption of cysteine, ornithine, arginine, lysine (COAL) Cysteine crystallizes to form stone |
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Candidiasis
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Vulvovaginitis
pH: <4.5 Color: white Odor: bready (yeast) Microscopic: germ tubes, pseudohyphae Cause: overgrowth of normal flora (Candida) - classic yeast infection DOC: miconazole (second line - fluconazole) Symptoms: pruritis, erythema, satellite lesions, curd-like or adherent white discharge |
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Trichomoniasias
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Vulvovaginitis
pH: >4.5 Color: yellow/green Odor: putrid Microscopic: darting trichomonads Cause: Trichomonas vaginalis (STD) DOC: metronidazole Symptoms: extreme pruritis, frothy green discharge |
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Bacterial Vaginosis
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Vulvovaginitis
pH: >4.5 Color: grey-white Odor: fishy Microscopic: clue cells Cause: overgrowth of normal flora of vagina (esp. Garnerella, Mobiluncus) DOC: metronidazole Symptoms: profuse grey-white discharge with or without pruritis, positive Whiff test |
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Gonorrhea
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Venereal disease
Cause: Neisseria gonorrheae (gonococcus) DOC: ceftriaxone (also give doxycycline or azithromycin to cover any undiagnosed chlamydia) Symptoms: purulent discharge at area of infection If left untreated in female, will ascend to cause PID |
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Non-Gonococcal Urethritis
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Venereal disease
Infectious urethritis in male due to anything but gonorrhea Cause: usually Chlamydia trachomatis DOC: doxycycline (for Chlamydia) plus ceftriaxone for empiric treatment of gonorrhea |
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Lymphogranuloma Venereum
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Veneral disease
Primarily found in tropics Cause: Chlamydia trachomatis DOC: doxycycline Symptoms: large palpable granulomas develop in inguinal lymph nodes and erupt on skin surface |
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Granuloma Inguinale
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Veneral Disease
Cause: Klebsiella granulomatis DOC: tetracycline Symptoms: Donovan bodies (visible etiologic bacterium seen in macrophage), granulomas develop on genitals and organsim blocks lymphatic drainage from genital region |
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Chancroid
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Venereal disease
Found mainly in tropics Cause: Hemophilus ducreyi DOC: ceftriaxone Symptoms: "school of fish" on microscopic exam, soft painful chancre |
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Syphilis
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Venereal disease
Cause: Treponema pallidum DOC: penicillin G 3 stages: 1 - painless hard chancre 2 - maculopapular rash on palms, condyloma lata on genitals 3 - gummas, tabes dorsalis, psychosis, dementia, luetic aneurysm, aortitis, aortic regurgitation |
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Condyloma Accuminatum
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Venereal disease
Also called genital warts Cause: HPV 6 and 11 (HPV 16, 18 are most dangerous for cancer development) TX: cryotherapy Symptoms: painless, koilocytes on biopsy (epithelial cells with perinuclear clearing) |
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Genital Herpes
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Venereal disease
Cause: HSV 1 and 2 DOC: acyclovir Symptoms: exquisitely painful fluid filled vesicles in a group on an erythematous base, tend to recur under stress, positive Tzanck test on fluid (screening, not confirmatory) Live virus becomes latent in sensory ganglion cells for reactivation at later date |
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Chlamydial Cervicitis
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Venereal disease
Cause: Chlamydia trachomatis DOC: doxycycline plus ceftriaxone for gonorrhea empiric therapy if not ruled out Symptoms: often asymptomatic If untreated will ascend to cause PID in female |
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Germ Cell Tumors
(Male) |
Tumors formed from cells that would ordinarily have become sperm
Seminoma Embryonal Choriocarcinoma Yolk sac Teratoma |
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Non-Germ Cell Tumors
(Male) |
Tumors formed from non-spermatozoan cells
Stromal sex cord tumors: Leydig cell Sertoli cell Non-stromal sex cord tumors: Lymphoma |
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Seminoma
(Male) |
Germ cell tumor (sperm derived)
Painless enlargement of testes +/- elevated hCG Peak occurrence at age 35 Most common germ cell tumor Always malignant Analogous to ovarian dysgerminoma Very radiosensitive |
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Embryonal Tumor
(Male) |
Germ cell tumor (sperm derived)
Painful with early metastases Elevated hCG Peaks under age 35 Second most common germ cell tumor Poor prognosis |
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Choriocarcinoma
(Male) |
Germ cell tumor (sperm derived)
Rare Peak in teens-20s Always malignant Analogous to ovarian choriocarcinoma Significantly elevated hCG |
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Yolk Sac Tumor
(Male) |
Germ cell tumor (sperm derived)
Also called infantile type embryonal carcinoma, endodermal sinus tumor Peak in infancy to early childhood Always malignant Elevated serum alpha-fetoprotein |
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Testicular Teratoma
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Germ cell tumor (sperm derived)
Comprised of 2 or more germ layers Usually malignant (usually comprised of immature neoplastic cells) Variable age of occurrence |
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Leydig Cell Tumor
(Male) |
Stromal sex cord tumor (non-germ cell)
Also called interstitial cell tumor Usually benign Testosterone producing Intracytoplasmic Reinke crystals Precocious puberty if occurs before puberty Gynecomastia if occurs after puberty (excess testosterone turned into estrogen by fat cells) |
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Sertoli Cell Tumor
(Male) |
Stromal sex cord tumor (non-germ cell)
Also called androblastoma Usually benign Endocrinologically asymptomatic |
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Testicular Lymphoma
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Non-stromal sex cord tumor (non-germ cell)
Occurs more frequently in elderly or immunocompromised |
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Ovarian Tumors
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Symptoms show up only late - vague (lower abdominal discomfort, mild digestive complaints)
Surface epithelium tumors - females over 20 Germ cell tumors of ovary - females under 20 Sex cord stromal cell tumors - variable age |
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Surface Epithelium Tumors of Ovary
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Tumors of outer epithelial lining of ovary
5 major types: Serous Mucinous Endometrioid Clear cell Brenner |
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Serous Tumor of Ovary
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Surface epithelium tumor
Cystadenoma (benign) or cystadenocarcinoma (malignant) Mass always cystic (fluid filled epithelial sac) Tumor lined with cells like fallopian tube epithelium (ciliated, watery secretions) Serous cystadenocarcinomas are half of all ovarian malignancies - often bilateral |
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Mucinous Tumor of Ovary
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Surface epithelium tumor
Cystadenoma (benign) or cystadenocarcinoma (malignant) Mass always cystic (fluid filled epithelial sac) Tumor lined with columnar cells that produce mucus May yield pseudomyxoma peritonei (rupture of mucinous cystadenocarcinoma to produce multiple intraperitoneal tumor implants) |
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Endometrioid Tumor of Ovary
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Surface epithelium tumor
Tumor comprised of glandular tissue resembling endometrial tissue Usually malignant Solid tumor |
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Clear Cell Tumor of Ovary
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Surface epithelium tumor
Rare Tumor comprised of large epithelial cells with large clear cytoplasm May occur in association with endometriosis or endometrioid carcinoma Usually malignant |
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Brenner Tumor of Ovary
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Surface epithelium tumor
Also called celioblastoma Rare Tumor comprised of cells like those found in bladder epithelium (transitional epithelium) |
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Germ Cell Tumors of Ovary
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Comprised of cells that would have normally become ova
25% of all ovarian tumors Most common type in women under 20 4 major types: Teratoma Dysgerminoma Endodermal sinus tumor Choriocarcinoma |
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Teratoma
(Female) |
Germ cell tumor
Comprised of 2 or more germ layers Comprised of either mature or immature cells (mature is more common - 90% of all germ cell tumors of ovary, 20% of all ovarian tumors) Dermoid cyst = mature teratoma Cyst lined by skin with hair follicles, nails, sebaceous gland, other cutaneous elements - may include bones, teeth, GI, neurological, respiratory, thyroid tissues Struma ovarii - variant of dermoid cyst - has only one tissue element (thyroid - can result in hyperthyroidism) |
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Dysgerminoma
(Female) |
Germ cell tumor
Comparable to seminoma of testicle Always malignant |
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Endodermal Sinus Tumor
(Female) |
Germ cell tumor
Comparable to yolk sac tumor of testicle Malignant Elevated alpha-fetoprotein |
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Choriocarcinoma
(Female) |
Germ cell tumor
Neoplasm of trophoblast (placental tissue) Aggressive and malignant Extremely elevated hCG |
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Stromal Sex Cord Tumors
(Female) |
Tumors derived from cells not destined to becomeova and not part of ovarian epithelial lining
3 major types: Granulosa-theca cell tumor Sertoli-Leydig cell tumor Fibroma |
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Granulosa-Theca Cell Tumor
(Female) |
Stromal sex cord tumor
Secretes large quantities of estrogen Call-Exner bodies (follicle filled with eosinophilic material Associated with causing secondary endometrial hyperplasia or endometrial cancer |
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Sertoli-Leydig Cell Tumor
(Female) |
Stromal sex cord tumor
Also called androblastoma, arrhenoblastoma Produces large quantities of testosterone Causes virilization in female (clitoromegaly, hirsutism, deepening of voice - irreversible) |
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Ovarian Fibroma
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Stromal sex cell tumor
Benign Solid tumor of spindle-shaped fibroblasts Can cause Meig's syndrome (ascites, pleural effusion, ovarian tumor) |
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Metastatic Disease of Ovary
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5% of all ovarian tumors are metastases (often from GI, breast, uterus)
Krukenburg Tumor: Tumor in ovary developed from cells that metastazied from elsewhere Bilateral replacement of ovaraies with mucin-producing signet-ring cells Primary site often stomach |
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Signet Ring Cell
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Cell of Krukenburg tumor (metastatic ovarian tumor)
Produces large quantities of mucin intracytoplasmically, displacing cell nucleus (giving appearance of signet ring) |
