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140 Cards in this Set
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- Back
- 3rd side (hint)
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Which drugs are the major P450 inducers/inhibitors?
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Induce:
Oral contraceptives (OCP) Phenytoin Barbiturates Alcohol Rifampin Levodopa Methadone (One Pharmaceutical Brings About Rapid Liver Metabolism) Inhibit: Sulfonamides Phenylbutazone Chloramphenicol Isoniazid Dicumerol Cimetidine (Some Pharmaceutical Classes Inhibit Drug Catabolism) |
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Explain why drug binding to albumin is an important factor.
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When drugs are bound to albumin, they are pharmacologically inactive.
Drugs that bind weakly (anionic drugs) or not at all (hydrophilic drugs) end up with a higher active concentration in the body. Drugs that bind strongly to albumin (hydrophobic drugs) are harder to displace from the albumin, leading to a lower active concentration. |
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Which drugs compete for renal transporters to be excreted from the body?
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Some Pharmaceuticals Plus Urate Stop Transporters
Sulfonamides Uric Acid (Urate) Probenecid Penicillins Salicylates Thiazides |
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What drugs are easily displaced from albumin? (i.e. have higher active concentrations per dose)
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Serum Proteins Can Spew
Sulfonamides Phenylbutazone Coumadin Sulfonylureas (Tolbutamide) |
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What is Serotonin Syndrome?
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Hyperthermia
Tachycardia Facial Flushing Severe Muscle Spasm Rhabdomyolysis Caused by combining MAOI + SSRI or TCA |
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What are the two stages of cell injury?
(and describe) |
Reversible (swelling, fatty change)
Irreversible (necrosis, apoptosis) |
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Describe the two types of wound repair.
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Primary Intention (wound edges attached, contraction may occur)
Secondary Intention (edges are not attached, granulation tissue forms, takes longer to heal) |
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What are the inflammatory responses and their mediators?
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Fever: IL-1, Prostaglandins
Vasodilation: Nitric Oxide, Prostaglandins Exudation: Histamine, Bradykinins Chemotaxis: Complement C5a, IL-8 Phagocytosis: Complement C3b (opsonin) Pain: Prostaglandins, Bradykinins |
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Name the two main complement pathways and their triggers.
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Classical: antigen-antibody complex
Alternate: contact with microbial surface |
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What stain is used to identify amyloid?
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Congo Red
Shows green birefringence under polarizing microscope |
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What are the three types of amyloid and their associated diseases?
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AL (amyloid light chains): multiple myeloma
AA (amyloid associated protein): chronic inflammation and aging Abeta (beta amyloid): Alzheimer's disease |
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What are the features of acute inflammation?
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rubor (redness)
dolor (pain) calor (heat) tumor (swelling) chronic: pallor, coolness, stiffness |
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How do prostaglandins cause pain?
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directly stimulate free (unmyelinated) nerve endings
bradykinins cause pain by same mechanism |
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How are prostaglandins produced?
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When cells are injured, some of their lipid bilayer cell membrane is freed. Phospholipase A2 converts these free lipids into arachadonic acid, which is metabolized by COX (cyclooxygenase) into prostaglandins.
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What cells produce histamine?
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Basophils
Mast cells Platelets |
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What inhibits the effect of bradykinins?
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Angiotensin Converting Enzyme (ACE) - tonic inhibition (happens all the time unless ACE is inhibited)
Bradykinin can help control BP - when ACE is inhibited, bradykinin can have full effect on body = causes vasodilation |
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Where are complement proteins made?
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Liver
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What is the first WBC to be found at any site of acute inflammation?
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Neutrophil
Because of C5a May not be predominant WBC as time passes, but will always be first |
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What do CD8 T cells kill?
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Fungi
Protozoa Viruses |
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What do B cells do when stimulated by CD4 T cells?
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Evolve into plasma cells
Can produce antibodies Fight microbes (especially bacteria) |
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Where is the MHC located?
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Histocompatibility genes on chromosome 6
Code for HLA (human leukocyte antigens) |
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When should we use CRP (C reactive protein) testing?
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Tests for acute inflammation
Not used for every case of suspected inflammation - wasteful Autoimmune diseases - monitors where pt is in process of exacerbation by measuring inflammation |
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What are the clinical features of acute phase response?
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Fever
Increased deep sleep Sleepiness during waking hours Decreased appetite Body protein breakdown Hypotension |
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What is an anaphylotoxin?
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Stimulate histamine releasing cells (basophils, mast cells, platelets) to release histamine
C3a and C5a complement proteins |
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What is the correct order of nomenclature for Fryette's?
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Type 1/Neutral - sidebending before rotation
Type 2/Flexion-Extension - rotation before sidebending |
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Who developed counterstrain?
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Lawrence Jones, DO
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Who developed Facilitated Positional Release?
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Stanley Schiowitz, DO
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Who developed myofascial release?
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AT Still
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Who developed muscle energy?
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Fred S. Mitchell, DO
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Who developed HVLA?
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AT Still
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What is a maverick point?
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Counterstrain point that does not have tenderness reduced below 70% after 3 counterstrain treatments
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Whats is facilitated positional release used for?
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Treatment of superficial muscles and deep intervertebral muscles
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How do you treat a maverick point?
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Fold away from tenderpoint (instead of in for normal counterstrain)
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What are some specific examples of things that activate the alternate pathway?
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Endotoxin
Cobra venom Complex polysaccharides (fungi capsules) |
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Adverse Effect of Mixing:
MAOI + SSRI |
Serotonin Syndrome
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Adverse Effect of Mixing:
MAOI + TCA |
Serotonin Syndrome
Severe sympathetic nervous system activation Hypertensive Crisis |
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Adverse Effect of Mixing:
Antiarrhythmics + Fluoroquinolone (except ciprofloxacin) |
QT prolongation
Torsades de pointe |
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Adverse Effect of Mixing:
Cation-containing Drugs or Citric Acid + Fluoroquinolone |
Severe impairment of FQ absorption
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Adverse Effect of Mixing:
Alcohol or Rifampin + Isoniazid |
Liver damage
Possible liver failure |
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Side Effect:
Bone Marrow Toxicity |
Ganciclovir
Zidovudine (AZT) Chloramphenicol Carbamazepine Chemotherapeutic agents Interferon Flucytosine Gargantuan Zebras Can Cause Certain Idiots Fear |
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Side Effect:
Hepatotoxicity |
Imidazoles
Nevirapine Interferon Statins (HMG-CoA inhibitors Valproic Acid Isoniazid I Never Invite Syphilitic Vaginas Inside |
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Side Effect:
Nephrotoxicity |
Foscarnet
Aminoglycosides NSAIDs Cidofovir Amphotericin Cyclosporine FAN CAC |
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Side Effect:
Tendon Rupture |
Quinolones
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Side Effect:
DVT |
Raloxifene
Tamoxifen Estrogens/Progesterones |
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Side Effect:
Orthostatic Hypotension |
All alpha blockers
Most TCAs |
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Side Effect:
Hypertensive Crisis |
MAO inhibitors
TCAs Most likely when mixed Malignant hypertension, tachycardia |
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Side Effect:
Serotonin Syndrome |
MAO inhibitors
SSRIs TCAs Decongestants containing pseudoephedrine SNRIs Most likely when mixed Hyperthermia, tachycardia, facial flushing, severe muscle spasm, rhabdomyolysis |
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Side Effect:
Cutaneous Flushing |
Niacin
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Side Effect:
Seizure |
Meperidine
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Side Effect:
G6PD Exacerbation |
Potentially any drug, but especially:
Sulfa drugs Primaquine |
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Side Effect:
Drug-Induced Lupus |
Hydralazine
Procainamide |
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Side Effect:
Malignant Hyperthermia |
Halothane
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Side Effect:
Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION) |
PDE-5 inhibitors
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Side Effect:
Ototoxicity |
Aminoglycosides
PDE-5 inhibitors |
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Side Effect:
Neural Tube Defects |
Carbamazepine
Valproic acid When used by mother during pregnancy |
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Side Effect:
Ebstein's Anomaly |
Lithium
When used by mother during pregnancy |
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Alpha-Interferon (INF-alpha)
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Produced by: Leukocytes (macrophages, T and B cells, granulocytes)
Action: Antiviral, Induces MHC-1 expression |
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Beta-Interferon (INF-beta)
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Produced by: Fibroblasts
Action: Antiviral, Induces MHC-1 expression |
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Gamma-Interferon
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Produced by: T-cells
Action: Activates macrophages, Induces MHC-2 expression on macrophages |
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IL-1
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Produced by: Macrophages
Action: Fever |
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IL-2
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Produced by: T-cells
Action: stimulates production of B cells, CD8 T cells, NK cells |
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IL-6
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Produced by: Macrophages, Fibroblasts
Action: stimulates B cells, stimulates acute phase response |
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IL-7
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Produced by: Bone marrow cells
Action: stimulates proliferation of T and B cells |
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TNF-alpha
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Produced by: Macrophages
Action: Fever, cachexia (muscle wasting), inhibits lipoprotein lipase, stimulates acute phase response, stimulates T and B cells |
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PDGF (platelet derived growth factor)
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Produced by: Platelets, Endothelial cells
Action: Proliferation of vascular smooth muscle cells |
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T Cells are activated by?
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IL-1
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B cells are activated by?
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IL-2, IL-4, IL-5
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Autoantibody:
Rheumatoid Arthritis |
Anti-IgG (rheumatoid factor)
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Autoantibody:
Systemic Lupus |
Anti-Nuclear Antibodies (ANA)
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Autoantibody:
Drug Induced Lupus |
Anti-Histone
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Autoantibody:
CREST |
Anti-Centromere
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Autoantibody:
Myasthenia Gravis |
Anti-ACh Receptor
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Autoantibody:
Graves' Disease |
Anti-TSH Receptor
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Autoantibody:
Hashimoto's Thyroiditis |
Anti-Microsomal
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Autoantibody:
Wegener's Granulomatosis |
Anti-Neutrophil Cytoplasm (ANCA)
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Autoantibody:
Primary Biliary Cirrhosis |
Anti-Mitochondrial
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Autoantibody:
Celiac Sprue |
Anti-Gliadin
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Autoantibody:
Goodpasture's Syndrome |
Anti-Glomerular Basement Membrane
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Type I Hypersensitivity
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IgE
Mediators: mast cells, basophils, histamine Signs/Symptoms: urticaria (hives) erythema bronchioles constrict laryngeal edema shock, death |
Examples:
anaphylaxis asthma hay fever eczema |
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Type II Hypersensitivity
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IgG, IgM
Mediators: antibody binding to cell surface activates complement Signs/Symptoms: hemolysis |
Examples:
transfusion reaction drug reaction erythroblastosis fetalis autoimmune diseases |
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Type III Hypersensitivity
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IgM, IgG
Mediators: immune complex deposits activate complement Signs/Symptoms: urticaria lymphadenopathy arthritis vasculitis glomerulonephritis |
Examples:
serum sickness Arthus reaction |
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Type IV Hypersensitivity
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Delayed Hypersensitivity
Mediators: T cells activate macrophages and killer cells Signs/Symptoms: erythema with induration |
Example:
Tuberculin reaction |
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Types of transplant rejection:
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Hyperacute (due to preformed antibodies)
Acute (mostly due to type IV hypersensitivity) |
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Oncogene:
c-myc |
Burkitt lymphoma
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Oncogene:
c-abl |
CML
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Oncogene:
bcl-2 |
Non-Hodgkin lymphoma
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Oncogene:
ras |
colon carcinoma
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Tumor Suppressor Gene:
RB1 |
Retinoblastoma
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Tumor Suppressor Gene:
BRCA-1 |
Breast Cancer
Ovarian Cancer |
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Tumor Suppressor Gene:
p53 |
Breast Carcinoma
Colon Carcinoma Bronchial Carcinoma |
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Tumor Marker:
CEA |
Adenocarcinomas
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Tumor Marker:
alpha-fetoprotein |
Hepatoma
Twin pregnancy Anencephalus |
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Tumor Marker:
PSA |
Prostate carcinoma
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Tumor Marker:
acid phosphatase |
prostate carcinoma
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Tumor Marker:
alkaline phosphatase |
Metastases to bones
Obstructive biliary disease Paget's disease |
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Most common primary site for metastases found in:
Brain |
Lung > Breast
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Most common primary site for metastases found in:
Bone |
Breast > Lung
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Most common primary site for metastases found in:
Liver |
Colon > Stomach > Pancrease
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Autosomal Recessive Diseases
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Cystic Fibrosis
Phenylketonuria Albinism Alpha-1 antitrypsin deficiency Thalassemias Sickle Cell anemias Glycogen storage diseases Mucopolysaccharidoses (except Hunter's) Sphingolipidoses (except Fabry's) Polycystic kidney disease, infant type Hemochromatosis Chediak-Higashi syndrome |
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Autosomal Dominant Diseases
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Familial hypercholesterolemia
Familial polyposis Spherocytosis von Willebrand disease Ehlers-Danlos syndrome Marfan syndrome Achondroplasia Phacomatoses Huntington's disease Polycystic kidney disease, adult type |
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X-Linked Recessive Diseases
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Hemophilia A and B
G6PD deficiency Fragile X Fabry disease Lesch-Nyhan syndrome Duchene and Becker muscular dystrophies Bruton's agammaglobulinemia Wiskott-Aldritch syndrome Chronic granulomatous disease |
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Turner Syndrome
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45 chromosomes, X0
Webbed neck Aortic Coarctation Broad chest with widely spaced nipples Short Stature Immature Genitalia Lack of menstruation "Streak" ovaries |
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Klinefelter Syndrome
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47 chromosomes, XXY
High Voice Lack of facial hair Gynecomastia Hypogonadism Lack of pubic hair Infertility Tall stature |
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Chromosomal Deletion:
5p |
cri du chat syndrome
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Chromosomal Deletion:
11p |
congenital absence of iris
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Chromosomal Deletion:
13q |
retinoblastoma
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Chromosomal Deletion:
15q11-13 (paternal) |
Prader Willi syndrome
severe infantile hypotony, obesity, mental retardation |
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Chromosomal Deletion:
15q11-13 (maternal) |
Angelman syndrome
happy smile, wide-based gate, epilepsy |
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Predisposition for HLA:
A3 |
Hemochromatosis
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Predisposition for HLA:
B27 |
Ankylosing spondylitis
Reiter's syndrome Ulcerative colitis |
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Predisposition for HLA:
DR2 |
Multiple sclerosis
Narcolepsy |
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Predisposition for HLA:
DR3 |
SLE
IDDM |
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Predisposition for HLA:
DR4, Dw4, Dw14 |
Rheumatoid arthritis
Juvenile rheumatoid arthritis |
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Which ones and where are they found:
HLA Class I |
HLA-A, HLA-B, HLA-C
Found on all cell surfaces |
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Which ones and where are they found:
HLA Class II |
HLA-D
Found mainly on B lymphocytes |
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Most common malignancies:
Men |
Incidence:
prostate > lung > colon Mortality: lung > prostate > colon |
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Most common malignancies:
Women |
Incidence:
breast > lung > colon Mortality: lung > breast > colon |
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Most common malignancies:
Children |
Overall: leukemia (specifically ALL)
Solid: brain tumors Solid outside CNS: neuroblastoma |
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Clinical features of:
SLE |
Skin: malar rash, photosensitivity
Organs: arthritis, pleuritis, pericarditis, renal disease (proteinuria) Blood: hemolytic anemia, leukopenia, lymphocytopenia Lab: antinuclear antibodies, false positive VDRL (cardiolipin antibodies), confirmed by negative FTA-ABS |
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Clinical features of:
Systemic Sclerosis |
limited disease = CREST
Calcinosis, Raynaud's, esophageal dysmotility, sclerodactyly, telangiectasis anti-centromere antibodies localized scleroderma (fingers, forearms, face) Diffuse Systemic widespread scleroderma, rapid progression, early visceral involvement, anti-Scl 70 (topoisomerase I) |
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Clinical features of:
Sjogren's Syndrome |
Dry eyes
Dry mouth SS-A (anti Ro) and SS-B (anti La) antibodies |
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Severe Combined Immunodeficiency Disorder (SCIDs)
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Lymphopenia
Death within first year |
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DiGeorge's Syndrome
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Absent T cells
Viral or fungal infections Tetany |
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Bruton's Agammaglobulinemia
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Absent B cells
X-linked Bacterial infections |
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Common Variable Immunodeficiency Disorder (CVID)
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B cells present but producing few antibodies
Bacterial infections |
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IgA Deficiency
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Low IgA
Sinopulmonary and gastrointestinal infections Most common congenital immunodeficiency |
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Wiskott-Aldritch Syndrome
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Low IgM
X-linked recessive Bacterial infections Thrombocytopenia Eczema |
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Planes of motion:
Flexion/Extension |
In Sagittal Plane
Around Transverse Axis |
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Planes of motion:
Rotation |
In Transverse Plane
Around Vertical Axis |
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Planes of motion:
Sidebending |
In Coronal Plane
Around AP Axis |
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IL-3
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Produced by: T cells
Action: stimulates bone marrow to produce white blood cells |
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IL-4
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Produced by: T cells
Action: stimulates B cells |
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IL-5
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Produced by: T cells
Action: stimulates B cells |
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IL-8
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Produced by: macrophages
Action: stimulates B cells |
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TGF-alpha
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Action: stimulates angiogenesis and tumor growth
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TGF-beta
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Action: inhibits T cells, promotes collagen formation
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TNF-beta
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Action: fever, stimulates actue phase response, stimulates T and B cells
(similar to TNF-alpha) |
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CSF (colony stimulating factor)
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Produced by: NK cells
Action: stimulates bone marrow production of white blood cells |
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RANTES (regulated and normal T cell expressed and secreted chemokine)
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Action: chemotaxis of monocytes
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SRS-A (slow reacting substances of anaphylaxis)
(aka leukotrienes) |
Action: mediates exudation, vasoconstriction, and bronchoconstriction
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