Exam 3 Tissue Injury & Host Defense
Alice is a 16 yold schoolgirl and admitted to hospital for 22nd time! Each admission is due to acute bacterial infection influding multiple admissions for acute pneumonia, meningitis, osteomyelitis, skin infections, sinusitis, and otitis media. Investigation shows she has _____? (not in review but imp.)
"Complete absence of C3" is an extremely rare cause of SEVERE "RECURRENT" BACTERIAL INFECTIONs. * Careful: don't confuse this with bacterial infections caused by absence of C5!
(1) Metabolic Pathways influencing Clinical decision-making: Phase I metabolized Opioids? Codeine, Morphine? Oxycodone, Oxymorphone & Hydrocodone? Hydromorphone, Fentanyl? Tramadol? Methadone? (2) CYP2D6 dependent Opioids (3) CYP2D6 & CYP3A4 dependent Opioids didn't spend more than 5 seconds onthis slide.2/23 ID (not from review)
(1) - In patients on multiple drugs it is best to use an opioid that is not metabolized by CYPs. - Most opioids that undergo only CYP-mediated oxidation have SUBSTANTIAL DDI POTENTIAL. Exceptions: MORPHINE, HYDROMORPHONE & OXYMORPHONE: They undergo ++ glucuronidation. - Some opioids produce multiple *active metabolites* after administration . Altered metabolism *due to medical comorbidities, genetic factors or DDIs* may disrupt the *balance of metabolites*, thereby altering the efficacy and/or tolerability of the drug. FENTANYL, OXYMORPHONE & METHADONE HAVE NO ACTIVE METABOLITES COMPLICATING CARE (1a) *Phase I metabolized Opioids:* Codeine, Morphine, Hydrocodone, Oxycodone, Methadone, Tramadol, Fentanyl (1b) Codeine, Morphine: - Codeine: is a prodrug that is converted to Morphine. POOR OR RAPID 2D6 METABOLIZERS do not respond well to Codeine. Codeine toxicity can occur in poor 2D6 metabolizers who are unable to form Morphine and in rapid 2D6 metabolizers who form too much Morphine. - Morphine: metabolized by 3A4 & then glucuronidated to 2 metabolites* Morphine-6-glucuronide *(M6G)* & morphine-3-glucuronide *(M3G) are the two metabolites .Renal disease => M6G & M3G (metabolites) accumulation => toxicity of morphine from inc. metabolites. [don't use full dose of morphine in immunocompromised patient - reduced dose]. MORPHINE METABOLITE HAS CNS TOXICITY: Poorly excreted in presence of Renal insufficiency. So REDUCE DOSE OR AVOID USING MORPHINE IN CIRRHOTIC PATIENTS. MORPHINE HAS VERY FEW DDIS THAT ARE 3A4 RELATED (1c) Oxycodone, Oxymorphone & Hydrocodone: - Oxycodone: CENTRAL OPIOID EFFECT OF OXYCODONE IS GOVERNED PRIMARILY BY THE PARENT DRUG. Oxycodone is primarily metabolized to Noroxycodone (a weaker agonist) by CYP3A4. Small portion of Oxycodone undergoes CYP2D6 metabolism to Oxymorphone. Oxymorphone then undergoes Phase 2 glucuronidation. Oxymorphone is present only in small amounts after Oxycodone administration. CLINICAL RELEVANCE OF OXYMORPHONE IS QUESTIONABLE. Oxymorphone has MINIMAL DDIs with SSRIs, TCAs, β-blockers & anti-arrhythmia meds. - Oxymorphone (Opana): undergoes PHASE 2 METABOLISM ONLY. - Hydrocodone: 2D6 converts Hydrocodone to hydromorphone, which then undergoes Phase 2 glucuronidation. (1d) Hydromorphone, Fentanyl: - FENTANYL, OXYMORPHONE & METHADONE HAVE NO ACTIVE METABOLITES COMPLICATING CARE - Hydromorphone (Dilaudid): Hydromorphone (Dilaudid) undergoes Phase 2 metabolism only. - Fentanyl: converted by CYP3A4 to nor-fentanyl, a nontoxic, INACTIVE METABOLITE. Less than 1% of the active metabolite of Oxymorphone is excreted in urine. The *CYP3A4 enzyme* is the *primary metabolizer of Fentanyl.* Fentanyl also DOES NOT CAUSE HISTAMINE release associated with other opioids. - Hydromorphone and Fentanyl ARE LEAST AFFECTED BY RENAL DYSFUNCTION & BEST IN CRF. (1e) Tramadol:- Pro-drug Tramadol converts to active metabolite, O-des-methyl-tramadol (M1). Parent compound Tramadol relies on both CYP3A4 & CYP2D6 for metabolism. M1 RELIES ON CYP2D6 ONLY. Both Tramadol & M1 metabolite exert analgesic effects through μ-opioid RECEPTOR & THROUGH SEROTONIN REUPTAKE INHIBITION + NOREPINEPHRINE REUPTAKE INHIBITION. M1 HAS MORE POTENT ACTIVITY AT THE Μ-OPIOID RECEPTOR. Tramadol + Tegretol/Carbamazepine (a 3A4 inducer) => ++ serotonin effect & seizures Tramadol + SSRIs/TCAs => ++ serotonin effect & SEIZURES. Tramadol is the MORE POTENT INHIBITOR of serotonin & norepinephrine reuptake. IS ALSO THE more potent promoter of SEROTONIN AND NOREPINEPHRINE efflux. Do not combine Tramadol with Morphine, SSRIs, TCAs or anti-seizure medications as it can precipitate serotonin syndrome. - SEROTONIN SYNDROME symptoms: *Agitation, confusion, HBP, twitching, headache, diarrhea, inc. temperature or death.* Low dose Tramadol OCCASIONALLY USED IN CIRRHOTICS BECAUSE OF ITS MOOD ELEVATION AFFECT. Lower Tramadol dose or avoid WITH RENAL FAILURE. Avoid Tramadol IN EPILEPTICS as it is known to LOWER the seizure threshold. (1f) Methadone: - Methadone is metabolized by 6 CYPs: CYP3A4 (main), 2B6, 2C8, 2C9, 2C19 & 2D6 (main). WITH METHADONE INVOLVING 6 CYP enzymes, THERE IS CONSIDERABLE INTERACTION POTENTIAL. Methadone is well-absorbed from the GI tract. Methadone has high oral bioavailability & low hepatic extraction. It undergoes considerable biotransformation in the liver - Methadone produces no active metabolites. It is associated with the HIGHEST INCIDENCE OF PROLONGED QTC INTERVAL. It exerts its activity, BOTH ANALGESIC & TOXIC through the parent compound. (a) WHEN PAIN MEDICATION IS NEEDED FOR A METHADONE USER: Methadone clinic MD can inc. Methadone dosing to tid/q8h {red} for maximum pain control. Methadone dose for chronic pain in an outpatient setting should be ≤ 40mg/day {RED}. KNOW THAT YOU SHOULD avoid adding other opioids to Methadone {RED}. Pharmacokinetics of Fentanyl & Methadone ARE NOT MUCH AFFECTED by Hepatic impairment. Also, Methadone & Fentanyl ARE LESS AFFECTED BY Renal impairment than other opioids. ALCOHOL inhibits THE METABOLISM OF METHADONE, leading to elevated plasma levels. In the absence of alcohol, METHADONE MAINTENANCE IS SAFE with advanced liver disease as benefits from abstinence far outweighs the risks. (1) *2D6 is entirely responsible for Phase I metabolism of*: 1. Hydrocodone -> Hydromorphone 2. Codeine -> Morphine 3. Dihydrocodeine -> Dihydromorphine 4. Tramadol -> O-des-methyl-tramadol (M1) All the above then undergo phase 2 glucuronidation. *The above drugs have significant interactions with: SSRIs, TCAs, β-blockers, Anti-arrhythmia drugs* (2) - In addition to 2D6, Oxycodone, Tramadol & Methadone are also metabolized by 3A4. - They have less 2D6 associated DDIs compared to Hydrocodone, Codeine & Dihydrocodeine. - Phase 2 Metabolism: Opioids undergoing Phase II metabolism only have minimal DDIs as no enzymes involved. - PHASE I METABOLIZED OPIOIDS + 3A4 substrates/inducers/inhibitors -> inc. DDIs. - Bergamottin in grapefruit juice is a strong inhibitor of 3A4 : Avoid use with medications. - Cafestol found in unfiltered coffee is an inducer of the 3A4 enzyme: Avoid use.
Before prescribing pain (acute/chronic) meds, what do you need to determine and ask yourself (ALWAYS)? What are you concerned mostly about in Elderly patients, and in the younger? Three things you must consider before prescribing meds? - id 2/23 *bold* caps red. (not from review)
(1) - Use SMART {red, know} acronym for pain outcome goals: Be "S"pecific, "M"easurable, "A"ction-oriented, "R"ealistic & "T"ime-bound - *Set Goals to regain activities lost from pain*: chewing/opening jaw/neck movements etc. - 1st try *Tylenol & NSAIDs* (if OK to use), then start an Opioid at the lowest effective dose: "START LOW & GO SLOW" = aka: "Have a "start low & go slow" approach to opioid titration. Especially with hepatic &/or renal disease. In general, dose reduction and/or prolongation of dose intervals may be necessary. NEVER ABRUPTLY STOP ER OR LA OPIOIDS IN PATIENTS ON CHRONIC OPIOIDS THERAPY. ALWAYS TAPER BY 10% EACH WEEK. THEN SWITCH TO SHORT ACTING FORMULATIONS PRIOR TO SURGERY. - *When choosing an Opioid consider the following:* Its potency, *onset of action*, half-life, *starting dose*, rapidity of titration & *ceiling dose*. *Consider comorbities* like advanced age, SLEEP-DISORDERED BREATHING & CONCURRENT MEDS: such as *Benzodiazepines, Anticonvulsants, Muscle relaxants.* (2) *Adjuncts:* - TOPICAL ANALGESICS: Diclofenac *(Voltaren) gel or Lidocaine patch* 5% (Lidoderm) or *Capsaicin gel* - TCAs (Amitriptyline/Elavil), SSRIs (Fluoxetine/Prozac) or MUSCLE RELAXANTS (Beclofen/Lioresal) - AN ANTICONVULSANTS (Gabapentin/Gralise, Carbamazepine/Tegretol, Phenytoin/Dilantin) - *Also concurrent use of the following* NON-PHARMACOLOGIC THERAPIES *should be considered:* (a) *PT*, exercise, *Yoga*, Relaxation training, *Biofeedback*, Cognitive behavioral therapy (b) *Always be sympathetic towards your patient!* (3) *Opioid metabolism is a SAFETY ISSUE IN OLDER & Medically Complex Patients (MCP) because:* Medically complex patients (MCPs) are typically taking *multiple medications: ~ 4-7 * MCPs may have *inflammation & thus may need long-term* opioid therapy MCPs may have IMPAIRED RENAL &/OR HEPATIC FUNCTION thus affecting opioid metabolism MCPs may have *impaired immunity* thus contributing to *inc. opportunistic infections* (3b) *In Younger patients the provider is more concerned with*: Opioid metabolism & occurrence of *tolerance, impairment of skills & mental function* Also *adverse events during pregnancy and lactation (highlighted this)* Plus *prevention of abuse by monitoring drug and metabolite levels* (4) Before Prescribing: - What SAFETY CONCERNS exist for the MEDICALLY COMPLEX PATIENT (MCP)? - How do NSAIDs & Opioids affect specific ORGAN FUNCTION OR DYSFUNCTION(S)? - What impact will NSAIDs &/or Opioids have on ASSOCIATED DISEASE STATES?
"Points to Consider..." ID 2/23 (1) Always prescribe ______ for ACUTE PAIN. (2) For the EXPECTED DURATION OF PAIN, how much should you prescribe? (3) More than a few days of exposure to unnecessary opioid use increases the likelihood of? (4) Prescriptions with fewer days' supply also minimizes the number of pills available for ? (5) In cases of acute pain that may require more than 3 days of opiod treatment, what range of days should you go with? (6) For Perioperative Pain, what do you check? (7) Points to consider - fix, mesh with rest an dhighlight these .
(1) Always prescribe lowest effective dose of immediate-release opioids for acute pain. - NON-OPIOID ANALGESICS OR IMMEDIATE-RELEASE OPIOIDS ARE MORE EFFECTIVE FOR ACUTE PAIN. (2) Do not prescribe greater quantity than needed for the expected duration of pain. - Limiting the days for which opioids are prescribed, also *minimizes the need to taper opioids* to prevent unpleasant withdrawal symptoms. (3) INCREASES LIKELIHOOD OF PHYSICAL DEPENDENCE *without adding benefit*. (4) UNINTENTIONAL OR INTENTIONAL DIVESION. (5) Some types of *acute pain may require more than 3 days* of opioid treatment -> In such cases go with a range of *≤3-5* days or *≤3-7* days when needed: *CANNOT GIVE FOR >7 DAYS* (6) PREOPERATIVELY CHECK PMP & assess risk for over-sedation & difficult to-control pain. Discharge with *Tylenol, NSAID, or 2-3 days of short-acting opioids* for some minor surgeries. (7) GIVEN THE LONGER half-lives and longer duration of effects (respiratory depression) w. ER/LA opioids (methadone, fentanyl patches, ER versions oxycodone, oxymorphone, morphine). AVOID PRESCRIBING ER/LAD OPOIODS FOR ACUTE PAIN. Anxiety disorders (and other mental health conditions) = more likely to receive Benzodiazepines, which CAN EXACERBATE PIOID-INDUCED RESPIRATORY DEPRESSION and increase risk for overdose. FOR TREATMENT OF CHRONIC PAIN in patients w depression, use TCA or SNRIs for their analgesic & antidepressant effects, If not otherwise contraindicated. WHEN COMPARED TO YOUNGER ADULTS initiate opioids at 25-50% lower dose IN OLDER ADULTS. Review the patients health history & H/o controlled substance prescriptions. USE STATE PRESCRIPTION DRUG MONITORING PROGRAM (PDMP) DATA to determine if the patient is getting opioid dosages elsewhere (this puts patient at high risk for overdose).
(1) Opiods - if you need to use in patient w. liver disease, what should you adjust to the opiod med? In patient with kidney disease, you cannot use? RECOMMENDED FOR USE IN LIVER/KIDNEY FAILURE, why? (2) vs. Non-opioids - Cox-1 or 2's cause more stomach upset and why? NSAIDs for patients with CVD? Do these have ceiling effect? ID 2/23
(1) Opioids & Liver Dis. = impaired metabolism in liver disease (liver failure -> dec. oxidation and clearance opiods) so use lower dose for longer interval (thats if u must use opioid in liver disease). Opioids & Kidney Dis. = impaired metabolism in kidney disease: AVOID: Pro-Drug Opioids [CODEINE-TYLENOL, VICODIN, TRAMADOL] w. Celecoxib, a 2d6 inhibitor ( opioids are 2d6 substrates and slow down intestinal absorption time). Use caution with Codeine, Morphine, Oxycodone bc their active metabolites r cleared thru kidneys. AVOID in Liver OR Kidney Disease = Meperidine, Propoxyphene, Pentazocine. Tramadol = can use reduced dose in pre-failure liver/kidney diseases; Avoid Tramadol (Ultram) with cirrhosis/dialysis. RECOMMENDED FOR USE IN LIVER/KIDNEY FAILURE = HYDROMORPHONE (DILUADID) OR FENTANYL; Hydromorphone & Fentanyl appear ARE LEAST AFFECTED BY RENAL DYSFUNCTION in Cirrhosis. (2) COX-1s cause more stomach issues, intestinal bleedings, ulcers; bc 1's decrease natural protective mucus lining of stomach more than COX-2s. Inc. risk for CV disease, use of COX-2s DO NOT PREVENT STROKES/HEART ATTACKS. COX-2s inc. platelet aggregation: Avoid with significant cardiovascular disease (CVD).IN GENERAL, AVOID PRESCRIBING ANY NSAID IN PATIENTS WITH SIGNIFICANT/UNSTABLE CVD. Non-opioids have max. analgesia/dose ceiling effect: No more pain relief with inc. in dose. -> HIGHER DOSING NEEDED WITH ANY NSAID FOR ANTI-INFLAMMATORY EFFECT, but ALWAYS USE INCREASED DOSING FOR THE SHORTEST TIME: 1-2 DAYS IF POSSIBLE...USE STEROIDS IF LONGER DURATION ANTI-INFLAMATORY EFFECT IS NEEDED. NSAIDS are generally better than opioids at routine doses.
NSAIDs & Gastric Bleeding or Ulcers
*Non-selective NSAIDs* can cause *stomach & intestinal bleeding, ulcers and perforation*. THESE EVENTS *CAN OCCUR AT ANY TIME* DURING TREATMENT *AND WITHOUT WARNING* SYMPTOMS. *ELDERLY PATIENTS ARE AT GREATER RISK* . *GI side-effects* can occur *SOON AFTER INITIATION OF THERAPY*.
Layers of Integument (review)
1) Epidermis 2) Dermis = CT layer, has spclzed glands, hairs, sensory receptors. 3) Hypodermis [not really a layer but some stuff extends to it]= subcutaneous adipocytes; has spclized glands, hairs, sensory receptors (cutaneous adnexa).
Opioids that are "THERAPY FOR HEROIN ADDICTS" (know ID, 2/23)
1) METHADONE 2) BUPRENORPHINE (SUBOXANE)
List of Bacteria that can cause diseases of the lungs? Each associated w. what disease, where are they found, how they spread, etc? (review)
1) Pertusis = whooping cough usu. in INFANTS (is MOST DANGEROUS in them) , can lead to death (many infants with it don't cough even; instead, apnea (pause in breathing pattern) and turn blue) = BORDETELLA PERTUSIS bacteria is gram negative: encounter via person-to-person (doesn't survive well in environment, highly contageous). Entry via inhalation Multiplication by adheres to respiratory tract. Damage bc produces toxins that immobilize the mucociliary escalator. - *Pertussis Vacccines*: Currently, use DTaP for baies and chidlren (first vaccination). Tdap for preteens, teens, and adults (booster). or, Tdap for *pregnant women*. (2) Pneumonia = infection of lung parenchyma (portion of lung involved in gas transfer: the alveoli, alveolar ducts and bronchioles) = is a bunch of related diseases that affect same location, thus cant diagnosis specific pathogen cause based on clinical symptoms (need to dx by bacteria culture) = ACUE PNEUMONIA caused by: (i) STREPTOCOCCUS PNEUMONIAE [if spread from oral to lungs will cause pneumonia], (ii) LEGIONELLA PNEUMOPHILA [come form environment / WATER SYSTEMS, NOT human-human trnsmsn; grows inside Macrophages], (iii) PSEUDOMONAS AERUGINOSA [Nosocomial (rarely, environmental); Opportunistic in Humans - normally won't cause disease, will tho in CF patient or immunocompromised, in HOSPITAL; has 2 properties that make disease caused by this bacteria difficult to treat: forms BIOFILMS, and is naturally ANTIBIOTIC RESISTANT]. (3) Pulmonary Actinomycosis = Rare Lung Infection = SYMPTOMS: Chest pain, cough, fever, lethargy, night sweats, shortness of breath, weight loss; Infection often develops slowly. RISK FACTORS: *POOR DENTAL HYGIENE*, *DENTAL ABSCESS*; alcohol abuse, emphysema, scars on lung = TREATMENT W. IV antibiotics 4-6 weeks = bacteria is Acinetobacter sp. OTHER NOTES ON RESPIRATORY INFCTIONS FROM LECTURE (NOT REVIEW): - Respiratory disease is caused by AIRBORNE ORGANISMS. - *Upper Respiratory Infections (URIs)* = Otitis media, pharyngitis, laryngitis, croup, Sinusitis, conjunctivitis, rhinitis, epiglottis, tracheatis. Viruses mainly cause URIs. - *Lower Respiratory Infections (LRIs)* = Pneumonia, bronchiolitis, bronchitis. Fungi and protozoa rarely cause disease in mmunocompetent persons but can cause pneumonia in the immunocompromised. - Cold air means increased transmission of pathogens -- Respiratory infections more common in winter: BC: confined indoors (poor ventilation, close to ppl); cold air breathing causing caugh, sneeze, runny nose. Cold and dry air results in smaller respiratory droplets which stay longer in air (smaller droplets can travel longer distances and reach lower respiratory tract). All resulting in *increased transmission of pathogens* C) Most do not cause infection and disease unless other factors interefere w host defences.
Pigmentation Variations
1. freckles - a.k.a "ephelides" -localized INC. IN MELANIN PRODUCTION. -develop in response to sun exposure 2. moles - a.k.a "nevus" -localized AGGREGATION OF MELANOCYTES. -appear soon after birth (if congenital, called "birthmark") 3. vitiligo -focal destruction of melanocytes -autoimmune disorder 4. albinism -lack of pigmentation -tyrosinase defect (Type I)
Abscesses - defintion? smells like? proximity/route (possible ways to get it)? Treatment would be aimed at... why? (review)
= A swollen, inflamed area in body tissues, in which pus gathers; foul-smelling. PROX/ROUTE (3 POS) = Extension from a nearby non-sterile area (dental work), penetration/trauma (deep wound), or hematogenous spread (brain). - Bacteria found in the abscess match those in the place of origin, e.g., oral. - are POLYMICROBIALmainly oral anaerobes, synergistic (become pathogens in presence of other bacteria). -> Treatment aimed at many species, not just one!
Mucosal Tissues of the Human Body immuno 2/24
= where pathogens most likely to get us bc at risk even when stuff blowed into face and gets into repiratory tract (infections in blood / spleen that deals w and filters blood aren't "as likely" bc we are sterile nowadays) = any site where there's secretion and mucous surfaces. MALT - mucosal associated lymphoid tissue. BALT - bronchus associated lymphoid tissue. GALT - gut associated lymphoid tissue.
What is the new black box warning placed on benzodiazapines? A. do not operate heavy machinery or a motor vehicle under the influence. B. do not lift heavy objects whil under influence. C. providers must warn patients about the interaction of this drug with alcohol D. avoid combination of this drug with opioid analgesics. star and see notes on this.
C. NOT on the slides, she said it in lecture. Benzo's are depressants, alcohol is a depresant -> double depressant is no gucci. D is very wrong. u can absolutely give benzos and opioids together. A is TRUE, but not the black box warning.
All three "Complement Pathways" converge on/cleave _____? (review)
C3 is common to all three pathways!
"Coat" around virus and define the viral genome?
Caspid is protein coat. Some viruses have a lipid coat or "envelope" as well. Viral Genome can be either Double-Stranded or Single-Stranded DNA or *RNA.*
Which of the following does NOT cause a disease of the lungs? A Legionella pneumophila B. Actinomyces baumanii C. Pseudomonas aeruginosa D. Streptococcus pneumoniae E. All of these can cause a disease of the lungs.
E (all them cause disease of lungs!)
Legionella pneumophila can be found in all of the following EXCEPT A. Air conditioning systems B. Dental unit water lines C. Hot tubs D. Lakes and ponds E. Normal human microbiota.
E (not found in normal human microbiota).
BABY IS BORN WITH? .... At 9 months / birth, what Ig does person have? Before vs. After birth? (review)
Full Adult Level of moms IgG. IgG has half life about 1 month, so after birth moms IgG goes down but babys igg starts going up and eventually will reach adult levels = passive immunity, preformed antibody. KEY POINT: "After birth, moms IgG decreases and baby's IgG increases until reaches "adult" levels." REMEMBER HALF LIFE OF IGG IS 3-4 WEEKS. - Fully adult level of IgG that came from mom. - But, Half life IgG 3-4 weeks. So, then maternal IgG goes down w/in a month after birth. - Newborn IgG starts after birth and will go up and meet up with the maternal IgG around 3 months.
Difference between injecting someone with "Immune Globin" versus giving vaccine?
Immune Globin = artificial PASSIVE immunity = = MORE EXPENSIVE THAN REG. VACCINE. VERSUS, giving them vaccine wouldnt be fast enough bc get lag phase.
What is IVIG?
Injection of pre-formed Immunoglobulin (antibody) in PASSIVE IMMUNITY. Intravenous Immunoglobulin is a solution of highly purified immunoglobulin G, derived from large pools of human plasma that contain antibodies against a broad spectrum of bacterial and viral agents. Indicated Uses: Primary humeral immunodeficiency disease; Certain autoimmune diseases including Autoimmune Thrombocytopenia, and Myasthenia Gravis [bc Dumping lot of IVIG into autoimmune patient -> patients lower amount of antibody they make and also lower amount of autoantibody they make].
Pregnancy & Vaccines (review)
MATERNAL IMMUNIZATION PROVIDES STRATEGY TO DECREASE SUSCEPTIBILITY TO INFECTION IN NEWBORN INFANTS. TETANUS, DIPHTHERIA, PERTUSSIS (Tdap), & INACTIVATED INFLUENZA VACCINES R NOW RECOMMENDED FOR USE DURING PREGNANCY. "Tetanus, diphtheria, pertussis (Tdap) and inactivated influenza vaccines are now recommended for use during pregnancy." Passive and Active Immunity - idea that if u immunize pregnant women against tetanus toxin, or boost them, then you make sure that baby will be born with "protective titer" of antibody against tetanus toxin, which can cause neonatal tetanus. Safe vaccines not infectious.
IMP. PROTEINS IN LECTIN PATHWAY? know the names.
MBL (mannose binding protein), MASP1, MASP2. Recall: activated by organisms w mannose on their surface. Draw pic!
m. avium-intracellulare
MYOBACTERIAL DISEASE ("other") know path 2/22
What are Melanocytes, Langerhans cells, and Merkel cells? Where do you find them?
Melanocytes -melanin pigment production (no keratinization, same w merkel cells). Langerhans Cells -immunosurveillance, antigen presentation, no desmosomes, few IF, derived from bone marrow Merkel Cells -sensory, mechanoreceptors (no keratinization, same w melanocytes) (lymphocytes) All are Epidermis Cells
Transcriptional Anti-Terminators (review)
N and Q proteins s.t. phage LAMBDA (a lysogenic/temporate phage capable of either pathway) continues with LYTIC Gene Expression. [A "new kind of transcriptional regulation" in phages].
Adverse side effects of opioids? star
Nausea, Vomiting, Constipation Drowsiness Respiratory- Depression Not Diarrhea! But, *dec side effects* when opioids (dec dose used) combination w. Tylenol (non-opiod), so combo is good for tx acute pain.
Lack of complement C7 means? (review)
No MAC. Results in Neisseria Infection e.g. Neisseria Ghonnorea.
Tramadol (ULTRAM)
Opioid. Dental Use = relief of mild to moderate pain. Efficacy equiv. to aspirin/codeine combination. Schedule IV drug. Mech of action: mu receptor agonist, inhibits pain ascending pathways, altering perception and response to pain. Also inhibits NE and 5-HT reuptake, which also modifies ascending pain pathway. Warnings/contraindications: elderly patients, patients w chronic respiratory disorders, liver disease, pregnancy, patients w history of drug or alcohol dependence, seizure prone patients.
What do you do when a kid is bit by crazy dog (rabies risk)? Even at six months after {tho this is rare possibility}.
Postexposure rabies vaccination (vaccine = active immunity) consists of = four doses of an "inactivated" rabies virus vaccine given on days 0, 3, 7, and day 14 after exposure. On day zero, rabies immune globulin (RIG) is also given to provide iMMEDIATE PROTECTION VIA *PASSIVE* imunity; which is done bc the vaccine takes 7-15 days to provide a protective antibody response from *active immunity* (and immune globin intramuscular shot will last few months and in that time you'll build up ur active immunity).
NSAIDs & Cardiovascular Risks & Events (not from review)
RISKS: - NSAIDs have many SE, including an INC. risk of adverse CV effects - Risk of events varies depending upon: The clinical context (CO-MORBIDITIES), WHICH NSAID Is being used, & What dose is being dispensed. - BOTH nonselective NSAIDs & COX-2 selective NSAIDs (Coxibs) INCREASE SUCH RISK. - ALWAYS BEST TO CONSIDER THE DURATION & FREQUENCY OF THERAPY BEFORE PRESCRIBING - Use nonselective NSAIDs at LOWEST EFFECTIVE DOSE & FOR THE SHORTEST DURATION required CV EVENTS: - Adverse CV events include: (KNOW LIST, IN RED) MI, stroke; Heart failure (HF); Atrial fibrillation ; CV death. - Absolute increase in risk is small in patients with no known CVD. - RISK OF CV EVENTS IS EXTREMELY SMALL WITH SHORT TERM THERAPY (2-3DAYS). - NAPROXEN IS BEST FOR SHORT-TERM/INTERMITTENT USE FOR THOSE WITH NO PAST H/O CVD. - IBUPROFEN IS ALSO A REASONABLE ALTERNATIVE GIVEN THE LOW BASELINE RISK IN SUCH PATIENTS. - NAPROXEN IS PREFERRED OVER OTHER NSAIDS FOR SHORT OR LONG-TERM USE. NSAIDs: Heart Failure & HTN: - NSAIDs & Heart Failure: - AVOID NSAIDS use in HF patients as NSAIDS can EXACERBATE Heart Failure by: (i) Promoting *sodium & water retention*; (ii) Causing higher *intravascular resistance*; (iii) Causing *reduced response to diuretics*. - *Patient with hypertension & diastolic dysfunction develop HF more easily.* - Risk of HF *doubles with Celebrex.* - Ibuprofen can interfere with the cardio protective effect of Aspirin. - USE OF NSAIDS SHOULD BE AVOIDED IN HEART FAILURE (HF). - *NSAIDs should be used with CAUTION in patients with Hypertension (HTN).* - CHRONIC NSAIDS CAN RAISE THE BP & CAUSE NEW ONSET HTN OR WORSENING OF EXISTING HTN. - NSAIDs DEC. action of Diuretics by *reducing renal blood flow* (prostaglandin inhibition). NSAIDs & CV EVENTS: - *Diclofenac & Celebrex* are associated with *increased CV side effects*. *CVD SE with Ibuprofen are* NOT STATISTICALLY SIGNIFICANT. - Most *nonselective NSAIDs at HIGH DOSES* INCREASE MAJOR CV EVENTS RISKS. *CV & GI risks increase* with *higher doses & increased dosing frequency.* - NAPROXEN APPEARS TO BE AN EXCEPTION. An *increased risk of MI/stroke* may be seen *at LOWER DOSES of Naproxen (220 mg bid).* *At higher doses*, NAPROXEN HAS A MORE SUSTAINED ANTIPLATELET EFFECT. Thus Naproxen is the *safest nonselective NSAID* WITH RESPECT TO CARDIOVASCULAR RISK. - HIGH-DOSE DICLOFENAC/CELEBREX CAUSE SIGNIFICANT INCREASE IN MAJOR CV OR CORONARY EVENTS. *Do not use NSAIDs in patients with* RECENT ACUTE MI, UNSTABLE ANGINA, OR POORLY COMPENSATED HEART FAILURE (HF). Yes/No CVD Risks: Which NSAID to use? (1) *In patients WITHOUT CVD risk* = 1st choice is best to dispense NAPROXEN for *short-term* or *intermittent* use. 2nd choice is IBUPROFEN is a *reasonable choice and cost effective*. - *Naproxen* is also the NSAID choice for *long-term use*, PARTICULARLY IF USED IN HIGH DOSES. (2) *Patients W. KNOWN CVD or AT HIGH RISK for CVD*: use NAPROXEN for *short-term or intermittent use*. HOWEVER, AVOID NSAIDs WHEN POSSIBLE IF AN ALTERNATIVE CHOICE IS AVAILABLE. Use "Naproxen* when *high doses* are needed for *long-term use*. - AVOID IBUPROFEN OR DICLOFENAC.
Specific uses of adrenal corticosteroids in dentistry? (not in review but red)
Specific Uses in Dentistry (know this list - red) = (1) ORAL LESIONS - topical fluoridated glucocorticoids such as Synalar or Lidex applied with an adhesive paste can be used topically to treat certain types of oral lesions such as chronic desquamative gingivitis (2) PULPAL SENSITIVITY - to reduce pain from pulpal hypersensitivity resulting from inflammation (3) TMJ PAIN - to treat pain in temperomandibular joint disorders using direct intraarticular injection. (4) POSTOPERATIVE TRAUMA - to lessen postoperative trauma such as edema and trismus following dental surgery. (5) ANAPHYLAXIS - not the primary drugs for treating the life threatening cardiovascular and respiratory failure of anaphylaxis. Administration of epinephrine and establishment of an airway are the immediate first course of action. (6) GLOVE RASH - should not be placed on hands and then have gloves worn over the drug as the increased heat will increase systemic absorption.
What is the difference between thin skin and thick skin?
Thick skin = palms/soles (only 2 places), NO hairs (no apocrine or sebaceous glands), fingerprint grooves, SSKE also. Thin Skin = everywhere else (besides palms/soles), hair usu. And hair-associated glands, SSKE also. Differentiation has to do with the epidermis.
13) Which if the following statements is FALSE? a) melanin is derived from tyrosine b) arrector pili muscle action causes "goose bumps" c) human papilloma virus infection causes warts d) sebaceous glands always empty into hair follicles e) loricrin is deposited intracellularly.
a. correct, no intermediate b. Yes c. True d. FALSE - answer. Anytime u have hair, u will have sebaceous glands dumping into them. But you can hair sebaceous glands w/o follicles = fordyce spots on lips & aerolar glands (around nipple).
Major surgery with bleeding risk, you should tell your patient to stop their aspirin when? Star
about a week (7-14 days, know 10 days) before the surgery.
G6PD (Fava Beans) star fix see notes why not
cannot have tylenol.
Chronic Inflammatory Granulomatous Response with Minimal Acute Inflammation know path 2/22 pic see bc in lecture
"Other Myobacterial Diseases" - LEPROSY (M. LEPRAE). - BOVINE TUBERCULOSIS: CERVICAL NECK NODES INVOLVED FROM DRINKING INFECTED COWS' MILK. - M. MARINUM: CHRONIC SKIN LESIONS ON HANDS. - M. SCROFULACEUM: ENLARGED LYMPH NODES OF THE NECK.
Understand concept of "Herd Immunity (Community Immunity)" (review)
"The protection of unimmunized individuals due to a large decrease in susceptible individuals as a result of high vaccination levels. Example: varicella (chicken pox) vaccination protects individuals no eligible for vaccination. varicella vaccination was introduced in 1995, and the incidence among infants, one ineligible group, declined 90% by 2009. Measles, the most contagious of the vaccine-preventable diseases, requires very high vaccine coverage, estimated at 92%-94% to achieve effective 'herd immunity'; herd immunity for other vaccine-preventable diseases range from about 80-86%" notes - protection of entire community/group IF enough people are immunized. High vaccination level for a particular bug. e.g. measles outbreak bc so many ppl in community need to be immunized; measles is highly infectious.
(1) IV Acetaminophen & (2) Mild-Mod Pain Rx, (3) Acetaminophen and Coumadin ID 2/23
(1) *IV Acetaminophen:*= FDA approved for postoperative pain in *adults & kids: VERY RAPID ONSET.* Used alone or w. opioids *prior to surgery or during intra-operative period.* * Avoids first-pass * in the liver thus *reducing the potential for hepatotoxicity.* IT IS PROVING TO BE SAFE IN PATIENTS WITH UNDERLYING LIVER DISEASE. *Contraindicated with severe liver disease.* You can easily switch to oral Acetaminophen once the patient tides over the acute phase. Dispensed as a *100mL single-use vial containing 1,000mg Acetaminophen*. (2)*Acute post-op Mild to Moderate Pain Management* = NSAID + Acetaminophen provides greater pain control than does either drug alone: They both inhibit prostaglandin synthesis but *act at different sites.* Do not exceed the daily recommended doses of Tylenol to avoid liver damage. Always begin pain management with non-opioids and add opioids, when needed. (3) Combination can increase INR within 18-48 hours. - *This DDI is enhanced by*: Decreased fluid intake, Dehydration, Alcohol consumption, Liver disease. - *Precautionary Steps*: Use only regular strength Tylenol for 2-3 days & avoid extra strength Tylenol. Increase the fluid intake. Consume 6-8 glasses of water per day. Avoid alcohol consumption These steps will minimize an increase in the INR.
Cochrane Review: Analagesic efficacy of drugs - (1) Highest analgesic efficacy (of individual drug interventions) in acute post-operative pain? How many mg voltaren for acute post-op pain? (2) Highest analgesic efficacy of drugs w. 8 hours or more analgesia effect? What combo of drugs can be used for both acute post-op pain, and, has 8 hours or more analgesia effect? ID 2/23 (not from review but red stuff)
(1) Analgesic efficacy of individual drug interventions "IN ACUTE POSTOPERATIVE PAIN "{RED}: - IBUPROFEN 200mg + ACETAMiNoPHEN (Tylenol) 500mg = HIGHEST EFFICACY for acute post-op pain. (know this, red}. - Ibuprofen fast acting 200 mg - Ibuprofen 200 mg + Caffeine 100 mg - DICLOFENAC POTASSIUM (VOLTAREN) 50 mg {bold}. - Ibuprofen acid 400 mg (2) Analgesic efficacy of drugs with "8 hours or more ANALGESIA EFFECT" {RED}: - DIFLUNISAL (Dolobid) 500 mg (HIGHEST EFFICACY) {bold}, but this is NSAID and should not be used in liver problem patient. - Tylenol 650 mg plus Oxycodone 10 mg - NAPROXEN 500/550 mg {bold}. - CELECOXIB 400 mg {bold} - IBUPROFEN 400 mg {RED} + TYLENOL 1000 mg {RED} NOTE: Cochran review - how applying to patient care. TAKE HOME: Whenever u have patient taking two drugs both for same common goal, don't need to use equal doses for each drug. Instead of using 400mg ibuprofen + 1,000 tylenol {analgesic ceiling}, you can use 200 ibu + 500mg tylenol (1/2 mg's) and have optimal effect for acute pain management. If you have analgesic that'll last for 8 hours or more, also good bc means don't have to medicate the patient more frequently. Notice that longer duration have higher dosage...
Medical uses of Adrenal Corticosteroids?
(1) Endocrine: - replacement therapy for acute or chronic adrenal insufficiency (Addison's disease) or to suppress ACTH in congenital adrenal hyperplasia (2) Non-endocrine: (relating to antiinflammatory, antiallergenic actions requiring much higher, non-physiological doses) - rheumatoid arthritis, bursitis - skin conditions or asthma, collagen diseases such as lupus - palliative management of leukemias and lymphomas - ulcerative colitis, Crohn's disease - acute episodes of multiple sclerosis COPD, severe alcoholic hepatitis
Healing By Repair (review)
(1) From Review slides: = SCAR FORMATION w. FIBROBLASTS (ANGIOGENESIS); CAPILLARIES FORM; ENDOTHELIAL CELLS; CONNECTIVE TISSUE. = GRANULATION TISSUE IS HEALING TISSUE. - MATURATION TO FORM A SCAR. - GROWTH FACTORS (TGF-B) aka Fibrinogenic Agents. - "Inflammatory response is NECESSARY for healing and involved in scar formation (aka inflammation isn't only for get rid of bugs). (2) other notes from path: = "primary Intention" - healing of closely opposed surfaces. - epithelial regeneration is principal mechanism of repair. - small scar w. minimal wound contraction.
Other Opioid Medications (know caps -red, pharm 2/23) (review)
(1) METHADONE - TREATMENT FOR ADDICTION; THERAPY FOR HEROIN ADDICTS (2) FENTANYL (3) CARFENTANYL (4) Pentazocine (Talwin, Talacen); mixed acting agonist/antagonist. (5) Meperidine (Demerole) - for codeine allergic patients, 50-150mg PO every 3-4 hours, dispense 16 tabs, no refills. Contraindicated in patients taking MAOIs (causes increased formation of toxic metabolite, normeperidine). (5) Oxycontin: time release oxycodone preparation.
NSAIDs & Blood Thinners, Lithium or Methotrexate
(1) NSAIDs and Blood Thinners: NSAIDs can affect *both immediate & delayed hemostasis.* They inc. bleeding by *decreasing platelet cohesiveness.* This can affect primary blood clot formation. When used with *Warfarin (Coumadin)*, BLEEDING COMPLICATIONS INCREASE. ALSO, *Ibuprofen, Naproxen, Celecoxib and Coumadin are CYP2C9 substrates:* WHEN ANY ONE OF THESE NSAIDS ARE TAKEN PO AT THE SAME TIME WITH COUMADIN, *the NSAID can compete with Coumadin for CYP2C9,* THUS AFFECTING COUMADIN RESPONSE. *Avoid NSAIDs with NOACs* (2) NSAIDs & Lithium/Methotrexate: NSAIDs decrease *elimination of Lithium* (Eskalith) & *Methotrexate* (Rheumatrex). This can potentially lead to *toxicity with either drug.*
Important Functions of Complement System (when activated by Classical Pathway): 1) in Opsonization?* 2) Chemotaxis?* 3) Anaphylatoxin Production?* 4) Lysis of Organisms?* (review)
(1) OPSONIN = C3b = (IgG is another imp opsonin; phagocytes have Fc receptors for IgG) = Coating of organisms with antibody and complement C3b so that they are more easily phagocytosed by neutrophils and macrophages. [without C3b or antibody (alone), phagocytic activity is slow to ingest stuff; W/O C3b but still with antibody, phagocytic activity IS increased bc number of bacteria dec in quicker number of min. (2) C3a and C5a - are chemotactic factors (and anaphylatoxins, see (3)) = phagocytic cells are attracted to the site of the antigen. (3) C3a and C5a = ANAPHYLATOXINS = innate way to degranulate mast cells and basophils, releasing Histamine granules {potent inflammatory chemicals /mediators}. (4) C5b-C6-C7-C8-C9 is the membrane attack complex (MAC) that mediates LYSIS = ESP. IMP IN NEISSERIAL INFECTIONS = Lysis of organisms coated w specific antibody - C8 and C9. = In the classical (activation) Complement Pathway, this is formed when late complement components, C6, C7, C8, and C9 bind to C5b. [first C5b67 complex binds to membrane via C7, then C8 binds complex and inserts into cell membrane, then C9 binds to complex and C9 polymerizes]. Together, complement proteins (complexes) form a complex PORE in phospholipid bilayer, allowing INRUSHING FLUIDS into CYTOPLASM of pathogen cell.
Advantages of Combination preparations of opiods? know, red pharm 2/23 (not from review)
(1) SYNERGISM / ADDITIVITY - PROVIDES THE PAIN RELIEF OF A HIGHER DOSE OF OPIOID COMPONENT *WITHOUT* THE SIDE EFFECTS ASSOCIATED W THE USE OF THE HIGHER DOSE {in red}. Combine the peripheral action of quick acting, but shorter duration aspirin or tylenol with the slow onset, but longer acting central pain relieving action of the opioid.
NSAIDs & Systemic Inflammatory Diseases + Psych Pharmacotherapy
(1) Systemic Inflammatory Diseases: *The effect of NSAIDs on CV risk is LESS CLEAR* in patients with systemic inflammatory disorders such as *Rheumatoid arthritis (RA)*. In general, CV risk is increased in patients with RA. Some disease-modifying anti-rheumatic drugs (DMARDs) have a protective effect. (2) Psych Pharmacotherapy: Celecoxib & most SSRIs are CYP2D6 inhibitors = *Avoid Celebrex use with SSRIs*. *AVOID* SHORT OR LONG-TERM DISPENSING OF NSAIDS IN COMBINATION WITH SSRIS. Combination can potentiate *gastrointestinal (GI) bleeds*. NSAIDs DECREASE *elimination* OF LITHIUM via prostaglandin inhibition. This leads to DECREASE IN LITHIUM EXCRETION which is EXCLUSIVELY THROUGH THE KIDNEYS. *This can potentially lead to Lithium drug toxicity.* ASPIRIN & CLINORIL (SULINDAC) ARE THE *EXCEPTIONS*. Use *Clinoril short-term* when NSAID is needed *with Lithium.*
(1) Pregnancy & Opioids - allowed or not? (2) Pregnancy & NSAIDs (3) Pregnancy category B drugs? ID 2/23
(1a) No known safe level of narcotic use (while preg.) - risks to fetus = miscarriage, stillbirth, premature delivery; risks if born = low birth weight, breathing dificult, xtreme drowsiness -> feeding problems. (1b) BUT, narcotic use occasionally allowed for preg. if benefits >> risks. *List of Drugs approved for SHORT-TERM use in 1st/2nd trimester/Prior to week 28 of pregnancy* {only prescribe *short-acting opioids* during pregnancy & for *short-term use* only. *In Mass, patients* CAN BUY NALOXONE *at the pharmacy* WITHOUT A SCRIPT} = (i) Oxycodone (Percocet): FDA CLASSIFIES OXYCODONE AS A PREGNANCY CATEGORY B DRUG. (ii) Fentanyl (Duragesic), (iii) Hydromorphone (Dilaudid), (iv) Morphine Sulfate. *"Less safe" narcotics for short-term use in 1st/2nd trimester before 28 weeks* = (i) Codeine-Tylenol with codeine; (ii) Hydrocodone + Tylenol (Vicodin). (2) Avoid NSAIDs (generally) in pregnancy - ESP. during 1st (miscarriage risk) & 3rd ( premature ductus arteriosus closure). BUT, can also (like opiods) be used if benefits outweigh risks (category B) for max time 48-72 hours. *Avoid Celecoxib: Pregnancy Category: C, but D with chronic use /with high dose*. (3a) Oxycodone (Percocet) [opiod] - it is approved for short-term use in first/second trimesters/prior to week 28 of pregnancy. Recall: opioid/narcotic use isn't safe, but occasionally allowed for preg. if benefits outweigh risks. (3b) Ibuprofen and Naproxen [NSAIDs]: Both Pregnancy Category B* only dispensed up to 48-72hours. (3c) Pregnancy Category B Acetaminophen is the safest nonopioid analgesic.
HEAD AND NECK ABSCESSES - KNOW: LOCATION, SYMPTOMS, AND CLINICAL DIAGNOSIS (review). (A)Peritonsilar/Parotid/Parapharyngeal & Submandibular Abscesses 2) Acute Bacterial Perotitis 3) Submental & Submandibular Abscesses 4) Parapharyngeal or Lateral Pharyngeal or Pharyngomaxillary Space Abscesses (all the same) / Infection (B) Pterygopalatine, Infratemporal, and Temporal Fossa Infections (5) Retropharyngeal Abscesses
(A) = SORE THROAT and TRISMUS (inability to open jaw) ....or worse (secondary) "I can't talk or eat, or breathe".... DYSPHAGIA & ODYNOPHAGIA (inflam of cricoaretenoid); DYSPHONIA & HOARSENESS (CN10); UNILATERAL TONGUE PARESIS (CN12); STRIDOR & DYSPNEA = physical findings: face/neck swelling, erythema, and purulent oral discharge. There may be pooling of saliva in the mouth and asymmetry of the oropharynx. Adenopathy is usually present. Fluctuation is not easily appreciated, because of the dense fascial structures. Characteristic signs of deep pus are pitting or a doughy feeling on firm deep palpation. (2) PAIN, SWELLING OF PAROTID GLAND and DYSPHAGIA. In elderly, dehydrated, intubated, or post-op people; salivary stasis -> retrograde seeding of parotid duct with virulent oral flora; risk factors = recent vigorous TEETH cleaning, use of anticholinergic drugs, and salivary calculi. Pus can be expressed from Stensen's duct, and it should be cultured and Gram stained. An abscess may be present. Hydration, and antibiotics directly against staphylococci and the mouth flora are used. (3a) Submandibular abscesses usually due to an infected submandibular lymph node or salivary gland. Fluctuation is easily appreciated here, as there is no overlying musculature and the fascia is not dense. (3b) Submental abscesses usually result from the spread of an apical abscess of the LOWER INCISORS through the thin buccolabial acrolar plate and below the myelohyoid diaphragm, or from suppuration of a submental lymph node. - Some elevation of the floor of the mouth may be seen, but the exuberant swelling of Ludwig's angina is not present. - Palpate to see infectted salivary gland or lymphnode; abscess down low under mandible. This is not ludwigs angina (similar presentation). (4) *Located in the upper neck, above the hyoid bone, between the pretracheal fascia of the visceral compartment medially and the superficial fascia, which invest the parotid gland, internal pterygoid muscle, and mandible laterally*. Its shape is an INVERTED CONE, with its BASE BOUNDED BY THE SKULL AND THE APEX DIRECTED DOWN TOWARD THE HYOID BONE. The *carotid sheath*, which runs in the posterior part of the parapharyngeal space, pierces the cone at its upside down apex to enter the mediastinum. Communicates with retropharyngeal space. = usu. a COMPLICATION OF PERITONSILLAR ABSCESS. Also spread of infections from PAROTID GLAND, DENTAL ROOTS, PETROUS PYRAMID, or AFTER DENTAL OR PHARYNGEAL SURGERY. Before antibiotics were available, half of all neck infections occurred in this space, usually as a complication of infection in the tonsils and pharynx. (4I) The TRIAD of: tonsillar prolapse with swelling of the lateral pharyngeal wall. trismus, and parotid swelling... Indicates an ABSCESS IN THE PARAPHARYNGEAL SPACE. Abscess can extend into the carotid sheath. Erosion of internal carotid artery leads to STROKES AND FATAL HEMORRHAGE. THROMBOPHLEBITIS of the internal jugular vein with intracranial extension of clot also occurs. Inferior extension to the pyriform sinus OBSTRUCTS THE UPPER AIRWAY, and MEDIASTINITIS occurs after extension from the retropharyngeal space or carotid sheath. (B) (side head, in front of ear @ eye level) The pterygopalatinate fossa is behind the maxillary antrum and below the orbital apex. It contains the maxillary nerve and branches, the sphenopalatine ganglion, and the internal maxillary artery and branches. The abducens nerve, the inferior branch of the oculomotor nerve, and the maxillary nerves are close by, and can be involved during infections of the maxillary and sphenoid sinuses.- Infections here usually ARISE AFTER EXTRACTION OF A MAXILLARY MOLAR TOOTH or after LOCAL ANESTHESIA OF THE SUPERIOR ALVEOLAR NERVE. A fulminant cellulitis develops, involving (in order) the upper molar gingiva, the pterygopalatine, infratemporal, and temporal fossae, and then abscess formation in these spaces ensues. - Clinical history: PAINFUL SWELLING OF THE MAXILLARY GINGIVA that SPREADS TO INVOLVE THE CHEEK. It INVOLVES THE ENTIRE SIDE OF THE HEAD, INCLUDING THE NOSE, EAR, AND THE UPPER NECK. PROPTOSIS OF THE EYE results from extension of pus and infection INTO THE ORBIT through the inferior orbital fissure. VISION IS LOST due to optic neuritis. Surgical drainage of the pterygopalatine abscess and any orbital abscess is mandatory, as are antibiotics. (5) DANGER SPACE {common spread from head/neck (oropharynx) to mediastinum} LYMPHATIC SPREAD OF INFECTN in PHARYNX or SINUSES to RETROPHARYNGEAL LYMPH NODES. Abscess in children is common, in adults is bc of ACCIDENTAL PERFORATION (lolipops, fishbones, toothpick). Infections are POLYMICROBIAL. - Classical presentation is: CHILLS AND FEVER AFTER PHARYNGITIS, problems swallowing and breathing; NECK HYPER EXTENDED (prsn trying to releive the pressure) - do dx. with LATERAL NECK RADIOGRAPH and see thickened pre-vertebral/tracheal space. Complications = Rupture of abscess can lead to ASPIRATION of the PUS INTO the LUNGS, PNEUMONIA & EMPYEMA (infection btwn the pleura); an abscess in danger space btwn alar and prevertebral facias may drain to mediastinum causing MEDIASTINITIS; INVOLVEMENT OF MAJOR BV's (suggested by hemorrage) and PHLEBITIS or THROMBOSIS of the IJV can occur. These are often/usually lethal!
Clinical application of Steroids Rx (not from review)
*20 mg* Cortisol is released in a normal healthy patient daily *between 2-8am*. 20 mg Cortisol = *5 mg Prednisone = 20 mg Hydrocortisone* Na+ Succinate. {RED}. Maximum endogenous Cortisol *release = 100-160 mg = 25-40* mg Prednisone {RED}. Prednisone potency is *4 times* that of Hydrocortisone (Solu-Cortef) {RED}. Max. Steroids *for stress* = 25-40 mg* Prednisone PO or 100-160 mg Hydrocortisone PO/IV {RED}. *The endogenous secretion by a normal gland is increased with:* Intense fear, fever, infection, inflammation, trauma or bleeding. Protocol for Patients on Daily Steroids: - For PLANNED surgical procedures, Use a step-up and step-down intake Start dose increase 48 hours pre op. Reach baseline intake 48 hours post op. see picture. *Steroid Protocol for Emergency Dental Surgery* = ONE hour prior to surgery give: 25-40 mg Prednisone, PO/IV/IM ... or ... 100-160mg Hydrocortisone Sodium Succinate (Solu-Cortef) PO/IV. *Typically Prednisone PO is given for step-down over 48 hours, post operatively.* Alternate Day Steroid Intake = Alternate day steroid use causes less inhibition of endogenous steroid secretion. *Schedule surgery on the day of steroid intake. * Frequently you may just need to *DOUBLE* the routine dose. see picture w step up step down. Steroid Boost for Mild/Moderate Stress = (a) *Mild stress* - *Example: 4 or less* extractions or *one quadrant* flap surgery -> Double the steroid dose if patient is currently on steroids.... Or Give *25 mg Hydrocortisone PO/IV or 6.25 mg (6.0 mg rounded)* Prednisone PO, 1 hour prior to surgery if the patient is not currently on steroids; 5 mg Prednisone will also suffice. (b) *Moderate stress* - *Example: 5-16* extractions or *2 quadrants* flap surgery. Prescribe *50-75 mg Hydrocortisone PO/IV or 12.5-18.75 mg* (15-20 mg rounded). Prednisone PO, 1 hour prior to surgery. Steroid Boost for Severe Stress: *Severe Stress Example* - 17 or more extractions or 3 or more quadrants flap surgery -> Prescribe *100-160 mg Hydrocortisone PO/IV or 25-37.5 mg*, (round off to 25-40 mg) Prednisone PO, 1 hour prior to surgery. Best to err by giving more steroids than giving less when needed. Always consult with the patient's MD to determine the amount of steroid boost needed for major dental surgery.
Acute Adrenal Insufficiency - clinical features, vital signs, and treatment? ID 2/23
*Clinical Features*: Extreme fatigue & Muscle cramps; Mental confusion; Nausea, Vomiting, abdominal pain. *Vital Signs:* Rapid thready pulse; Rapidly falling BP; Respiration slow and shallow. *Treatment:* Supine position & Maintain ABCs; Call EMS; Give 5% glucose IV; Give Solu-Cortef and by BVM: 15L/min O2. my notes: - Lacking in steroid. If don't compensate/ recognize problem -> won't give that as replacement therapy -> detrimental situation. - Brain needs carbs for functioning. Acute adrenal insufficiency is when brain is without carbs. - Mineralcorticoids and glucocorticoids maintain the blood pressure, BP sinking. ...Patient collapses. - Give 5% gluco's IV -> need to go in right away to brain. Replacement therapy.
Abscesses of the head and neck (review)
- "interfascial spaces" are potential areas in which abscesses can sit, and the fascia are borders for infections. - Submandibular, parotid, parapharyngeal, temporal fossa, retropharyngeal. - Ludwig's angina is not an abscess, is cellulitis.
Fixed-Dose Combinations of Analgesic Drugs, according to Cochrane Review, produce.... what type of efficacy? Analgesics are used to relieve what type of pain? ID 2/23 red (not from review)
- Analgesic efficacy of single dose oral analgesics & fast acting formulations. - SIMPLE FIXED DOSE COMBINATIONS of DRUGS PRODUCE GOOD, LONG-LASTING ANALGESIA AT RELATIVELY LOW DOSES. - Acute postoperative pain is a manifestation of inflammation due to tissue injury. - MANAGEMENT OF POST-OPERATIVE PAIN & INFLAMMATION IS CRITICAL COMPONENT OF PATIENT CARE. Analgesics used for relief of postoperative pain include: (1) "MILD" OR STEP 1 ANALGESICS = ACETAMINOPHEN & NSAIDS (Ibuprofen and Celecoxib) - NSAIDS [except *aspirin* special bc *irreversibly* blocks Cox-1] inhibit production of prostaglandins (and thromboxane A2) and prostaglandins mediate: maintenance of GASTRIC mucosal barrier, regulation of RENAL blood flow, regulation of ENDOTHELIAL TONE, INFLAMMATORY & NOCICEPTIVE (PAIN) process role. (2) "MODERATE" or STEP 2 ANALGESICS = weaker opioids e.g. CODEINE. (3) "STRONG" or STEP 3 ANALGESICS = strong opioids e.g. OXYCODONE & FENTANYL. - OPIOIDS CAUSE adverse effects: DROWSINESS & RESPIRATORY DEPRESSION; binding prim. to GI receptors causing NAUSEA, VOMITING, CONSTIPATION. But, *dec side effects* when opioids combination w. Tylenol (non-opiod) bc in this formula, there's dec. opioid dose used. & when you use LOWER DOSES OF DRUG -> GENERATES good analgesia. Drugs with LONGER EFFECTS are likely to be MORE USEFUL and EFFECTIVE in clinical practice, compared to drugs w. shorter duration of action. SIMPLE DRUG COMBINATIONS and FAST ACTING FORMULATIONS can DELIVER GOOD ANALGESIA in many patients with ACUTE PAIN at relatively low doses.
Syphilis (STD) (review)
- Caused by Treponema pallidum, a spirochete that has never been cultured. - Primary (localized disease) => Secondary (systemic) => Tertiary (long-term inflammation of the CNS, aorta, brain, skin, spine, eye...). - Congenital (systemic, chronic inflammation). - Those with syphilis often have HIV, other STDs. - Diagnosis and treatment at different stages. "SCREWDRIVER" SHAPED INCISORS WITH NOTCHING (HUTCHINSON'S TEETH); A "MULBERRY" MOLAR.
Human papilloma virus (review)
- Cutaneous and ano-genital warts and cervical cancer. - Respiratory pap - death by suffocation - during vaginal delivery, infant's oropharynx infected. - Subunit vaccine is available against SOME HPV strains.
How can DNA-damaging antibiotics induce the ____ response, causing exacerbation of disease symptoms in pathogenic lysogens? Fix after review - needa know this?
- E. Coli outbreak of 1998 in undercooked burgers; many deaths from hemolytic uremic syndrome (HUS). - Transcription mechanism: DNA Damage -> Activated RecA (host) protein -> phage repressor undergoes autoproteolysis -> prophage induced (Q protein now expressed which is the transcription anti-terminator => lysis). (1) Plate = regulatory region of phage carrying Shiga-Like toxin {fix - google what this is}. (2) Q protein {recall only expersed after prophage induced in} enhances expression of stx A and B {= toxin genes}. (3) Ciproflaxin antibiotic treatment is stx phage inducer, causes bacteriolysis and release of toxin, resulting in increased risk of hemolytic-uremic syndrome in children w. E. Coli (strain O157:H7).
Multimodal Analgesia (MMA) - what is it most imp. for? Indicated uses (timing..)? What type of pain relief / mech of doing this? Differences btwn management moderate - - > severe post-op pain? 2/23 ID red caps; *bold* (not from review)
- Multimodal analgesia is the 'STANDARD OF CARE' for preventing pain following procedures. - MMA IS "PERI-OPERATIVE" ANALGESIA (Analgesia before, during & after procedures). It is safe, effective, with minimal side-effects & is easily managed by patient once home. - Achieves acute & chronic pain relief by TARGETS PAIN TRANSMISSION AT multiple levels using analgesics and/or adjuvants, IN COMBINATION. - Combination of PREVENTIVE centrally & peripherally acting OPIOID & NON-OPIOIDS are used in AROUND-THE-CLOCK (ATC) DOSING. - * "PREVENTIVE" ANALGESIC regimen is started IN PRE OR EARLY POSTOP PERIOD & continued for ~3-5 days* dependent on the extent of the procedure (nothing given for more than 7 days it's the law for acute opioids!) (2) Stepwise Multimodal Acute Post-op Analgesia Algorithm: - *Best* to provide the analgesic(s) *prior* to surgery *Next best*: intra-operative or prior to loss of anesthesia. (a) *Mild to Moderate Postoperative Pain:* NON-OPIOIDS +/- ADJUVANTS W. "PRN" SHORT-ACTING OPIOID {PERCOCET OR CODEINE OR VICODIN OR TRAMADOL} - she said to note that this is PRN only dosing, so your adding percocet or codeine or vicodin. (c) *Moderate to Severe Postoperative Pain*: - *Stop* the short acting opioid. - TO THE NON-OPIOIDS +/- ADJUVANT, now ADD AN IMMEDIATE ACTING STRONGER OPIOID {IMMEDIATE RELEASE (IR) OXYCODONE OR METHADONE OR FENTANYL OR LOW DOSE MORPHINE THE OPIOID} GIVEN ATC / PRN. (d) *Severe Postoperative Pain*: - Stop the immediate release opioid. - *To the non-opioids +/- adjuvant ADD a long-acting or sustained-released opioid {sustained release (SR) oxycodone* OR *morphine* OR *fentanyl*} GIVEN ATC (around the clock) - SHE SAID TO NOTE: NOT PRN DOSE ANYMORE, BUT NOW ATC.
Gonorrhea (STD) (review)
- Neisseria gonorrhoeae, a gram negative diplococcus on Gram stain which infects mucus-secreting epithelial cells. > 95% OF MEN SYMPTOMATIC; OFTEN NO SYMPTOMS IN WOMEN (but can get PID and ectopic pregnancy). Pelvic inflammatory disease with abscesses, subsequent ectopic pregnancies or sterility in women. Gonorrheal PHARYNGITIS = SORE THROAT W. NEG STREP TEST AND SEXUALLY ACTIVE PERSON.
Chlamydiae (STD) (review)
- Strict intracellular bacteria, genome small; cannot generate ATP; has no oxidative enzymes, flavoproteins or cytochromes; can make own proteins. - Two unique stages: (1) RETICULATE BODY stage [ACTIVE METABOLISM, only stage that responds to ANTIBIOTICS] and (2) Elementary body (transit form that goes from one cell to another). - Most common cause of urethritis and cervicitis in the US.
Actinomycosis
1) *Actinomyces* bacteria = oral and gut microiota; gram positive bacilli; faculative or obligate anaerobe; grow in chains and appear similar to fungi; slow-growing in culture = associated w. *periodontitis and caries* = polymicrobial infections. 2) *Pulmonary Actinomyocosis = "rare infection of lung" Lower Respiratory Tract Infection (LRI)*. Symptoms = chest pain, cough, fever, lethargic, night sweats, shortness breath, weight loss; infection develops slowly usu. Risk factors = *POOR DENTAL HYGIENE*, *DENTAL ABSCESS*; Alcohol abuse, emphysema, scars on lung. Tx = IV antibiotics 4-6 weeks. 3) *cervicofacial actinomycosis* (lumpy jaw) = *MOST COMMON FORM ACTINOMYCOSIS*. *POOR DENTAL HYGIENE AND DENTAL ABSCESS* are risk factors. 4) Other forms of Actinomyocosis: Abdominal actinomycosis (surgery or trauma); Pelvic actinomycosis (intrautarine devices), Brain Abscess (spread from other infected site).
"COMPLEMENT DEFICIENCIES" 1) Absence of C1q, C2, or C4 2) Absence C3 3) Absence C5 4) Absence C6, C7, OR C8 5) Absence alternative pathway components. 6) Absence Lectin pathway components 7) Absence/Deficiency/Dysfunction of C1-INH
1) Associated with SLE. 2) Severe recurrent bacterial infections. 3) Bacterial infections 4) Overwhelming Neisserial Infections e.g. N. Meningitidis and N. Gonorrhea [to control gonorrhea, you need C6, C7, or C8]. 5) RECURRENT BACTERIAL INFECTIONS [but still have classic pathway, so not as bad as person lacking C3] [recall: alternative pathway comoponents = C3b (from natural breakdown C3), Factor B, Factor D, Properidin (together generate C3bBbP that splits C3 into C3a and C3b and continues the complement cascade). Factor H and Factor I are inhibitors of alternative pathway and regulate activation of the system]. 6) Infection in Childhood [recall: lectin pathway components = MBL, MASP1, MASP2] 7) Hereditary Angeioedema = rare autosomal dominant genetic disorder resulting from inherited deficiency or dysfunction of the C1 inhibitor. Characterized by recurrent episodes of angioedema, without urticaria (hives) or pruritus (itching), which most often affect the skin, as well as mucosal tissues of upper resp. and GI tracts. Although the swelling is self-limited, laryngeal involvement may cause fatal asphyxiation.
Dermis - layers and whats found in each layer (sensory structure, cell types)? (review)
1) PAPILLARY LAYER = sensory structures (MEISSNER CORPSUCLES) & capillaries (for thermal regulation) 2) RETICULAR LAYER [thickest, contains most adnexa] = hair follicles w arrector pili muscles (thin skin only, bc thick skin doesn't have hairs); sweat glands (everywhere; secretory portions may extend to hypodermis); Sebaceous glands (thin skin only bc thick doesnt have hair); Apocrine Sweat Glands (specialized locations); and sensory structures are PACINIAN CORPUSCLES {may also be in hypodermis}
List of FACTORS INFLUENCING REPAIR (tissue repair?)? know path 2/22 all
1. Infection 2. Nutrition 3. Glucocorticoids 4. Mechanical variables 5. Poor perfusion 6. Foreign bodies 7. Type and Extend of tissue injury 8. Location of injury 9. Keloids = PROMINENT RAISED SCARS RESULTING FROM EXCESS PRODUCTION OF EXTRACELLULAR MATRIX (KNOW).
What are the two types of phages? Examples of each? (review)
1. Lytic / Virulent Phage = T4 Phage consisting of HEAD W. DNA, tail, base plate w. spikes = ALWAYS undergo the lytic (release) growth pattern - stages: KNOW: PHAGE ABSORB TO SPECIFIC RECEPTORS {E. Coli proin protein is receptor for T4 phage} ON BACTERIA CELL SURFACE (attachment, and membrane fusion); FROM REVIEW, KNOW STAGES OF LYTIC GROWTH CYCLE: 1 Absorption, 2 Penetration {injection, membrane fusion}, 3 gene Expression, 4 Nucleic Acid Replication, 5 Synthesis structural Proteins, 6 assembly virions, 7. Lysis / Release. 2. Lysogenic Phage /Temperate phage = Bacteriophage Lambda = Can undergo EITHER lytic or lysogenic existence(/growth mechanisms) [know all this, review] - Favor LYTIC growth when infecting bacteria growing in RICHmedium; Favor LYSOGENIC existance when infecting bacteria growing POORly. EXAMPLES: 2a) - Vibrio Cholerae is a lysogen = Cholera toxin is encoded by genes located on the ctx (pro)phage. Lysogeny = expression of BOTH phage repressor and ctx toxin genes. 2b) Bacterophage LAMBDA - know transcription regulation: (i) Lysis occurs if = Rich medium -> high levels of bacterial protease -> All of CII is degraded -> No repressor (CI) is made -> Q protein (transcriptional anti-terminator (another one is N protein) transcribed in lytic cycle) accumulates -> Lysis. (ii) Lysogeny = poor medium -> low lsvels of protease. Enough CII is spread to activate transcription resulting in High levels of CI repressor {not transcribed in lytic cycle; is expressed by Prophage that is made when Integrase (Int. Protein) integrates bacteriophage gene into E. Coli Chromsome. (lysogeny is repressor of lytic growth). (iii) Key Players to know defns of: - N and Q = Transcriptional anti-terminators. - Cl protein is the repressor of Lytic growth and Cl gene is only gene NOT transcribed in the lytic cycle. Repressor protein is only one expressed by the prophage - lysogen is immune to any other lambda "infection." (LYSOGENY = repression of Lytic Growth). Int protein "Integrase" required for integration of bacteriophage gene into E. Coli chromsome, to create a "Prophage" w chromsome of lambda lysogen
What are three things that are major side effects of prolonged use of corticosteroids for dentists? (in red must know pharm 2/23) (not from review)
1. SUPPRESSION OF PITUITARY ADRENAL AXIS (acute adrenal insufficiency) s.t. patients unable to normally respond to stress of dental procedure and may need extra (double or triple) doses of steroid before and after surgical procedures (dose then tapered down over sev. days to normal maintenance dose). Need therapy supplementsto prevent acute adrenal insufficiency crisis and recovery of normal adrenal function can take up to 1 year after cessation of therapy. is NOT a PROB IF use is restricted to 1-2 weeks. Systemic Prednisone is a corticosteroid. 2. IMMUNOSUPPRESSION so patients may have INC. SUSCEPTIBILITY TO INFECTION. so if ur planning dental surgical procedure, u might needa give antibiotics to patients on long-term steroids (minor or superficial infections may become systemic; quiescent infections may become active) - don't use in patients w. latent tuberculosis (use is contraindicated), also dont use in tx herpes. 3. SUPPRESSION OF BENEFICIAL INFLAMMATORY PROCESSES - patients will show slow healing of wounds (inflammatory imp for efficient healing of wounds and tissue injury) so you need to manage/monitor them after oral surgery. Also careful bc dec. inflam. response could mask some early symptoms of disease and interfere w making proper diagnosis. Asthma tx can use corticosteroid- containing inhalers, but bad bc using these types has been associated with increased occurrence of oral Candida related problems.
Define Comlement. (1) Classic Complement System is activated by? (2) Alternative complement pathway activated by? (3) Lectin Pathway activated by? (not from review but know it)
= series of proteins working in cascading manner, to generate imp. host defense mechanisms. Three different pathways of complement activation: 1) Classical 2) alternative 3) Mannan binding ligand (MBL). (1) Classical Complement System is activated by Ag-Ab complexes (ANTIGEN BINDING ANTIBODY). - C1q, C1r, and C1s bind to complement binding site on Fc portion of antibody molecule. Complex of C1q, C1r and C1s is called "Activated C1." - "Activated C1" splits C4 into C4a and C4b. - C4b sticks to the activated C1 and this complex is called "C14b complex" - C14b splits C2 into C2a and C2b; C14b2b splits C3 into C3a and C3b. - The complex of "C14b2b3b" splits C5 into C5a and C5b. - C6, C7, C8 and C9 bind to C5b forming the "membrane attack complex (MAC)." (2) Activated by BACTERIAL OR VIRAL PRODUCTS e.g. Lipopolysaccaride {LPS} (of outer leaflet of outer membrane). (3) Lectin path activated by ORGANISMS W MANNOSE ON THEIR SURFACE.
10) Which cell type is NOT found in the epidermis? a) myoepithelial b) Langerhans c) Merkel d) melanocyte e) keratinocyte
A
Adjuvant - exampl of one (found in what)? (review)
A substance that, when administered with an antigen (vaccine), Increases its immunogenicity. Adjuvants provoke local inflammation, Drawing immune system cells to the site and *triggering the maturation of dendritic cells.* Many vaccines include ALUM (aluminum salts) as an adjuvant. Yields a STRONGER RESPONSE. FUNCTION = ACTIVATING DCs BY STIMULATING PRR PATHWAYS = basically turns on immature DC via PRR (innate immune, dc's sense there's an infection) into mature DC that'll then express B7 and go to lymph node (B7-B28) = and this is the innate system telling Adaptive system that theres and infection..."An Innate Immune Response is needed to Initiate and Adaptive Response."
Chronic Inflammation vs. Acute Inflammation - onset? inflammatory cell infiltrate? tissue injury/fibrosis? local/systemic signs? Type of immunity? (review)
ACUTE = minutes-hours; mostly Neutrophils [eosinophils, basophils]; tissue injury/fibrosis is Mild/Self-Limited; Prominent local/systemic signs = INNATE IMMUNITY CHRONIC = days; monocytes/macrophages and lymphocytes [and plasma cells]; tissue injury/fibrosis is Severe/Progressive [is often w. fibrosis]; Less Prominent (Often Subtle) local/systemic signs = ADAPTIVE IMMUNITY = Mediated by cytokines produced by lymphocytes (especially T cells) and macrophages.
C1-INHIBITOR (C1-INH)
AN INHIBITOR OF THE CLASSICAL COMPLEMENT PATHWAY. Recall: Absence of it results in Hereditary angioedema.
Analgesics & Anemia ID 2/23
AVOID ALL NSAIDS FOR PAIN CONTROL *due to inc. bleeding risk &* WORSENING OF ANY ANEMIA. Aspirin & NSAIDs cause platelet dysfunction, gastric erosion & acidosis. All NSAIDs are acidic drugs: They all cause hemolysis in the congenital types of anemia. *SAFE Analgesics* = (i) Regular strength (RS) Tylenol; (ii) Oxycodone/Codeine/Hydrocodone with Tylenol. *Analgesics for G6PD* = (i) Use Codeine Phosphate *or* OxyContin WITHOUT Tylenol or Tramadol; (ii) *Use Codeine Phosphate*: 15-60 mg/dose q4-6 h: *Typically 30mg q4-6h*; (iii) *Oxycodone (OxyContin)* is dosed at 20mg oral, q8-12h: ONLY GIVEN IF ALREADY IN USE; (iv) *Tramadol (Ultram), 25-50 mg q6h PRN* can be prescribed SHORT-TERM if a *non- narcotic analgesic* is needed: Tramadol is now a Schedule *IV drug*.
Classification of Adrenocorticosteroids - Differences in potency (numbers)?
According to duration of action: 1) short-acting: hydrocortisone, cortisone. 2) intermediate-acting: prednisone, triamclinolone, methylprednisone. 3) Long-acting: dexamethasone, betamethasone. According to activity (can also be classified this way): 1) w. BOTH gluco- and mineral-corticoid activity: hydrocortisone and cortisone. 2) WITHOUT mineralcorticoid activity: prednisone and dexmethasone. Corticosteroids (systemic) Differ in Potency: 1. Dexamethasone - long-acting activity - 25 potency. 2. Prednisone - Intermediate Acting - 4 potency. 3. Methylprednisolone - intermediate acting - 5 potency. 6. Hydrocortisone - short-acting - 1.0 potency.
What lab value would you select in order to determine the status of patient's renal system? A. GFR B. LFT C. CBC D. All of the above
Answer = A. Renal status measured by = serum creatine level and GFR. - As kidney function *decreases*, the serum creatinine *levels rise* - DIET, MUSCLE MASS, OLD AGE CAN ALSO AFFECT SERUM CR. VALUE. (it wont rise as much if diet poor, etc.) - *always estimate renal function by GFR * - CHRONIC ELEVATION OF S. CR OF 2.0 MG/DL *indicates moderate to severe decrease in GFR* - GFR IS USED TO DETERMINE THE SEVERITY OF KIDNEY DISEASE. - chronic chronic kidney disease (compromised renal status) = GFR less than 60 for 3 MONTHS. (GFR more than 60 means healthy) - know:*ALWAYS help prevent progression of kidney disease by using appropriate AAAAAs {Anasthetics, Analgesics, Antibiotics, Antivirals Antifungals = "the five A's"}* - Insist patient *control the associated diseases* like hypertension and/or diabetes . - These conditions commonly cause chronic kidney disease (CKD).
4) Which of the following statements is INCORRECT regarding melanocytes? a) they are derived from neural crest b) their numbers differ between races c) they synthesize tyrosinase d) they are located superficial to the epithelial basal lamina e) they pass melanosomes t keratinocytes by "pigment donation"
Answer = B. their numbers are consistent between races!
11) Which of the following pairs DO NOT fit together: a) melanocyte - stratum basale b) myoepithelial cell - sweat gland c) apocrine sweat gland duct - hair follicle d) hair follicle - hypodermis e) tyrosinase - keratohyalin granule
Answer: E - tyrosinase is made by melanocyte. Statum granulosum - keratohyalin.
Asthma: Link with NSAIDs &/or Opioids
Asthmatics *are at higher risk* for experiencing *serious allergic reactions to NSAIDs*. NSAID USE IS NOT CONTRAINDICATED IF PAST USE HAS NOT PRECIPITATED AN ALLERGIC REACTION OR AN ASTHMA ATTACK *Drugs that can frequently precipitate allergies and/or precipitate Asthma attacks* = Aspirin; Indocin, ibuprofen, Anaprox; Codeine; Morphine; Penicillin. -> So always clarify before use. Use these drugs only if they have caused no reactions & no DDIs with med(s)
When a phage undergoes the lysogenic cycle: A. it must excise from the chromosome. B. it must integrate its genome into the host chromosome to maintain its genes in the bacterial population. C. it must integrate its DNA into the chromosome in order to express the repressor protein. D. it need not integrate its DNA. E. it must express the genes for capsids and tails. (review)
B (phage integrate genome to host chrom to maintain its genes in bacterial population = definition of lysogenic cycle). Not C b/c even though does express repressor, its not...
You are asked to fit a 15-year old adolescent boy with orthodontic bands and note that two of the boy's molars have a central crown, and that two of the central incisors have a V-shaped defect. What do you suspect? A. Tertiary syphilis B. Congenital syphilis C. Congenital gonorrhea D. Oral injury E. That he is really an alien creature.
B - V-shaped defect central incisor is congenital syphallis.
30 female presents for tooth extraction. She is 12 weeks pregnany. After the extraction, she asks you what she should take for the pain? Which of the following drugs would you recommend? A. ibuprofen B. acetaminophen C. celebrex D. Aspirin E. none of the above star Based on previus patient scenerio, if patient fails to have pain alleviated by acetaminophen, what would be ur next choice for opioid analgesic? A. Vicodin B. Percocet C. codeine + tylenol D. codeine E. none of the above.
B. Acetaminophen (tylenol) is first choice liver, kidney, pregnancy. Not C because celebrex is cox-2 inhibitor = NO for pregnant. B. Percocet is first choice for an OPIOID for pregnancy (tylenol is first choice overall dont foreget). Know: next choice would be: Fentanyl or Geladid = liver, kidney failure, prgnancy ok in. Not A because vicodin is one of the least safe ones for pregnant, star search notes
Patients who are poor or rapid 2D6 metabolizers do not respond well to which opioid analgesic? A. Fentanyl B. Codeine C. Morphine D. Hydromorphone (Dilaudid) star
B. POOR or RAPID 2D6 METABOLIZERS do not respond well to Codeine => Codeine toxicity.
Single implant placement (minor). Surgery well, little trauma associated. Best analgesic to prescribe for your patient post-op? A) codeine 5 mg every 8 hours B) 200 mg ibuprofen (advil) and 400 mg acetaminogen every 8 hours. C) 200mg ibuprofen and 1000mg acetaminophen every 8 hours D) 200 mg ibuprofen and 500 mg acetaminophen and percocet (5/325) every 8 hours fix - star
B. bc we never start w codeine (never first choice as opioid); c is wrong bc dose for acetaminophen is high and usu wanna start w lower dose of advil and tylenol first to see if it works, and the purpose of giving both together is that u dont hae to give the full dose of both (usu ppl take 400mg advil or 1000 tylenol separate).
Statement 1: Phase 1 metabolisms are modification reactions, such as oxidation and hydrolysis, that occur in the liver. Statement 2: Phase 2 metabolism are predominately glururonidiation reactions, that are cleared by the kidney. Star
BOTH STATEMENTS TRUE. Statement 1 is true - DRUG METABOLISM in general OCCURS IN the Liver via 3 mechanisms: (1) PHASE I: *Oxidation, reduction or hydrolysis* involving hepatic CYP450 enzyme system. Statement 2 is false - (2) PHASE II: *Conjugation* to glucuronic acid/sulfate/acetate/glycine/glutathione/methyl group. (3) BILE: Biliary excretion & elimination {know if have drugs that need bile to remove drug out of system, but if there is a bile duct obstruction, then levels will build up in the patient eek}
Tissue Repair - BRAIN know path 2/22 (not from review)
BRAIN DAMAGE AND REPAIR IS UNIQE = NOT REPAIRED THRU PROLIFERATION OF FIBROBLASTS, BUT THRU PROLIF. OF BRAIN SUPPORT CELLS {ASTROCYTES}. NECROTIC TISSUE REPLACED BY FLUID. CYSTIC LESION SURROUNDED BY COMPACTED GLIAL FIBERS PRODUCED BY ASTROCYTES CALLED CLIAL SCAR {ASTROCYTE GLIOSIS}
Understand how respiratory pathogens can overcome host defenses
Bacteria mechanisms that can counteract host "defenses" = (1) Capsule (Streptococcus Pneumoniae), (2) Growth Within Macrophages (Legionella pneumophila), (3) attachment factors (biofilms - pseudomonas aeruginosa); (4) toxins
Bacteriophage structure? 2/24 ID
Bacteriophage Structure: (1, start w) Empty head = 1 major protein & 7 minor proteins. Add DNA, 10 Proteins (2) full head w. collar (3) spontaneously get Complete tail which was made from Base plate (15 proteins) + 3 proteins to make base plate & core/needle, +1 protein to add sheath, +3 proteins to complete tail. (4) Complete tail fibers (5 proteins) added (6) = Completed Bacteriophage = Head w. Collar, Tail (base plate, core/needle, sheath), & Tail fibers.
What are some general things you should be considering regarding corticosteroid use on ur patient?
Because of the wide ranging effects and potency of these drugs, it is virtually impossible to achieve clinical improvement w.o producing some adverse side effects. Thus, its desirable to limit use, when possible to: Emergency Situations, or to Short-Term Therapy at the Smallest effective Dose. Many instances of inflammation can be just as effectively treated using NSAIDS.
Temperate phages that encode virulence factors are likely to have acquired these genes by which of the following mechanisms? A. transformation B. conjugation C. misexcision D. misintegration E. transcription
C - misexcision is way temperate phages move virulence factors from cell to cell.
How long does it take for the irreversible effect that aspirin has on platelets to wash out? A. 24-48 hours B. 3-4 days C. 7-10 days D. 14-20 days star
C. = On one slide it says 10-4 days, sooo just know 10 days. Nsaids has irreversible effect on platelets; thus when have major surgery and theres a bleding risk, tell ur patietns to stop their aspirin about a week before.
Old man comes to clinic with abscess. HE gives you latest lab results along w note from PCP. CUrrently treated for chronic kidney failure. HIS LATEST S. CREATININE IS 14mg/dL (H). He says that multimodal analgesia previously prescribed has not been effective and is seeking more powerful pain medication. Which one of the following opioids would be the safest for this patient given his current medical history? A. codeine B. Tramadol C. Fentanyl D. Advil E. None of the above
C. FENTANYL & HYDROMORPHONE (DILUIDAD) - star fix search fentanyl bc need spelling. ARE the TWO OPIOIDS that r safe for people w. Kidney and Liver failure!!!! D, advil, is NOT safe bc / maybe worst u can give to the patient, since it is type of NSAID and NSAIDS inhibit prostaglandins, and prostaglandins directly inhibit renal profusion; thus, someone already undergoing kidney failure already doesnt have best kidney profusion so dont wanna add to that. = AKA: Advil (NSAID) + Kidney Failure = BAD => kidney profusion too much! - if a patient is explicitly seeking opioids, you should probably not give them opioids (has asked this on exams in past). - tylenol: best for pregnancy, okay for liver and kidney, nothing about clotting / cv disease / anything like that. Thus, if tylenol was an option here, that would be the first choice!!! know.
A patient comes to your office for an emergency visit. He has a hoarse voice and keeps his head tilted back. Swallowing seems difficult and unusually, he asks to spit into a cup. On the basis of this you suspect: A. Carotid involvement B. Mediastinitis C. Retropharyngeal abscess D. Submandibular abscess E. Tonsillar abscess
C. Hoarse voice, tilted head back, swallowing difficult => Retropharyngeal Abscess.
8) Which one of the following pairs is mismatched? a) merocrine secretion - eccrine gland b) apocrine glands - product storage c) holocrine glands - ducts reach epithelial surface d) apocrine glands - become active at puberty e) eccrine glands - myoepthelial cells f) holocrine glands - ~8 day turnover
C. Holocrine glands (like sebaceous glands) secrete into air shafts. All others are right.
A patient observes that she has had a sore throat for 2 weeks, and that multiple tests have been negative for streptococci. On exam, she has an erythematous pharynx and no discrete circular lesions. She is sexually active. Which of the following is the most likely explanation for this scenario? A. Strep throat due to Streptococcus pyogenes B. Oropharyngeal syphilis C. Oropharyngeal gonorrhea D. Oropharyngeal papillomavirus ("warts") E. Retropharyngeal abscess.
C. Sore throat w. neg strep test & no circular lesion & no warts => Oropharyngeal Gonorrhea.
Which drug has dose ceiling effect and is contraindicated in patients with biliary stasis? A, codeine B, methadone C. suboxone D. tramadol star and see notes
C. know SUBOXONE known for having Dose-Ceiling effect, and is contraindicated in patients w. biliary stasis. - biliary = gallbladder. - codeine: prodrug, 2d6 morphine gets converted. - methadone: heroine; methadone clinic. KNOW you would not be prescribing a patient on methadone (recovering addict) an opioid; but if ur gonna give them an opioid, you refer them back to the clinic and they can do it, but you yourself will not prescribe anything.
Important proteins in the Alternative Complement (activation) Pathway? Inhibitors of the pathway? know the names.
C3b (generated from natural breakdown of C3), FACTOR B, FACTOR D, PROPERIDIN => Together they generate "C3bBbP" that splits C3 into C3a and C3b and continues the complement cascade. FACTOR H AND FACTOR I are inhibitors of alt. pathway and regulate the activation of the system. recall: activated by bacterial or viral products e.g. lipoplysacc (LPS) on outer leaflet of outer membrane of bacteria.
TUBERCULOSIS is caused by*? Induces what type of immune response*? Histopathology hallmark*? Main site of infection*? What leads to military Tb, to Tb bronchopneumonia*? Can the disease come back*? *="key facts" Characterized by what? More severe in what patients? PRIMARY, SECONDARY, MILITARY Tb? Diagnosis? know path red 2/22 (not from review)
CAUSED BY MYOBACTERIUM TUBERCULOSIS. TYPE IV HYPERSENSITIVITY REACTION (i.e. induces type 4 hypersensitivity response), MORE SEVERE IN IMMUNOCOMPROMISED. HISTOPATHOLOGY HALLMARK IS CASSEATING GRANULOMAS {key fact} = CENTRAL CASEOUS NECROSIS SURROUNDED by bunch OF ACTIVATED EPITHELIOID HISTIOCYTES. MAIN SITE OF INFECTION IS IN LUNGS. VASCULAR SPREAD LEADS TO MILITARY TB. BRONCHIAL SPREAD LEADS TO TB BRONCHOPNEUMONIA. REACTIVATION OF DEASE IF HOST RESPONSE IS WEAKENED. (2) LANGHANS GIANT CELL = LG. MULTI-NUCLEATED CELLS SEEN IN GRANULOMATOUS DISEASES - MANY NUCLEI AROUND PERIPHERY AND LG. CENTRAL CYTOPLASMIC MASS. (i) PRIMARY TB = DISEASE IN UNSENSITIZED PATIENTS; BACTERIA INHALED AND PROLIFERATE; BACTERIAL ORGANISM NOT DESTROYED; GHON PRIMARY COMPLEX OF INFLAMMATION FORMS IN AREA OF SENSITIZATION, WITH DISSEMINATION TO LYMPH NODES; CAUSES DAMAGE TO ADJACENT LUNG (xray given in lecture presentation) ; FOCI OF SCARRING. (ii) SECONDARY TB = PATTERN OF DISEASE {5% OF PATIENTS} ARISING IN PREVIOUSLY SENSITIZED HOST. MAY FOLLOW SOON AFTER PRIMARY TB, BUT MORE COMMONLY AFTER REACTIVATION OF DORMANT ORGANISMS. CLASSICALLY LOCALIZED TO APICES (apex). (iii) MILITARY TB = ORGANISMS DISSEMINATE THRU VASCULAR SYSTEM TO HEART AND PULMONARY ARTERIES, LIVER, BONE MARROW, SPLEEN, AND OTHER ORGANS. DIAGNOSIS: (A) Mantoux or PPD Skin Test = DETECTS CELL-MEDIATED HYPERSENSITIVITY REACTION AT LEAST 2-4 WEEKS AFTER INTIAL EXPOSURE.
Most common cause of urethritis and cervicitis in the US? (review)
Chlamydiae
"Prolonged host response to persistent stimulus" is known as? (review)
Chronic Inflammation (adaptive immunity; Mediated by cytokines produced by lymphocytes (especially T cells) and macrophages). e.g. Periodontal Disease (periodontitis) is an inflammatory response DRIVEN by something, an antigen!
Which complement pathways are "Adaptive Immune Responses" and which are "Innate"? (review)
Classical Pathway = adaptive immune response bc involves Ab = IgM and IgG (know) are the antibodies that activate complement system and cleave C3, resulting in opsonization (c3b), anaphylaxis (), and MAC. But, "complement is an innate system" = alternative and lectin pathways which is good bc dont need to presensitize w. Ab.
Advantages of conjugated polysaccharide vaccines? What are they (doing)? (review)
Conjugate Vaccine (review) [Subunit Vaccine - Active Immunity] = Thymus independent (cant give T cell repsonse) polysach. turned INTO Thymus-Dependent antigen by basically making glycoproten (protein+polysach). = from review slide: "CONJUGATE VACCINE AGAINST THE BACTERIUM, Haemophilus Influenzae Type B (Hib) = vaccine consists of capsular polysaccharide of Hib CONJUGATED TO (linked) a protein antigen (tetanus toxoid). B cells specific for the polysach will internalize the conjugate. Peptides from the protein are presented to the B cell's MHC class 2. T helper cells specific for the protein portion of the conjugate activate the B cell via CD40/CD40L...Bc T helper cells provide a second signal, the B cell undergoes class switch, hypermutation, and strong memory cell generation." *Limitations of Polysach Vacines, Thymus Independent* = Primarily IgM (minimal class switching; no CD40-40L for instance and no T cell help); Poor responses for children under 2 years old; No memory response to subsequent immunizations. *Children under 2 years of age (where u need responses to strep pneumonia), don't response to thymus independent. So what scientists did is make conjugated vaccine....* *Advantages of Conjugated Polysaccharide Vaccines* = helper T cell = Good serum IgG response (Class switch recombination); Good immunologic memory; Strong response in young children. = *conjugate vaccines are*: Conjugate vaccine against specific bacteria; vaccine consists of the capsular polysaccharide of that bacteria conjugated (linked) to a protein antigen (such as tetanus toxoid). B cells specific for the polysaccharide will internalize the conjugate. Peptides from the protein are presented on the B cell's MHC class II. Th cells specific for the protein portion of the conjugate activate the B cell via CD40/CD40L. Because Th cells provide a second signal, the B cell undergoes class switch, hypermutation, and strong memory cell generation. Notes: fix and summarize hwile studying - B cell here is specific for the polysac (blue thing) - that's the B cell u wanna turn on. Since B cell are antigen presenting cell, when binds polysacarride w specificity, if you coupled protein with polysach, it'll take that antigen into the cell and when it takes polysach in itll also take protein in. Chops up all them -> foreign peptide from protein on conjugate -> recognized by CD4+T cells; and then get CD40-CD40L interaction to switch to thymus-dependent response - and then immunizing children many times with this conjugate vaccine, u give them lots of levels of IgG specific for polysach (boost each shot s.t. get more and more).
7) Which of the following statements is INCORRECT: a) sebaceous and apocrine glands typically empty their contents into hair follicles b) sweat glands secrete sodium c) sebaceous glands secrete sebum using a holocrine mechanism d) apocrine sweat glands are important for thermoregulation e) infection of sebaceous glands may produce acne
D - apocrine sweat glands are only in a few spots in body.
Adult female for 4 teeth extracted today in conjunction with her implant surgery. She has no contributory health problems. What would be the most effective ANALGESIC to prescribe her in order to help minimize her pain following her surgical procedures? A. advise patient to take 200mg Ibuprofen and 250mg Tylenol period to surgery. B. advise the patient to continue taking either Ibuprofen or Tylenol (or combination) around the clock every 6 hours post-surgery C. if pain persists post-op prescribe patient NSAIDs, Benzodiazepines along with Percocet as needed D. All of the above
D. *Severe Postoperative Pain*: - Stop the immediate release opioid. - Use Non-Opioid + either (long acting, sustained released opioid) oxycodone* OR *morphine* OR *fentanyl*} GIVEN ATC (around the clock) - SHE SAID TO NOTE: NOT PRN DOSE ANYMORE, BUT NOW ATC.
All of the following are relative contraindications for prescribing opioids EXCEPT? A. old age B. pregnancy (29 weeks) C. sleep apnea D. chronic constipation star and see notes
D. Know the contraindications for prescribing opioids. THere are some poeple that CANNOT have opioids. Pregnancy we dont prescribe opioids if we can help it but we can, 29 weeks is third trimester when cant prescribe... what about second and first trimesters?. Sleep apnea dont give opioids bc respiratory depression. CHronic constpiation (small bowel obstructions) - opiods cause rly bad constpiation like so bad sometimes we give them laxitives, thus dont combine the two. Old People can have opioids.
Medically complex patient, which category of drugs when prescribed along codeine would lead to increased avaliablity of morphine in the circulation, leading inevitably to respiratory arrest? A. antidepressants B. NSAIDs C. H2 blockers D. Anticonvulsants E. Antibiotics star and see notes on this
D. = Anticonvulsants are 2D6 INDUCERS, will lead to inc. morphine in blood -> respiratory arrest eventually.
Which of the following statements regarding prevention and treatment of STDs is FALSE? A. Erythromycin drops are administered to all neonates to prevent conjunctivitis due to potential maternal gonorrhea infection. B. Vaccine is currently available to prevent infections with certain types of HPV. C. Syphilis infections are typically treated with intramuscular injections of penicillin. D. Antibiotics currently used to treat chlamydia infections are active against the elementary body form of the bacterium.
D. Antibiotics for chlamidia are against reticulate body form.
56 male presents to ER w tooth infection. Past history of alcohol abuse and is currently cirrhotic. Analgesic BEST choice for this patient? A. Ibuprofen B. Aspirin C. Percocet D. Tylenol E. None of the above
D. Tylenol is first choice liver, kidney. Cirrhotic = Liver = NO nsaids {ibuprofen}. B is wrong bc if you see aspirin on test as something "I could prescribe", its probably not the answer. red flag. C percocet is not the best choice star fix why isnt it?
A temperate phage infects a host bacterium that is growing in a poor environment. Which of the following cycles does the phage enter and why? A. the lytic cycle to escape from the poorly growing host cell. B. the lytic cycle because that is the cycle that produces the most progeny phage. C. the lysogenic cycle because that is the cycle that produces the most progeny phage. D. the lysogenic cycle because the poor growth environment may not be adequate to support the production of even one progeny phage particle. E. neither the lytic nor the lysogenic cycle. (review)
D. note: u needa figure out what progeny phage particle she's referring to.
Macrophages - all red path 2/22 - role in chronic inflammation? - where would you find them? - derived from? - fusion of them forms what? - what does the "mononuclear phagocyte system (reticuloendothelial system) include? and what is it activated by? (not from review)
DOMINANT CELLS OF CHRONIC INFLAMMATION. "TISSUE" CELLS DRVED FROM "BLOOD" MONOCYTES. FUSION OF ACTIVATED MACROPHAGES FORMS MULTINUCLEATED GIANT CELLS. MONONUCLEAR PHAGOCYTE SYSTEM [RETICULOENDOTHELIAL SYSTEM] INCLUDES CELLS SCATTERED IN CT, LIVER (KUPFFER CELLS), SPLEEN AND LYMPH NODES (SINUS HISTIOCYTES), CNS (MICROGLIAL CELLS), AND LUNGS (ALVEOLAR MACROPHAGES). ACTIVATED BY EITHER: CLASSICAL (INDUCED BY MICROBIAL PRODUCTS, CYTOKINES, OR FOREGN MATERIAL), OR ALTERNATIVE {OTHER CYTOKINES OR OTHER CELLS INCLUDING MAST CELLS AND EOSINOPHILS) PATHWAYS.
Defense mechanisms of the respiratory tract include the following EXCEPT: A. Changes in direction of airflow B. Coughing reflex C. Alveolar macrophages D. Mucociliary escalator E. Tongue.
E (tongue is not a defense mech)
25 year old female coes to ur clinic for minor surgery. Tells u that she gets steroid shots (5mg prednisone) in her knee every week for past three years. WHich following would be a consideration for her dental treatment today? A. give patient morning appointments. B. work with PCP to double the dose of steroid on the day of surgery. C. consider prescribing benzodiazepines for stress management. D. all of the above. E. none of the above. star
E is the answer. - rule of 2 for steroids are for systemic steroids aka not in knee or in muscle or steroid inhaler. Since she gets shots in her knee, it doesnt get in her blood. But for systemic steroids, need to follow rule of two's = patient needs to be on steroids for two weeks or longer in the past two years. if patient takes steroids every day for one week in the past two years that doesn't qualify. - there is nothing wrong in giving someone extra steroid dose... but you cannot not give them enough bc thatll not be good for them. SO if we are planning major surgery yand following rule of twos, we will double on the day of surgery (so say they are taking 10, then take 20 on day of surgery.,, and then you need to wean them off with 'step down approach!" TO check - is it going in systemically, going in for two weeks or longer in past two years, major surgery (never do rule of twos for minor filing or cleaning bc thats not lot of stress/pain inflammation).
Which statement about abscess formation is FALSE? A. Usually there is local introduction of organisms. B. Abscesses usually involve endogenous organisms. C. Organisms may be introduced by trauma. D. Oxygen is present in the beginning of the process. E. Growth of organisms increases oxygenation and makes the affected site aerobic.
E. Growth of organisms does not Inc. oxygenation, it actually decreases oxygenation. Normal healthy tissue is well oxygenated.
Which of the following patients would be considered a medically complex patient? A. 24 year old female with history of Schizophrenia B. 58 year old male with history of hypertension treated with two medications C. 75 year old male patient with history of diabetes, hypertension and uncontrolled hypothyroidism D. All of the above E. A and C only. star
E. MCP is NOT patient who's already been treated! duh. Defintion MCP: Patient presenting with: - MULTIPLE CHRONIC ILLNESSES - Mental health concerns On MULTIPLE MEDICATIONS including ANTI-PSYCHOTIC MEDICATIONS ! - Often an OLDER patient Often WOMEN - Frequent CLINIC VISITS to MANY PROVIDERS. - More likely to MISS APPOINTMENTS & COMPLIANCE ISSUES. - Social and financial issues. Living in lower income neighborhoods. - PSYCHOSOCIAL BARRIERS TO MEDICAL CARE. KNOW, IN MEDICALLY COMPROMISED PATIENT, DO NOT USE MORE THAN 2g TYLENOL per day in divided doses. USING 1,000MG (1g) TYLENOL {ceiling effect}.= EXCEEDING THAT A LOT.
Extreme pain presentation from post-op extraction wisdom teeth. Also on prozac for depression. Prozac is 2d6 inhibitor. Which drug should u NOT prescribe to the patient, due to its innefectiveness in the presence of a 2D6 inhibitor? A) morphine B) codeine C) tramadol D) hydrocodone E) B, C, and D star
E. See 2D6 in question, immediately know you CANNOT prescribe three drugs: Codeine, Tramadol, Hydrocodone (has codeine). - You should know the list of pro-drugs (activated by 2D6 enzyme) these three are 2d6, whenever you see these three know that SSRI's will alter its effectiveness.
Granulomatous Disorders are due to? Example of one? know path 2/22 red caps and recognize rest. (not from review)
FOREIGN MATERIAL {ORGANIC OR INORGANIC} HAT CANNOT BE PHAGOCYTOSED BY NEUTROHPILES: - Endogenous (keratin, urate crystals, degenerated altered collagen, degerated altered elastin (artery walls)). - Exogenous (sutures, talcum powder, vegetable matter). example = SARCOIDOSIS (gran. disorder) = IDIOPATHIC multisystem DISORDER w. enlargement lungs and lymph nodes and can result in pulmonary fibrosis. Discrete granulomas w histiocytic giant cells mainly in lymph nodes, lungs, liver, spleen, and skin (rarely brain, bone).
Define Lysogenic Conversion?
Getting a new property (phenotype) from host bacterium due to a temperate phage came in and established a lysogeny.... Or... How temperate viruses can convert NONPATHOGENIC BACTERIA to PATHOGENIC BACTERIA.
Specific histiopathologic pattern of chronic inflammation? (review)
Granuloma= collection of MACROPHAGES ("epitheliod histocytes"); also usu. multinucleated giant cells, lymphocytes, fibroblasts, and/or CT; may/maynot exhibit caseous necrosis. (Granulomatous Inflammation: looks red bubble-like-boilyish inflammations.
Case: Episodes of abdominal pain since age of 14. On this occasion developed an attack of severe abdominal pain at the end of school. Pain was unbearable. No point tenderness on examination but an exploratory laparotomy was performed which revealed a moderately swollen and pale jejunum but no other abnormalities. His mother, a maternal uncle and his sister also had recurrent episodes of abdominal pain. When he was 7 years old a blow with a baseball bat caused his entire arm to swell to twice its size. Swelling was not painful and disappeared after 2 days.
Hereitary Angioedema (AD genetic disorder / inherited characterized by recurrent episodes of angioedema w/o hives or itching, affecting (swelling of) skin, upper respiratory, or GI tract)
Lymphocytosis is most often caused by? red path 2/22 in caps (not from review)
Increased number of lymphocytes in the peripheral blood. MOST OFTEN CAUSED BY VIRAL INFECTIONS: Influenza, mumps, rubella, infectious mononucleosis. Less common by certain bacterial infections (whooping cough, tuberculosis).
Codeine (opioid)
Indicated for mild to moderate pain. Good oral efficacy, but 1/12 analgesic potency due to ceiling effec - must be converted to morphine to produce analgesic effect. Side effects: Nausea, constipation of parent molecule limit dosing. Allergic reactions - opioids trigger histamine release leading to rash, pruritis -> substitute with another opioid not structurally related to codeine, e.g. propoxyphene or meperidine. is Cytochrome p540- 2D6 substrate. Most used in combination form in dentistry: (1) w. Aspirin: Empirin #2, #3, #4. (2) w. Acetaminophe: Tylenol #2, #3, #4. (3) Schedule II drug when used alone.
Long term use of Prednisone (review)
It problematic to use corticosteroids long-term => (1) HPA AXIS SUPPRESSION by SYSTEMIC PREDNISONE (bc no make of cortisol from adrenal to negative feedback on hypothalamus and pituitary); (2) since it's ANTI-INFLAMMATORY -> SLOWS WOUND HEALING; & (3) IMMUNE SYSTEM SUPPRESSED: INFECTIONS BY OPPORTUNISTIC MICROBES e.g. CANDIDA.
Analgesic ceiling of Acetaminophen (Tylenol)?
KNOW, IN MEDICALLY COMPROMISED PATIENT, DO NOT USE MORE THAN 2g TYLENOL per day in divided doses. USING 1,000MG (1g) TYLENOL {ceiling effect}.= EXCEEDING THAT A LOT.
Induction of Prophages involves?
Key: DNA damage results in prophage excising and becoming lytic. - prophages can escape from lysogenic state {poor medium -> low protease -> CII made, CI repressor made} through the SOS response, elicited by DNA DAMAGE. This is a Universal Mechanism evolved by Temperate Phage Repressors. (1) SOS (DNA repair) genes aren't expressed in general bc they are repressed by LexA protein. - LexA repressor protein does autoproteolysis when interacts with activated host RecA (activated once after it has picked up DNA/bacterial chromsome damage/DNA fragments that r result from DNA damage {i.e. UV light}) => allowing SOS genes to be transcribed = SOS response to DNA damage. - SOS Response impact on prophage: Similar to LexA repressor, phage repressors are triggered to self-destruct after interaction w activated host RecA protein. This results in phage gene transcription leading to prophage exclusion from the chromsome and initiation of lytic growth cycle.
(A) What are defense mechanisms of the respiratory tract? (B) What are the risk factors for respiratory diseases? (review)
Know - Although topologically open, the respiratory system is well protected 1) Nose - Nose hairs, nose turbinates (air currents), Nasal Mucus. 2) Throat and Bronchi - coughing reflex, *mucociliary escalator* (ME) {= of bronchi, bronchioles and nose actually. Has two parts: goblet cells that produce mucous, and cilliated epithelial cells creating upward flow. ME is major marrier against infection. The cilia are continually beating, pushing mucus up and out into the throat, and microorganisms are caught in the sticky mucous and moved up}. 3) Alveolar macrophages. (B) Anything that impairs defense mechanisms of respiratory tract is a *risk factor* know this. Smoking (not the nicotin, but rather the toxins in the smoke) - paralyzes the cilia of the *Mucociliary Escelator (ME)* that r supposed to be continuoulsy beating and pushing mucous up and out into throat, along with microorganisms that get caught in the sticky mucus and moved up. Dry Air; Pollutants; Allergens; Asthma.
Low dose aspirin and Ibuprofen DDI? Ibuprofen-Aspirin associated DDI & other NSAIDs ? ID 2/23
LOW DOSE ASPIRIN & IBUPROFEN -> DDI: - *Ibuprofen competes with Aspirin* for a *common binding site on COX-1* and PREVENTS ASPIRIN FROM BINDING. - Take Ibuprofen *8h prior* or *30 min-2 hours* after taking a regular/non enteric-coated low-dose Aspirin. FDA suggestions are *only for regular, immediate-release low-dose aspirin (81 mg).* The ability of Ibuprofen to interfere with the anti-clotting effects OF ENTERIC-COATED ASPIRIN OR LARGER DOSES OF ASPIRIN, such as an adult Aspirin (325 mg), is not known. - INHIBITORY EFFECT OF NAPROXEN ON PLATELET FUNCTION *is greater than that of Ibuprofen.* *Half-life of Naproxen is significantly longer than that of Ibuprofen.* IBUPROFEN-ASPIRIN ASSOCIATED DDI & OTHER NSAIDS: - *The Ibuprofen-Aspirin DDI is NOT seen with: Celecoxib (Celebrex), Diclofenac (Voltaren), Ketorolac (Toradol), Sulindac (Clinoril)* - THESE NSAIDS ARE TYPICALLY USED FOR CHRONIC OR MAJOR PAIN. Remember: In patients *with and without CVD MOST NSAIDS & CELECOXIB* are associated with *AN INCREASED RISK of adverse CV events.* - *When needed (and safe to use) the above NSAIDs are prescribed as follows*: *Sulindac (Clinoril)*: 150mg bid; *Diclofenac (Voltaren)* : 50mg bid/tid; * Celecoxib (Celebrex)* : 100/200mg OD/bid; * Ketorolac (Toradol)* : 10mg q4-6h, maximum dose: 40mg/day.
Case #2 In 1976, there was an American Legion convention in Philadelphia. Mysteriously, 182 participants in the convention became ill and 29 of them died. The organism responsible for the outbreak was initially difficult to culture but it was eventually grown in the laboratory and studied. The cause of these infections was a bacterium, Legionella pneumophila.
Legionella pneumophila colonizes plumbing systems: air conditioning units, hot tubs, hot water tanks and heaters, *DENTAL-UNIT WATER SYSTEMS.* - Replicates inside Amoeba (natural reservoir). - believed that Legionella contaminated the AC system, and people at the convention were inhaling organisms in aerosols from the AC. - There have been other outbreaks, e.g. Pontiac, Michigan state office building. - Encounter: ENVIRONMENTAL - contaminated WATER SYSTEMS. - Entry: inhalation. - Growth: INTRACELLULAR. - Survival Strategy: GROWS INSIDE MACROPHAGES - it does NOT have capsule to prevent phagocytosis. Thus, organism is taken up by macrophages but not killed!. - Damage: due to host inflammatory response. - Transmission: NO HUMAN-HUMAN transmission (humans are "dead-end" hosts).
In general, what are opiods and where do they act? Receptors? Is there a ceiling dose for analgesic effects? Why don't we like to use opioids trivially? (spent a lot of time on this pharm 2/23)
Moderate to severe pain management. Used in dentistry (primarily) in form of combination medications - exist in wide range of analgesic efficacies. Act on specific receptors, prim. in CNS. There's an "endogenous opiod" system that contributes to the effect, and may underlie the placebo analgesia effects. No dose or ceiling dose for analgesic effects. NAH TRIVIALLY BC: Lack anti-inflammatory effects; have bad side-effects like CNS depression (limits their use); Patients may be allergic or more sensitive to nausea; problematic bc drug seeking patients, abuse, tolerance, and physical dependent development => subject to Controlled Substance Act (limitaitons on prescribing). 3 SPECIFIC RECEPTORS: (1) MU {Supraspinal (mu1) and spinal analgesia; Respiratory depression (mu2); Euphoria; Physical dependence}; (2) KAPPA {Spinal (K1) and Supraspinal (K3) analgesia; miosis; sedation; hallucinations; dysphoria. (3) DELTA {excitement, hyperkinesia, mydriasis, reinforcement, analgesia} = receptors r found in nerve endings in areas of chronic inflammation -> LOCAL EFFECTS of these drugs bc can provide pain relief that does NOT require CNS activity. TWO MAIN ACTIONS (see pic): (1) alter interpretation of, and emotional reaction to, pain @ thalamus and limbic system. (2) Dec. nociceptive pain input from periphery, altering pain threshold -> dec. release of substance P and Glutamate. @ periaqueductal gray (enkephalins and endorphins) & @ substania gelatinosa.
Corticosteroids - indicated use? what happens during stress?
Most commonly prescribed category of steroids for medical conditions (help control metabolism, inflammation, immune function, salt and water balance, development of sexual characteristics and your ability to withstand the stress of illness and injury; steroid medications are chemically related to some of your body's own steroids. duplicate their actions) that mimic ur body hormones cortisone and hydrocortisone (made by the outer portion (cortex) of your adrenal glands). Indicated use to dec. inflammation (but, this only happens w. med doses that exceed ur natural levels, which is disadv. since often the level of corticosteroids is not enough to deal w the inflammation/stress condition.) Regulated: HPA Axis: Hypothalamus makes CRF -> Pituitary makes ACTH -> Adrenal Cortex makes cortisol, which pos/neg regulation onto hypothalamus. STRESS (responded to by higher brain centers) = CORTISOL INC -> INC METABOLIC RATE, SODIUM AND WATER RETENTION, BLOOD VESSELS MORE RESPONSIVE TO NE.
Cirrhosis Types & Diagnosis, Liver & Analgesics ID 2/23
No cirrhosis = albumin (from liver) is normal. Hepatitis (active, acute, chronic, faccid, etc): albumin levels normal. - Cirrhosis of liver(end stage liver disease) dx = (1) ALBUMIN levels DEC (telling you production capacity of liver). (2) PT/INR also tells you production capacity of liver: when PT/INR starts getting prolonged, means clotting factor pool is dec. in patient. (2a) normal PT/INR = "compensated phase" (stage 1 and stage 2) of cirrhosis w no varicies for stage 1 or yes varicies for stage 2, no ascities in either; (2b) Prolonged PT/INR = "decompensated phase" (stage 3 and stage 4) of cirrhosis w. ascities +/- varicies. - PHARMACOKINETICS OF ANALGESICS rely heavily ON LIVER & RENAL FUNCTION. - *Efficiency of DRUG REMOVAL BY THE LIVER relies on: (1) Hepatic BLOOD FLOW (compromised in decompensated cirrhosis). (2) Hepatic ENZYME CAPACITY. (3) Plasma PROTEIN BINDING (Albumin is dec in ALL types of Cirrhosis).* - DRUG METABOLISM in general OCCURS IN the Liver via 3 mechanisms: (1) PHASE I: *Oxidation, reduction or hydrolysis* involving hepatic CYP450 enzyme system. (2) PHASE II: *Conjugation* to glucuronic acid/sulfate/acetate/glycine/glutathione/methyl group. (3) BILE: Biliary excretion & elimination {know if have drugs that need bile to remove drug out of system, but if there is a bile duct obstruction, then levels will build up in the patient eek} - CLEARANCE OF DRUG METABOLITES DECREASES WITH LIVER DISEASE. - This results in ALTERED PARENT DRUG or METABOLITE BIOAVAILABILITY. - THIS RESULTS IN INCREASED TOXICITY IN CIRRHOTIC PATIENTS. - If a drug is *highly protein bound* LOW ALBUMIN LEVEL leads to *inc free drug levels* - THIS CAN LEAD TO INCREASED ADVERSE EFFECTS & TOXICITY. - * OPIOIDS are CONTRAINDICATED with:* (a) RESPIRATORY DYSFUNCTION: *Severe asthma, COPD or trouble breathing.* (b) GI ISSUES: Such as *bowel obstruction or narrowing of the stomach or intestines* Suboxone & Methadone: (1) BUPRENORPHINE (SUBOXONE): has a ceiling reffect - recall. - Typically dispensed as SL Suboxone at Suboxone Clinics to heroin/other narcotic addicts - SUBOXONE ELIMINATION IS COMPROMISED WITH SEVERE CHOLESTASIS AS IT IS CLEARED VIA BILE. - Thus Suboxone requires DOSE REDUCTION/DRUG AVOIDANCE (2) METHADONE: - Typically dispensed daily at Methadone Clinics to heroin or other narcotic addicts - Methadone has a *LOW hepatic extraction/first-pass metabolism.* Methadone is heavily protein bound - LIVER DISEASE DOES NOT impact BIOAVAILABILITY (bc not involved in first pass!) - Methadone metabolism does not yield toxic metabolites. - However HEPATIC CLEARANCE may be ALTERED SUBSTANTIALLY. - Methadone requires *reduced dosing* IN CIRRHOTICS. Meperidine, Morphine & Fentanyl: (3) MEPERIDINE: (she hates it, but will be on boards) - Meperidine is metabolized by *CYP2B6 and CYP3A4* to nor-meperidine. (two enzymes) -> Nor-meperidine a NEUROTOXIC METABOLITE, particularly with concomitant RENAL DYSFUNCTION. - AVOID Meperidine WITH LIVER DYSFUNCTION because of the increased bioavailability (HEAVILY PROTEIN BOUND) AND PROLONGED HALF-LIFE OF ITS TOXIC METABOLITE. (4) MORPHINE or FENTANYL: - Both *NORMALLY* have *HIGH* hepatic EXTRACTION/FIRST-PASS METABOLISM & *LOW bioavailability* - In *Cirrhotic patients*: Both have "HIGHER" BIOAVAILABILITY - *Like Methadone, Fentanyl is also heavily protein bound* - *Like Methadone, Fentanyl requires reduced dosing* IN CIRRHOTICS - Like Methadone, metabolism of Fentanyl *does not* yield *toxic metabolites* - *Methadone, Fentanyl & Hydromorphone*, ARE BETTER TOLERATED IN LIVER DISEASE! Liver & Analgesic Guidelines: - *SEVERE COMPLICATIONS from ANALGESIA in Cirrhotics include: Hepatic encephalopathy, Hepatorenal syndrome, GI bleeding*: This leads to substantial morbidity . - CIRRHOTICS OFTEN HAVE *impaired Renal function* DESPITE A normal SERUM CREATININE LEVEL. This is because of poor nutrition & reduced muscle mass RESULTING IN LESS CREATININE PRODUCTION. Cirrhotics need prostaglandins TO COUNTERACT RENIN-ANGIOTENSIN-ALDOSTERONE & SYMPATHETIC SYSTEMS that reduce Renal perfusion. Hepatorenal syndrome is frequently a FATAL COMPLICATION of advanced Cirrhosis. - Analgesics with PREDOMINANT Renal elimination REQUIRE DOSE ADJUSTMENT with Liver disease. *Tylenol at ≤ 2 g/d* (& no alcohol intake) IS FINE *if needed long-term* (>14 days) IN CIRRHOTICS. - Best to AVOID NSAIDs to avert RENAL FAILURE. AVOID OPIATES OR USE with low & infrequent dosing, TO AVOID ENCEPHALOPATHY. Liver & Analgesic use Guidelines: - *With ASYMPTOMATIC chronic liver disease WITHOUT Cirrhosis: Analgesic metabolism is similar to that in the general population* - *With SEVERE liver disease but WITHOUT Cirrhosis as in SEVERE HEPATITIS:* Drug metabolism may be altered and THUS DOSE REDUCTIONS MAY be *warranted* - COMPENSATED CIRRHOSIS and NEAR-NORMAL synthetic function (PT/INR): (i) Drug metabolism will be impaired but less than WITH decompensated cirrhosis. (ii) REDUCE DRUG DOSE and/or USE LESS FREQUENTLY. - KNOW THAT CIRRHOTIC PATIENTS HAVE *low serum protein and low albumin concentrations.* Liver: Analgesic Summary: - long-term Acetaminophen dose in Cirrhotics (not actively drinking alcohol): ≤ 2 g/d. - FOR SHORT-TERM USE OR 1-TIME DOSING,, A DOSE OF 2-3 G/D APPEARS TO BE SAFE - Reduced dose NSAIDs & opioids OK WITH chronic liver disease WITHOUT Cirrhosis. - AVOID NSAIDS IN compensated AND decompensated CIRRHOSIS DUE TO risk of acute Renal failure FROM PROSTAGLANDIN INHIBITION. - Opiates should be avoided or used sparingly AT LOW AND INFREQUENT DOSES because of the risk of precipitating HEPATIC ENCEPHALOPATHY. - Patients with a HISTORY OF ENCEPHALOPATHY OR SUBSTANCE ABUSE should NOT take Opioids. - Anticonvulsants & antidepressants are alternate options for chronic neuropathic pain in patients with advanced liver disease Liver & TCAs (Tri-Cyclic antidepressants): - TCAs such as *Amitriptyline & Imipramine are used for neuropathic pain* (off-label use) . - They possibly BLOCK PRESYNAPTIC SEROTONIN AND/OR NOREPINEPHRINE REUPTAKE in neurons involved in pain transmission. - TCAs undergo *1st pass* hepatic metabolism mainly *via CYP2D6 & Renal elimination*. - Nortriptyline & Desipramine are less potent, *less sedating & less constipating* TCAs - Also Nortriptyline & Desipramine have *less tachycardia and hypotension* compared to Amitriptyline and Doxepin.
Sensory Nerve Endings of Integument
Non-encapsulated: - FREE NERVE ENDINGS = thermoreceptors (temp), mechanoreceptors, nociceptors (pain), extend to stratum granulosum. Encapsulated: - MERKEL ENDINGS (merkel cells) = slow-adapting mechanoreceptors. note: All three (acinian Corpuscles, Meissner's Corpuscles, Merkel Cells) are mechanoreceptors that are sensitive to PRESSURE (not temp, pain, etc).
Elderly and Vaccinations
Old people = bad immune system = running on T cell memory, don't make them every day. - immunodeficiency comes with being older -> Shingles is chicken pox virus - kids get chicken pox when younger and then remains dormant in their body bc immune system keping it in check. But when get old and immunoscenescent, immune system cant keep that virus in check all the time, so same virus is coming out but in different way as shingles. So shingles vaccine is same as the chicken pox virus vaccine, bu shingles cavvine is at a higher concentrated dose - why does old man need 15 times more viruses? Bc old and immunocompromised (weakener immune systems) even though has lots of memory.
Opioids and ALcohol ID 2/23
Opioids should not be prescribed if alcohol is being consumed. OPIOIDS SHOULD NOT BE PRESCRIBED IF ALCOHOL IS BEING CONSUMED. Always know that *alcohol favors RAPID RELEASE OF OPIOIDS in the stomach*. DEATH CAN OCCUR IF *OPIOIDS, ALCOHOL & BENZODIAZEPINES* ARE TAKEN TOGETHER *DOCUMENT THAT YOU HAVE INFORMED THE PATIENT ABOUT THIS BLACK BOX WARNING*!!!
Hydrocodone/Oxycodone (opioid)
Oral bioavaliability similar to codeine, but greater analgesic efficacy allows use of doses that provide analgesia w. less nausea and constipation. Hydrocodone, but not oxycodone, analgesic action reduced by 2D6 inhibition. 200mg codeine, 30 mg hydrocodone, 30mg oxycodone, are equipotenet and equianalgesic with 10mg morphine IM.
Passive & Active Immunity - define each and give examples? (review)
PASSIVE: transfer of pre-formed antibodies to give Immediate Protection thats short-lived = a few months (transient immunity bc antibodies /IgG half-life is 3-4 weeks). - Examples: (1) Natural - Maternal IgG passed through placenta "to provide passive immunity to neonate." (2) Natural - Maternal IgA (dimer secretory form) passed in milk {note this doesn't get absorbed into child, just goes to gut}; "infant receives antibodies, primarily dimeric IgA (colostrum/milk)". (3) Artificial - Injection of pre-formed Immunoglobulin (antibody) e.g. IVIG (intravenous Immune globin), RIG (rabies immune globin given Intramuscular), MAb (monoclonal antibodies). = Ig preparations that have high protective titer for specific pathogens prepared using sera from donors that are immune to a particular pathogen, thus will protect someone who is exposed to that particular pathogen = e.g Ig with protective titers for: rabies (Rabies Immune Globulin, RIG); tenanus toxin (TIG); hepatitisB (HBIG); varicella zoster (VZIG). ACTIVE: responds to antigen, mediated by adaptive immune response to Ag. Takes time to develop, but more long-lived response (results in memory). - Examples: (1) Natural - Infection w pathogen. (2) Artificial - Immunization (vaccination).
Adverse Effects of Prolonged Use of adrenocorticosteroids - affecting what biological mechs?
PROLONGED USE of corticosteroids can lead to widespread problems affecting => (1) Metabolism— your body tends to accumulate fat in your abdomen, around your face ("moon face") and on the back of your neck. Also, levels of blood sugar increase, sometimes leading to or worsening diabetes. Muscular weakness develops. (2) Bones - formation of new bone is inhibited and calcium is lost in the urine. Osteoporosis and, sometimes, joint damage result. (3) Eyes -incidence of cataracts increases. (4) Skin--thinning occurs. Blood vessels near the surface of your skin become more visible. Skin bruises more easily. Wounds heal slowly. (5) Blood pressure - elevations are common. (6) Immune system -your body produces fewer disease-fighting antibodies, making you more susceptible to viral, bacterial and fungal infections. (7) Emotions - some people develop agitation, euphoria, insomnia and, rarely, psychosis. (8) Peptic ulceration- thus use in patients with existing peptic ulcers is contraindicated. Better Ways to Prescribe Steroids Reduce Side Effects
Who is the Medically Complex Patient (MCP)? how is it defined) caps red ID 2/23 (not from review)
Patient presenting with: - MULTIPLE CHRONIC ILLNESSES - Mental health concerns On MULTIPLE MEDICATIONS including ANTI-PSYCHOTIC MEDICATIONS ! {she said to know: most of these r inducer drugs, meaning will wash out the drug from system; e.g. give codeine to patient who is also on anti-convulsant (inducer drug) -> will wash out codeine from the patient, but before the codeine starts working in patent needs to be converted to morphine. So rapid rid of codeine -> turnover of codeine so rapid -> very high morphine levels in patients at any given time, bc everything being pushed out by anticonvulsant}. - Often an OLDER patient Often WOMEN - Frequent CLINIC VISITS to MANY PROVIDERS. - More likely to MISS APPOINTMENTS & COMPLIANCE ISSUES. - Social and financial issues. Living in lower income neighborhoods. - PSYCHOSOCIAL BARRIERS TO MEDICAL CARE.
Case #1 A 58 year old salesman who is a heavy smoker and an alcoholic, noted that he had nasal congestion and a low grade fever. Two days later he abruptly developed a shaking chill, cough and severe pain on the right side of his chest that got worse with breathing. The cough produced rust-colored sputum. When he was seen in the ER, he appeared acutely ill and had a temperature of 104oF. His respiratory rate was relatively rapid and his breathing was shallow. The laboratory reported that his white blood cell count was increased. A chest X-ray revealed consolidation of the right upper lobe. Analysis of his sputum showed many neutrophils and lancet-shaped Gram-positive P-disk sensitive diplococci. Blood was obtained for culture and treatment was begun with penicillin. Both the blood cultures and sputum cultures were positive for the pneumococcus, Streptococcus pneumoniae. Two days later, the patient was much improved and, after 8 more days on penicillin, he recovered completely.
Pneumonia - S. pneumoniae, L. pneumophila, P. aeruginosa. - Lower Respiratory Infection (LRI). - Cause can be many dif. microbes, sometimes w distinct clinical manifestations. Pneumonia is not one disease but many dif ones that share a common anatomical location. - Is *infection of lung parenchyma* which is portion of lung involved in gas transfer incl. alveoli, alveolar ducts, and bronchioles. - Stages in pneumonia: (1) alveoli fill w fluid, (2) *consolidation* {defined as alveolar space that contains liguid instead of gas. Dense material/cellular exudate fill up alveoli and small airways; fluid in the airspaces of lungs leads to hardening of normally soft tissue/ soildifcation of alveolar parenchhyma. Lung becomes firm and inelastic; vs *bronchitis => no consoludation*), (3) Resolution (1) *Acute* Pneumonia "Syndrome" = sudden onset, symptoms progress over a few days; may be *community acquired* via Streptococcus pneumonia (person-toperson) or Legionella pneumophilia (environmental), may be *hospital acquired (nonsocomial) via Pseudomonas aeruginosa. *BACTERIA = Streptococcus Pneumoniae* - *Encounter*; INFECTED PERSON person (50% gen. popln r carriers); fomites. - Entry: inhalation. - *Growth/Multiplication*: EXTRACELLULAR. - *Survival mechanism*: CAPSULE allows organism to resist phagocytosis by macrophages. - Damge: no endotoxin, Pneumolysin {toxin/virulence factor}, acute inflammation, & fluids in lung. - *Major dangers posed by S. P. penumonia* = may develop BACTEREMIA; organs may spread to other organs, e.g. meninges (meningitis), heart valves (endocarditis). Before there were antibiotics, often fatal - recovery depdnt on antibody production, there are 85 sterotypes. Now though, disease response quickly to antibiotics -> can have complete recovery of lung!. (2) *Subacute or Chronic* = Fungal Pneumonia = Histoplasma capsulatum.
Polio Outbreak
Polio Outbreak - It attacked everyone no matter location or invcome -> paralysis result. - Polio virus infects gut, and sometimes polio gets into blood travels to CNS and causes paralysis (polio myolitis). - Oral Polio Vaccine = prevention of infection, transmission, no longer used in USA since year 2000 (we still get immunized tho bc its still in world but with "Salk's vaccine - reason is bc: atenuated virus has mutations that make it less pathogenic, antime u mutate something it can mutate back to norm./wild-type). - Would give natural immunity; largely IgA -> good mucosal immunity. - SIgA = secretory igA. - Prevention of infection very well, and prevention of transmission from one person to tohre v well. - Virus that comes out in diper is covered with secretory IgA, so actulaly had bee nnurilized. - Used world wide Get rid of small pox - we don't have to immunize aginst thia anymore, its gone! But we do stockpile these vaccines. fix see pic and summarize.
Case #3 A 57-year-old woman with current renal cancer and a history of smoking developed pneumonia seven days after a nephrectomy. The patient was undergoing chemotherapy. A physical examination revealed a temperature of 37.1 °C and crackles (rattling) in the left lung. Chest radiography indicated infiltration shadows in the left lung field. P. aeruginosa was identified in blood cultures and respiratory specimens. Intravenous antibiotics improved the chest X-ray findings and the pneumonia.
Pseudomonas aeruginosa - Can infect invertebrates and plants. - Gram negative, rod shaped. - Serious infections = in *hospitals* and/or in people with weakened immune systems -> e.g. Patients on *ventilators*, with catheters, wounds from surgery or from burns; or *Cystic fibrosis patients* (risk factor). - Mild infections = in healthy people -> e.g. Ears: exposure to contaminated water; or Eyes: contaminated contact lense solutions. - *pathogen* = OPPORTUNISTIC pathogen IN HUMANS. Naturally resistant to antibiotics - *Encounter* = NONSOCOMIAL (RARELY, EVNRIONMENTAL), & HOSPITALS. - *Growth* = NEEDS IRON. - *survival strategy* = BIOFILMS, ANTIBIOTIC RESISTANCE {Multiplication: facultative aerobe, needs iron, forms biofilms}.
Define Tissue repair? Regenerative capacity depends on? REGENERATION KEY FACTS? know path 2/22 red chronic ifnammation. (not from review)
RESTORATION OF TISSUE ARCHITECTURE AND FXN AFTER INJURY. OCCURS EITHER BY: REGENERATION (proliferation of residual cells that retain capacity to divide, and by replacement from stem cells. typical response in organs w rapidly dividng cells, incl. skin, intestines, liver) OR BY SCAR FORMATION (repairs occur by laying down connective tissue. fibrous tissue cannot preform function of previous tissue, but provides stability. Fibrosis = deposition of collagen in organs after chronic inflammation). REGENERATIVE CAPCITY DEPENDS ON ABILITY OF TISSUE TO PROLIFERATE: 1) LABIAL CELLS (labile tissue is continuously dividing) = HIGH TURNOVER RATE; HIGH REGENERATIVE CAPACITY; E.G. SQUAMOUS, GLANDULAR, AND GI EPITHELIUM; BONE MARROW. 2) STABLE CELLS (stable tissue has quiescent cells w minimal replicative activity) = LOW TURNOVER RATE; CAN PROLIFERATE RAPIDLY WHEN CALLED UPON; E.G. FIBROBLASTS, OSTEOBLASTS, LIVER, KIDNEY, AND ENDOTHELIAL CELLS. 3) PERMANENT CELLS (permanent tissue is terminally differentiated) = CANNOT DIVIDE, CANNOT REGENERATE; HEAL W SCAR TISSUE; E.G. NEURONS AND CARDIAC CELLS. REGENERATION KEY FACTS = RESTORATION OF NORMAL STRUCTURE & FUNCTION W/O SCARRING. ACUTE INFLAMMATORY EXUDATE REMOVED BY LIQUEFACTION AND PHAGOCYTOSIS. SUPPORT STROMA MUST BE INTACT. DAMAGED CELLS MUST BE ABLE TO REGENERATE. (Know the lists; draw/write this all out and note assoc's).
Renal Status - measured by? when does patient have kidney failure/ stages of disease (numbers)? ID 2/23
Renal status measured by = serum creatine level and GFR. - As kidney function *decreases*, the serum creatinine *levels rise* - DIET, MUSCLE MASS, OLD AGE CAN ALSO AFFECT SERUM CR. VALUE. (it wont rise as much if diet poor, etc.) - *always estimate renal function by GFR * - Normal S. Creatinine in most labs: *0.4-1.2mg/dL* - CHRONIC ELEVATION OF S. CR OF 2.0 MG/DL *indicates moderate to severe decrease in GFR* - GFR IS USED TO DETERMINE THE SEVERITY OF KIDNEY DISEASE. - *The 5 levels of severity or Stages of severity are: * (1) *Stage 1*: GFR ≥ 90mL/min/1.73m2 (2) *Stage 2 (Mild)*: GFR 60-89mL/min/1.73m2 (3) STAGE 3 (MODERATE): GFR 30-59ML/MIN/1.73M2. (4) STAGE 4 (SEVERE): GFR 15-29ML/MIN/1.73M2 STAGE 5 (KIDNEY FAILURE): GFR <15ML/MIN/1.73M2 - *Patient is said to have chronic kidney disease (compromised renal status) when the* GFR IS LESS 60 ML/MIN/1.73 M2 FOR 3 MONTHS in patient. (GFR more than 60 means healthy) - know:*ALWAYS help prevent progression of kidney disease by using appropriate AAAAAs {Anasthetics, Analgesics, Antibiotics, Antivirals Antifungals = "the five A's"}* - Insist patient *control the associated diseases* like hypertension and/or diabetes . - These conditions commonly cause chronic kidney disease (CKD).
Lung abscesses - risk factors, prevention? (review)
Risk Factors = -Often aspiration of oral contents; -Anaerobic flora common in the general community; - Alcoholics, people who have been in the hospital, or with little gastric acid may have different flora. "You can prevent lung abscess" = Key: prevent oral fluids from being aspirated; Common circumstance: Dental work on caries (Caries are a risk factor for having both more; and more varied; kinds of oral bacteria) = RUBBER DAMS protect oropharynx from aspiration, protect soft tissues, provide a clean and dry environment
M cells - transport what to where? Then what happens to the thing they transported? (review)
SELECTIVELY TRANSPORT ANTIGENS TO LYMPHOID FOLLICLES [PEYERS PATCHES]. ANTIGEN TRANSPORTED ACROSS M CELLS IS PRESENTED BY DENDRITIC CELLS TO T CELLS. OTHER NOTES (NON REVIEW): Cell in mucosa = M cell = transport antigens in selective (unkonwn mech) way to lymphoid tissue = antigen-sampling cell = decides (mech unknown) what antigens to transport through to the lymphoid tissue at the mucosal site. When there Is an infection or pathogen causing damage to mucosal surfae , that might allow antigen to get thru bc its descriucted mucosal barrier. But without pathogen or damage, the M cell is prevened from getting to B or T cells. With damage, M cell helps move the B and T cells to site. Certain things it recognizes on pathogens. Picture of mucosal surface. Top in green shows M cell. Below M cell is lymphoid tissue (lymphoid fillicle or peyer's pathces in gut) which aren't encapsulated (dif. sructure from lymph node) but u have tmv cells and lymphoid presenting cells. M cells will select cells that can go through. B cells that are here are already pre-destined to become IgA = IgA comitted B cells. Although committed B cell turned on at mucosal site, it'll travel thru lymphatic system (to nearest draining lymph node), where it'll full develop via undergo class switching and somatic mutation.They will develp The Path: Induction of immune response and turning on of B cells and T cells happens locally at the mucosal site, but finishes the job in lymph node 9 cells travel via lymphatics ly,ph node. Blood vessel at mucosal site have receptor regoc. By IgA secreting cell, and then IgA stops there and goes to mucosal site. 'Honing" to the iste [note: these don't hone to only one site, hone to multiple sites - makes sense to put that protection on all ur mucosal sites] e.g. mothers IgA want them to hone to secretory sites including the milth. E.g.2. vaccine to gut of Iga can still get it to the mucosal surfaces. Epithelial Cells make IgA (recall). Most imp function of IgA is that its transported to mucosal surface or in secretion, neutralizes pathogen and prevents it from getting in. IgA in gut goes to surface and prevents toxin from attaching ot cells and ding adamage. IgA is able to bind antigens in the cell.
Epidermis - what type of epithelium? types of cells? layers? turnover? sensation and blood supply? (review)
SSKE; CELLS = Keratinocytes (most cells); Melanocytes (only cells that produce melanin, then transfer it to other cells); Langerhans (wandering APCs); Lymphocytes (passing through). LAYERS = 1. Stratum Corneum 2. Stratum Lucidum 3. Stratum Granulosum 4. Stratum Spinosum 5. Stratum Basale (Germinativum). TURNOVER = 15 days to 1 month. FREE NERVE ENDINGS {Nociception, thermo, mecha} contained in it. AVASCULAR.
Combunox (opioid)
Schedule II. - FDA approves it for tx of acute, moderate, to severe pain. - Ad copy: "the first and only oxycodone (5mg) and Ibuprofen (400mg) combination long-lasting pain relief). - is dosed as 1 tablet q6h, with daily maximum of 4 tablets. The maximum length of treatment is 1 week.
Statement 1: Always estimate renal function by serum creatinine. Statement 2: Patient w. S. creatinine of 2 mg/dL is operating under 50% renal function. star and see notes on statement two
Statement 1 is false. You estimate renal function by GFR. serum creatinine gives u a great estimate, but its not ur "go to", ,GFR is go to. Statement 2 is true - Serum creatinine shoots up when 50% of ur kidneys stop working.
Statement 1: In prescribing younger patients opioid medications, it is important to consider patient's tolerance, abuse history and impairment of skills and mental function. Statement 2: When prescribing older adults opioids, it is important to consider patient's renal and liver function as the functions increase with age. star
Statement 1 is true - *In Younger patients the provider is more concerned with*: Opioid metabolism & occurrence of *tolerance, impairment of skills & mental function* Also *adverse events during pregnancy and lactation (highlighted this)* Plus *prevention of abuse by monitoring drug and metabolite levels.* Statement 2 is false - they dont inc. w age.
Statement 1: NSAIDs, including aspirin, inhibit the production of prostaglandins and thromboxane A2. Statement 2: Aspirin, unlike other NSAIDs, inhibits Prostaglandins, Thromboxane A2 and reversibly blocks COX-1. star
Statement 1 true, 2 is false - NSAIDS inhibit production of prostaglandins (and thromboxane A2) and prostaglandins; aspirin is special bc *irreversibly* blocks Cox-1 to do that.
Analgesics are prescribed in the dental setting for 3-5 days only to avoid misuse and to ensure patients come in again for follow-up appointments. Is the statement and reason true/false? STar
Statement is true but reasoning is false. Dentist prescribes analgesics for 3-5 days ONLY (nothing given for more than 7 days, its law for acute opioids). Multimodal analgesia (MMA) is the 'STANDARD OF CARE' for preventing post-op pain [it is also "PERI-OPERATIVE" ANALGESIA aka for before, during & after procedures] = safe, effective, minimal side-effects, easily managed by patient once home = acute and chronic pain relief bc TARGETING PAIN TRANSMISSION AT multiple levels using analgesics and/or adjuvants, IN COMBINATION. - Combination of PREVENTIVE centrally & peripherally acting OPIOID & NON-OPIOIDS are used in AROUND-THE-CLOCK (ATC) DOSING. - * "PREVENTIVE" ANALGESIC regimen is started IN PRE OR EARLY POSTOP PERIOD & continued for ~3-5 days* dependent on the extent of the procedure (nothing given for more than 7 days it's the law for acute opioids!)
Common Mucosal Immune System - what is it? (review)
System of lymphoid tissues beneath mucosal surfaces, so that if you immunize at ONE mucosal site -> ends up getting secretory IgG at ALL mucosal sites (think like roost underground tree). Flu mist = only way we know how to use vaccine to make mucosal immune response is by using Live-attenuated vaccine. STORY: M Cell, a specialized epithelial cell "gate" for what Ag's get pushed thru to B and T cells => activation of these B cells (at these sites) then travel to germinal center of lymph node (B cells fully develop)=> leave, Go to /in blood randomly through body. But mucosal site has proteins expressed on its' epithelial cells, so plasma cells know to come in and stick & become "Plasma cells that secrete DIMERIC IgA that "HOME"/migrate back to mucosal sites....Then, that Dimeric IgA (needs to go through secretory process) is taken up/recognized by Poly-Ig [Poly-Antibody] Receptor [made by epithelial cells] which COVALENTLY [permanently (unique bc other Ig-receptor's dont)] binds dimeric IgA => transports dimeric IgA into secretion or on mucosal surface; gets released by enzyme cleaving polyIG receptor, but leaves most of the receptor stuck to the IgA = SECRETORY COMPONENT. SECRETORY IgA (dimer IgA w. polymerized j chains, plussss Secretory Component that's from poly-Ig epithelial receptor that transported dimeric iga into secretions) = PASSIVE IMMUNITY = mucosal surfaces, saliva, tears, milk secretions = looks like dimer, with J chain (polymerization, polymeric) and other protein stuck to it (secretory igA/in secretions e.g. from saliva) called secretory component {part of receptor used to transport dimeric IgA into secretions} = poly Ig (polymeric immunoglobulin ) Receptor, on epithelial cells on mucosal or secretory sites. (2) see picture of "Secretory IgA" = Dimeric with j chain Covalently linked poly Ig Receptor = secretory igA. You make more IgA every day than any other class of antibody (reglardness that IgG is most in tissue fluids, etc) since we use it like everyday.
20 year old presents surgical extraction for all four wisdom teeth. Due to his severe asthma, your patient has been on 20 mg of Solu-Cortef every other day for the pats three years. How will u manage the patient's dental treatment prior to and after surgery? A. give patient 20 mg of solu-cortef on the day of procedure and see patient for a 9am appointment. B. Have patient take 10mg of prednisone on the day of procedure, 5mg prednisone the day after and then return to his regular steroid schedule. C. patient should take 40mg of drug on day of procedure then return to his regular steroid schedule the next day.
This question WILL apply to rule of two's! B is answer. C could also be answer, but step down is imp. know conversion bc WILL BE ON EXAM: 20mg Cortisol = 5mg prednisone = 20mg hydrocortisone. star search what is solu-cortef - its what makes up cortisol,
Which combination opioid is a Schedule IV drug (unlike other combination opioid containing meds)? (not from review)
ULTRACET {know this fact, red pharm 2/23}. - for moderate to moderately severe acute dental pain (e.g. extractions). Combines short-acting, rapid onset analgesic (acetaminophen - 325mg) with long-duration opioid analgesic (Tramadol 37.5mg). Reduced incidence of opioid related side effects i.e. constipation, nausea, dizziness, and somnolence. Avoid in seizure prone patients.
Melanocyte activity promoted by? Forms of melanin?
UV light & Melanocyte Stimulating Hormone (MSH). 1. eumelanin 2. phaeomelanin = -less effective at blocking UV rays -weaker antioxidant -thus risk of melanoma/skin cancer is higher -permits vitamin D synthesis under low light conditions
MOST commonly prescribed analgesic by dentists for Moderate to Severe Pain? Type of drug, what it contains (strengths), and dosing? know this all, red pharm 2/23! (not from review)
VICODIN - most commonly prescribed analgesic by dentists for moderate to severe pain. - SCHEDULE II. - CONTAINS HYDROCODONE & ACETAMINOPHEN IN VARIETY OF STRENGTHS: (hydrocodone mg / acetaminophen mg) (A) VICODIN 5/300 (B) VICODIN ES 7.5/300 (C) VICODIN HP 10/300 (recall: is strongest vicodin). - DOSING: q4-6h, MAX # PILLS PER DAY DEPENDS ON PREPARATION, USUALLY LIMITED BY THE ACETAMINOPHEN COMPONENT.
Opioids Efficacy
Wide range of efficacy Very Potent (1) TO less: (1) Fentanyl = fix see picture. (2) Butorphanol (3) Oxymorphone = hydromophone (4) Morphine = methadone (5) Oxycodone * (6) Hydrocodone (7) Pentazocine (8) Meperidine* (9) Tramadol* (10) Codeine* 200 mg codeine = 30 mg hydrocodone = 20 mg oxycodone = 10 mg morphine IM - fix do we needa know this.
Do NSAIDs retain sodium and water? ID 2/23
Yes -> in cardiocompromised patients, will worsen status of patient. Prostaglandin inhibitors -> compromises renal perfusion (and circulation). NSAIDs are contraindicated any time patient has kidney disase (above 1.2? )
Types of Vaccines and what each type activates? They ALL activate? (review)
[vaccines = active immunity]. ALL activate B cells. 1. Live attenuated (weakened), so that only a mild (subclinical) infection occurs = ACTIVATES BOTH CD4+ (MHC2) & CD8+T (mhc1, HLA a/b/c) cells {EXAM!}. 2. Inactivated (killed) = whole organism (virus or bacteria) is made non-infectious (e.g. polio treated with formaldahyde) = Activates primarily CD4+ T cells. 3. Subunit = purified component(s) of pathogen (from microbe or recomibant), which can be: proteins, toxoid (inactivated toxin), bacterial capsular polysaccharide, virus-like particles (VLPs) spontaneously assembled coat proteins) = Activates primarily CD4+ T cells. *Live vs. Inactivated or Subunit Vaccines*: (a) An *inactivated vaccine or subunit* vaccine will induce: Humoral immunity (antibodies); CD4+ T cells. (b) live vaccine (virus or other intracellular pathogen) will induce: Humoral immunity (ANTIBODIES); CD4+ T cells (T-HELPER CELL PRODUCING CYTOKINES); CD8+ T cells (CTL / CYTOTOXIC T LYMPHOCYTES) = KNOW ADV: *Live vaccines are generally more potent (greater immune response with longer lasting memory) compared to inactivated or subunit vaccines* [are better for mucosal immune e.g. *FluMist live intranasal vaccine for influenza virus (alternative vaccine to the injected/killed virus one) will yield better mucosal immune response and thus better protection s.t. less cases of Flu happen.* = DIADV: have potential to cause disease if the attenuated pathogen mutates back to a pathogenic form (reverts to wildtype); Immunodeficient individuals may be unable to control the normally mild infection caused by the live vaccine; For these reasons, polio vaccination in the US now uses the inactivated polio virus (IPV) instead of the highly effective oral polio virus (OPV.)
Granulomatous Inflammation Includes what disorders/diseases? red path 2/22(not from review)
a) FOREIGN BODY REACTIONS b) INFECTIONS = TUBERCULOSIS, TERTIARY SYPHILIS, CAT-SCRATCH DISEASE, LEPROSY, DEEP FUNGAL INFECTIONS (know this list red). C) IMMUNE- MEDIATED DISEASES = CROHN DISEASE, OROFACIAL GRANULOMATOSIS, GRANULOMATOSIS W. POLYANGIITIS. (know this list too) D) IDIOPATHIC DISORDERS = SARCOIDOSIS.
Dental Use of Opioids (not from review, red)
primarily in combination analgesics. List of Mild (1) TO Strong: (1) Tylenol w. codeine #2 {15mg}, #3 {30mg}, and #4 {60mg} (2) Vicoprofen - hydrocodone {7.5 mg} and Ibuprofen {200mg} (3, know red) VICODIN - HYDROCODONE {5 MG} AND ACETAMINOPHEN {300 MG}. (4, know red) VICODIN ES - HYDROCODONE {7.5 MG) AND ACETAMINOPHEN {300 MG}. (5, know red) VICODIN HP - HYDROCODONE {10 MG} AND ACETAMINOPHEN {300 MG} = strongest vicodin. (6) Percodan - oxycodone (4.88 mg) and aspirin (325 mg). (7) Percocet - oxycodone (5mg) and acetaminophen (325 mg). (8) Combunox - oxycodone (5mg) and Ibuprofen (400mg).
Specialized transduction?
specialized bc only specific genes adjacent to the order of the prophage are transduced. only temperate phages can do specialized transduction.
75 man presents for multiple teeth extractions. Previous history of drug abuse and tells u he had an MI 6 months ago, as a result he had two stents placed. Which of the following drugs would be BEST for this patient's pain management? A. codeine B. percocet C. ibuprofen D. celebrex E. acetaminophen.
star search notes fix this bc confused A. codeine - eliminate. B. percocet - eliminate, opioid.. C. ibuprofen - this COULD be given, it wouldnt be ur best choice. but if tylenol wasn't answer, this would be ur answer. D. celebrex - no, cardiovascular E. acetaminophen = answer. tylenol first choice. - no opioids.
Statement 1: albumin levels r typically normal in patients w hepatitis Statement 2: albumin levels only decrease in patients with decompensated cirrhosis. Statement 3: PT/INR is increased in hepatitis. star
statement 1 = TRUE. Statement 2: = FALSE. Statement 3 = false. FIRST - Hepatitis of any type is liver inflammation = liver normally making Albumin. THEN - if it gets rly bad, liver scarring happens (abnormal tissue scarred becomes nonfunctional, liver can be scarred 50-80% but still fxn normally) = CIRRHOSIS = function of liver starts to decrease, so ALBUMIN levels start to DEC. THIRDLY - Once scarring so bad s.t. cannot compensate for amt of scarring = "DECOMPINSATED cirrhosis" = when SYMPTOMS APPEAR (jaundice, enphalopothy/confusion, acitis (belly filled w fluid)) = liver no longer makes clotting factors -> bleed more: PT/INR increased (increases as scarring continues). note: Blood values tell you difference btwn hepatitis, cirrhosis, and decompinsated cirrhosis.
