Download - Primer Worksheets.pdf
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es3 QUESTION WARM-UP1. What portion of the brachial plexus is injured in Erb-Duchenne Palsy? What are the
symptoms? (FA11 p375) (FA12 p410)
2. What is the clinical appearance of internuclear ophthalmoplegia? With what disorder is it commonly associated? (FA11 p424) (FA12 p464)
3. Which lipid-lowering agent matches the following description? (FA11 p282) (FA12 p308) 7)JEGMEPYWLMRK SE: elevated LFTs, myositis SE: GI discomfort, bad taste Best effect on HDLBest effect on triglycerides/VLDLBest effect on LDL/cholesterolBinds C. diff. toxin
OSTEOARTHRITIS AND TREATMENTH: Chapter 332R: Chapter 26GG: Chapter 34
Osteoarthritis (FA11 p382) (FA12 p417)Aspirin (FA11 p391) (FA12 p429)NSAIDS (FA11 p391) (FA12 p429) (H p2835, Table 332-1)COX-2 inhibitors (FA11 p392) (FA12 p430)Acetaminophen (FA11 p392) (FA12 p430)
QUICK QUIZ4. What is the mechanism of treating acetaminophen overdose? (FA11 p392) (FA12 p430)
5. What is the classic feature of osteoarthritis? (FA11 p382) (FA12 p431)
6. By what mechanism do NSAIDS cause renal disease? (FA11 p391) (FA12 p430)
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3 Joint Diseases
OTHER JOINT DISEASES H: Chapters 331, 333, 334R: Chapter 26GG: Chapter 34
Rheumatoid arthritis (FA11 p383) (FA12 p418)Juvenile idiopathic arthritis
- Polyarticular - Pauciarticular - Systemic Onset (Stills Disease)
Sjogren syndrome (FA11 p383) (FA12 p418)Gout (FA11 p 384) (FA12 p419)Gout drugs (FA11 p392) (FA12 p431) (GG p994)Pseudogout (FA11 p384) (FA12 p419) (H p2839)Infectious arthritis (FA11 p384) (FA12 p420) (H p2842)
END OF SESSION QUIZ7. A man presents with pain and swelling of the knees, subcutaneous nodules around the
joints and Achilles tendon, and exquisite pain in the metatarsophalangeal joint of his right big toes. Biopsy reveals needle-like crystals. What is the diagnosis?
8. What medications are used in the treatment of an acute gout exacerbation?
9. What drugs can be used in the treatment of chronic gout? (FA11 p393) (FA12 p431)
10. What are the classic symptoms of Sjgren syndrome? (FA11 p383) (FA12 p418)
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3 QUESTION WARM-UP1. What diseases might be found immediately above the pectinate line vs. immediately below
the pectinate line? (FA11 p313, FA12 p342) (COA p416)
2. How many ATP are generated during aerobic metabolism? During anaerobic metabolism? (FA11 p97, FA12 p103) (Phys 860-861)
3. What enzyme is inhibited by the drug fomepizole? (FA11p94) (FA12 p100) (GG p86, Fig. 4-11)
ENTEROBACTERIACEAE, UTI, AND ANTIBIOTICSH: Chapter 133,137R: Chapter 8
Enterobacteriaceae (FA11 p137-138 150) (FA12 p147-148, 163)E. coli (FA11 p151) (FA12 p163)ProteusKlebsiella (FA11 p151) (FA12 p163)Urinary tract infections (FA11 P177) (FA12 p197) (H p2388)UTI bugs (FA11 p178) (FA12 p199)Sulfonamides and trimethoprim (FA11 p189) (FA12 p210)Sulfa drug allergies (FA11 p189) (FA12 p246)Trimethoprim (FA11 p189) (FA12 p211)NitrofurantoinFluoroquinolones (FA11 p190) (FA12 p211)
4. Enterobacteriaceae (E. coli, Salmonella, Shigella, Klebsiella, Enterobacter, Serratia, Proteus)Gram (-) rodsAll species have somatic (O) antigenCapsular (K) antigen- related to the virulence of the bug Flagellar (H) antigen- motile speciesAll ferment glucose and are oxidase negative
5. E. coli diarrhea, UTI, neonatal meningitis/pneumonia/sepsisEntero-toxigenic (ETEC) Most common form of travelers diarrhea (Montezumas revenge)
6\81471
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6. What is the most common cause of gram negative sepsis?
7. Proteus spp. (P. mirabilis, P. vulgaris)Very motile no distinct colonies can be grown (common cause of UTI)Carries urease: urea NH3 + CO2 ammonium-magnesium-phosphate stones staghorn calculi
8. What organisms most commonly cause UTIs? (FA11 p178, FA12 p198)
Antibiotics9. What is the mechanism of action of sulfonamides? (FA11 p189, FA12 p210) What is the
mechanism of action of trimethoprim? (FA11 p189, FA12 p211)
10. What drugs have photosensitivity reactions?
11. What other drugs should be avoided in patients with an allergy to sulfa? (FA11 p189,246) (FA12 p273)
12. What drugs can cause Stevens-Johnson syndrome (SJS)? (FA11 p245) (FA12 p272)
13. What are the clinical uses for TMP-SMX? (FA11 p189) (FA12 p211)
14. NitrofurantoinMechanism: Bacteriocidal. Reduced by bacterial proteins to a reactive intermediate that inactivates
bacterial ribosomes Indication: UTI cystitis (not pyelonephritis) by E. coli or Staph. saprophyticus (not Proteus) 7)VEVIP]REYWIE,%EXYPIRGI Safe in pregnancy
;LEXMWXLIQIGLERMWQSJEGXMSRSJUYMRSPSRIW#;LEXEVIXLIGPMRMGEPYWIWJSVYSVSUYMRSPSRIW#*%T*%T
;LEXEVIXLIWMHIIJJIGXWSJYSVSUYMRSPSRIW#*%T*%T
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QUICK QUIZ17. Which form of E. coli causes hemolytic-uremic syndrome (HUS)? (FA11 p151) (FA12 p163)
18. What infections is Klebsiella pneumoniae known for causing? (FA11 p151) (FA12 p163)
19. What organisms are the most common causes of UTI? (FA11 p177) (FA12 p198)
20. What is the function of the enzyme urease?
DIARRHEA AND FOOD POISONINGR: Chapter 17
Salmonella vs. Shigella (FA11 p152) (FA12 p164)Campylobacter jejuni (FA11 p152) (FA12 p164) (R p799)Vibrio cholera (FA11 p152) (FA12 p164) (R p797)Yersinia enterocolitica (FA11 p152) (FA12 p164) (R p802)'HMJGMPI*%T*%TBrief review of protozoa that cause diarrhea (R p805)Bugs causing food poisoning (FA11 p175) (FA12 p195) (R p800-801)Bugs causing diarrhea (FA11 p176) (FA12 p196) (R p798, Fig. 17-7)
21. Salmonella (FA11 p152, FA12 p164) Common cause of osteomyelitis in sickle cell patients S. enterica and S. enteritidis: the most common cause of food associated diarrhea in developed countries
(poultry, eggs, reptiles)Antibiotics should be avoided because they may prolong the carrier state in Salmonella GI tract
infections. S. typhi: causes typhoid fever
22. Shigella (FA11 p152, FA12 p164) Bacterial dysentery can be caused by 7LMKIPPEI\RIVM7LMKIPPEWSRRIMor Shigella dysenteriae 7LMKIPPEI\RIVM associated with causing Reiter syndrome
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END OF SESSION QUIZ23. What medications are commonly used to treat C. diff colitis? (FA11 p147) (FA12 p158)
24. What infectious agent most likely corresponds to the following statement? (FA11 p175) (FA12 p195) Food poisoning as a result of mayonnaise sitting out too longDiarrhea caused by Gram (-) nonmotile organism that does not ferment lactoseRice-water stoolsDiarrhea caused by a C- or S-shaped organism
Diarrhea transmitted from pet feces Food poisoning resulting from reheated rice (Chinese food)Diarrhea caused by Gram (-) motile organism that doesnt ferment lactoseMost common cause of travelers diarrhea
Diarrhea after a course of antibioticsDiarrhea caused by Gram (-) lactose fermenting bacteria, no feverDiarrhea caused by Gram (-) comma-shaped organism, no feverDiarrhea + recent ingestion of water from a stream Food poisoning from undercooked hamburger meat
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ycology3 QUESTION WARM-UP1. What problem/abnormality is associated with the following buzzwords?
(FA11 p269) (FA12 p294, p467) (R p537)Boot-shaped heartContinuous machine-like murmurTendon xanthomasCaf-au-lait spotsTuft of hair on lower back
2. What structures are at risk for injury with an anterior shoulder dislocation? (FA11 p371) (FA12 p 405) (H p2823)
3. What are the layers of the epidermis? (FA11 p370) (FA12 p404) (COA p12)
MYCOLOGYH: Chapters 163, 164, 169R: Chapter 8Mycology (FA11 p157-159) (FA12 p171-174)
4. What are 4 molds that are considered dermatophytes (fungal species commonly found MRZEHMRKWYTIVGMEPPE]IVWSJWOMR#
5. What infections are commonly caused by dermatophytes?
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yQUICK QUIZ6. Which fungus matches the following statement?
Found in SW U.S. including west Texas and California Found in Mississippi and Ohio River basinsCauses San Joaquin Valley fever Found in rural Latin AmericaAssociated with plant thorns and cutaneous injury Found in states east of the Mississippi River Found in bird and bat droppingsMold form contains barrel-shaped arthroconidiaAssociated with dust stormsBroad based budding of yeastMultiple budding of yeast form
Causes diaper rashOpportunistic mold with septate hyphae that branch at a 45 angleOpportunistic mold with irregular nonseptate hyphae that branch at wide angles (>90 degrees)Causes thrush in immunocompromised patients and vulvovaginitis in womenKnown for causing pneumonia in AIDS patients start Bactrim prophylaxis when CD4
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ycologyECTOPARASITES H: Chapter 357
Lice (H p3578)Scabies (H p3576)Bed bugs (H p3582)
10. Pediculosis capitis and pediculosis pubis: Treatment Pediculosis capitis (caused by Pediculus humanus AKA lice) wash scalp normally then towel dry
saturate scalp with permethrin cream (OTC Nix 1%) or pyrethrin (OTC Rid) for 10min then rinse repeat on day 9 due to resistance (CDC rec.) - Malathion lotion 0.5% (Rx) may be used instead of permethrin - Ivermectin can be used in resistant cases (not FDA approved). 200 mcg/kg po x1, repeated in 2wks - Lindane is not used due to potential neurotoxicity and widespread resistance - If younger than 2 years, then wet combing with conditioner or olive oil rather than insecticides
performed q3-4 days for weeks - 'LMPHVIRQE]VIXYVRXSWGLSSPEJXIVXLIVWXXVIEXQIRXWIWWMSR[IXGSQFMRKSVMRWIGXMGMHI
Pediculosis pubis (caused by Phthirus pubis%/%GVEFW permethrin 1% cream (OTC Nix 1%) or pyrethrin (OTC Rid) for 10min then rinse repeat on day 9-10 - Malathion or Ivermectin can used as alternatives (see above) - Sexual partners need to be treated at the same time - Bedding and clothing should be machine washed and dried in a hot dryer, dry cleaned, or bagged for a
min of 72 hrs
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yEND OF SESSION QUIZ ;LMGLJYRKYWXWXLIJSPPS[MRKWXEXIQIRX#
Causes San Joaquin Valley fever Found in rural Latin AmericaAssociated with plant thorns and cutaneous injury Found in states east of the Mississippi River Found in bird and bat droppingsMold form contains barrel-shaped arthroconidia
12. An HIV (+) patient with CSF showing 75/mm3 lymphocytes suddenly dies. Yeast is MHIRXMIHMRXLI'7*;LEXMWXLIQSWXPMOIP]HMEKRSWMW#
13. A patient presents with rose gardeners scenario (thorn prick with ulcers along lymphatic drainage). What is the infectious bug?
14. Which two agents are usually used in the treatment of pediculosis capitis and pediculosis pubis?
15. Why is lindane not the preferred agent in the treatment of lice?
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Viruses
3 QUESTION WARM-UP1. Which antibiotics are safe during pregnancy? (FA11 p196, 120) (FA12 p127, 219)
2. What nerve is most at risk of injury with the following types of fractures/injury? (FA11 p374) (FA12 p409) (COA p695-686, 710) Shaft of the humerus Surgical neck of the humerus Supracondyle of the humerusMedial epicondyleAnterior shoulder dislocation Injury to the carpal tunnel
3. What makes Lewy body dementia unique? (FA11p 425) (FA12 p465) (R p1321)
RNA VIRUSES PART 1H: Chapters 190-197
RNA viruses (FA11 p168) (FA12 p186)Reoviruses (FA11 p168) (FA12 p186)
- Coltivirus: Colorado tick fever (FA11 p168) (FA12 p186) - Rotavirus (FA11 p169) (FA12 p187)
Picornaviruses (FA11 p169) (FA12 p187) - Poliovirus (FA11 p411) (FA12 p451) - Echovirus - Rhinovirus - Coxsackievirus - HAV (FA11 p171) (FA12 p190)
Caliciviruses (FA11 p168) (FA12 p186)Flaviviruses (FA11 p168) (FA12 p186)
- HCV - Yellow fever virus - Dengue - St Louis encephalitis - West Nile virus
Rubella virus (FA11 p170) (FA12 p188)Retroviruses (FA11 p169) (FA12 p187)Coronaviruses (FA11 p169) (FA12 p187)
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QUICK QUIZ6. The X-virus has one virulence factor that causes an upper respiratory tract infection (factor
A) and one virulence factor that causes gastroenteritis (factor B). In order to determine which segment of the X-virus gene determines the manifestation of the infection, researchers rearrange each of the virulence factors to each of the 3 segments: L, M, and N. Which segment is most responsible for the clinical manifestation of a X-virus infection?
Segment L Segment M Segment N Manifestation A A A viral URI
B B B gastroenteritis
A A B viral URI
B A A viral URI
A A A viral URI
B B A gastroenteritis
B B B gastroenteritis
7. What is the #1 cause of fatal infantile gastroenteritis?
8. What virus is commonly associated with outbreaks of gastroenteritis on cruise ships?
9. Which RNA virus matches the following statement? Hand, foot, and mouth disease Break bone fever Common cold Fever, jaundice, black vomitMeningitis in summer monthsTourniquet test helps diagnose hemorrhagic disease Infects motor neurons of the anterior horn
4. Dengue Fever (H: p1621)Most prevalent mosquito-borne viral disease worldwide> 50 million annual, worldwide infectionsDisease severity ranges from mild to life-threateningClassic dengue fever = Break Bone Fever: muscle/joint pain, headache, retro-orbital painHemorrhagic fever: developed by < 20% of dengue patients 8SYVRMUYIX8IWX ;,3IPHXIWXJSVLIQSVVLEKMGJIZIV &4MREXIHXSETSMRXFIX[IIR7&4ERH(&4 - If excess petechiae = increased capillary wall fragility and thrombocytopenia
5. West Nile Virus (H: p1625)Birds are the reservoir, and mosquitoes are the vectors. Humans, horses, and dogs are incidental hosts. 7\YWYEPP]SRP]LIEHEGLIQEPEMWIFEGOTEMRQ]EPKMEERHERSVI\MEJSVHE]WYPMOI 7IZIVI7\MRQIRMRKMXMWIRGITLEPMXMWMRGPYHMRKQYWGPI[IEORIWWERHEGGMHTEVEP]WMWZME
anterior-horn involvement), alterations in consciousness, possibly deathDx: serology for IgM anti-WNV antibodiesTreatment: supportive
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Viruses
RNA Viruses Part 2 H: Chapter 186-187, 192-194, 197
-RYIR^E*%T*%T,T - %ZMERMRYIR^E,T - ,2MRYIR^E,T
Paramyxoviruses (FA11 p170) (FA12 p190) - 4EVEMRYIR^EGVSYT,T - RSV bronchiolitis (H p1488) - Rubeola (measles) virus (FA11 p170) (FA12 p188-189) (H p1600) - Mumps virus (FA11 p170) (FA12 p189) (H p1607)
Rabies virus (FA11 p170) (FA12 p190))FSPEZMVYW,THanta virus (H p1628)Anitvirals
- %QERXEHMRI^EREQMZMVSWIPXEQMZMV*%T*%T - Ribavirin (FA11 p195) (FA12 p216)
%ZMER-RYIR^E,TH5N1 It is only spread from bird-to-human (but great fears of mutation that would allow human-to-human spread) Sx: URI, GI symptoms (diarrhea), fever, pancytopenia, elevated aminotransferases (ALT, AST)Dx: reverse transcriptase PCR or viral cultureRx: oseltamivir
,2-RYIR^E,T SwinI*PYJVSQX[SW[MRIYWXVEMRWSRILYQERWXVEMRERHSRIEZMERWXVEMR 7\X]TMGEPY+-W]QTXSQW 6\SWIPXEQMZMVSV^EREQMZMVXSLMKLVMWOSVWIZIVIP]MPPTEXMIRXWFYXPSGEPWYVZIMPPERGIHEXEWLSYPHKYMHI
drug choice)
4EVEMRYIR^E'VSYT,T Laryngo-tracheo-bronchitis Sx: characteristic barking seal cough, respiratory distress (may mimic asthma), inspiratory stridor 4VMQEVMP]EKIWQ]VW8LIPIEHMRKGEYWISJLSWTMXEPM^EXMSRMRGLMPHVIR]SYRKIVXLER]IEVWDx: clinical, x-ray may show steeple sign 6\GSSPQMWXLYQMHMIVRSTVSZIRFIRIXVEGIQMGITMRITLVMRISRIHSWISJHI\EQIXLEWSRI
supportive, oxygen as needed
13. RSV bronchiolitis (H p1488)Bronchiolitis pneumonia 7\GLEVEGXIVMWXMGFVEWW]GSYKL[LII^MRKVIWTMVEXSV]HMWXVIWWQE]QMQMGEWXLQE 7IEWSR[MRXIVWEQIEWYWIEWSR 4EWWMZIMQQYRM^EXMSR[MXL4EPMZM^YQEFQSRSGPSREP67:MQQYRSKPSFYPMRQSRXLP]HYVMRKXLI[MRXIV
months in premature infants or infants with chronic lung diseaseRx:
- Albuterol or racemic epinephrine - Supplemental oxygen as needed - Steroids are not used (ineffective unless coexisting asthma) - 6MFEZMVMRMWRSXKIRIVEPP]YWIHMRGLMPHVIRYRTVSZIRIJGEG]MRGLMPHVIR%%4VIGSQQIRHWEKEMRWXXLI
use of ribavirin for RSV) - Ribavirin may be used in adults especially if RSV develops after a bone marrow transplant
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sEND OF SESSION QUIZ14. Which antiviral(s) matches the following statement?
4VSTL]PE\MWJSVMRYIR^E% Inhibits CMV DNA polymeraseUsed in treatment for chronic hepatitis C First-line for HSV or EBVBlocks viral penetration and uncoating 8VIEXWFSXLMRYIR^E%ERH& Second-line for CMV retinitisDerivative of amantadine with fewer side effects Inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase
15. Which RNA virus matches the following statement?Characteristic barking seal coughAfrican hemorrhagic feverChildhood diarrhea in winter monthsAsthma-sounding infection in infants (esp. premies)
;LEXZMVYW62%SV(2%XWXLIJSPPS[MRKWXEXIQIRX#*%T (FA12 p183-194)Can cause conjunctivitis or diarrhea *IZIVNEYRHMGIFPEGOZSQMXEnlarged cell with owls eye inclusions -HIRXMIH[MXLE4ETWQIEVBarking seal coughBrassy coughNegri bodiesHides in trigeminal gangliaDiarrhea in children during winter months2 most common causes of common coldDowney cellsAseptic meningitis
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PARASYMPATHETIC ACTIVATIONGG: Chapters 8-10Phys: Chapter 60
Central and peripheral nervous system (FA11 p235) (FA12 p262)Effects of parasympathetic activation (GG p179-181, Table 8-1) (Phys p734-736, Table 60-2)Cholinergic agonists (FA11 p238) (FA12 p265) (GG p222)Alzheimer anticholinesterases (GG p252)Myasthenia gravis (FA11 p386) (FA12 p422) (GG p251)Cholinesterase inhibitor poisoning and pralidoxime (FA11 p238) (FA12 p265) (GG p247-249)
4. How do the sympathetic and parasympathetic nervous systems affect the following body structures?
Sympathetic Parasympathetic
Heart
Eye
Salivary glands
Bronchiolar smooth muscle
Bladder
Male GU
GI tract
5. What are the symptoms of excess parasympathetic activity? (FA11 p238) (FA12 p265)
PHA
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3 QUESTION WARM-UP ;LMGLGSPPEKIRMWX]TMGEPP]HIGMIRXMR)LPIVW(ERPSWW]RHVSQI#-RSWXISKIRIWMW
imperfecta? (FA11 p80) (FA12 p83)
2. What regulates the progression of G1 phase of the cell cycle to S phase? (FA11 p76) (FA12 p 79)
3. What cranial nerves innervate the tongue in the following ways? (FA11 p129) (FA12 p137)Taste in the anterior 2/3Taste in posterior 1/3 (main innervater)Motor Sensation in the anterior 2/3 Sensation in the posterior 1/3
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6. Alzheimer disease anticholinesterases(SRITI^MPGalantamineRivastigmine
7. Myasthenia Gravis (FA11 p386) (FA12 p422)Antibodies to the acetylcholine receptorMost common board question presentation: that worsens throughout the dayTensilon testThymus pathology:
50% associated with thymic 20% associated with thymic 15% associated with thymic
Myasthenic crisis rapidly progressing weakness esp. in musclesRx: , , ,
QUICK QUIZ8. What drug regenerates acetylcholinesterases after organophosphate poisoning?
(FA11 p238) (FA12 p265)
9. What is the antidote for organophosphate poisoning? (FA11 p238) (FA12 p265)
10. Which anticholinesterases are used in the treatment of Alzheimer disease?
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PARASYMPATHETIC INHIBITION GG: Chapters 9, 11
Anticholinergics (FA11 p239) (FA12 p266) (GG p225) Atropine (FA11 p239) (FA12 p266) Muscarinic antagonists (FA11 p239) (FA12 p266) Urge incontinence treatment (GG p231, p232 Table 9-3)
Contraindications to anticholinergics (GG p234)Other drugs with anticholinergic side effectsNicotinic acetylcholine receptors (GG p255)
Central and peripheral nervous system (FA11 p235) (FA12 p262) ACh receptors (FA11 p235) (FA12 p262)
Hexamethonium (FA11 p239) (GG p272)
11. What are the symptoms of inhibiting parasympathetic activity? (FA11 p239) (FA12 p266)
12. What drugs inhibit parasympathetic activity? What are their uses? (FA11 p239) (FA12 p266)
13. What anticholinergics are used in the treatment of urge type urinary incontinence?OxybutyninTolterodine(EVMJIREGMRERHWSPMJIREGMRTrospium
14. In what patient populations is atropine contraindicated? (FA11 p239) (FA12 p266)
15. What other medications have anticholinergic side effects? First generation H1 blockers: diphenhydramine (Benadryl), doxylamine (Unisom), chlorpheniramineTraditional neuroleptics (FA11 p453) (FA12 p498)Tricyclic antidepressants (FA11 p455) (FA12 p500)Amantadine (FA11 p195) (FA12 p216)
PHA
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END OF SESSION QUIZ16. What are the symptoms of excess parasympathetic activity? (FA11 p238) (FA12 p265)
17. What are the symptoms of inhibiting parasympathetic activity? (FA11 p239) (FA12 p266)
-HIRXMJ]XLIJSPPS[MRKHVYKWEWEHMVIGXGLSPMRIVKMGEKSRMWXERXMEGIX]PGLSPMRIWXIVEWIERXMmuscarinic, or cholinesterase regenerator:PhysostigminePilocarpine EchothiophateOxybutyninAtropine(SRITI^MPPralidoximeBethanecholNeostigmine(EVMJIREGMR Ipratropium
TropicamideBenztropine ScopolamineEdrophoniumTolterodineTrospiumRivastigmineHomatropinePyridostigmine Carbachol
19. A gardener presents with shortness of breath, salivation, miosis, and diarrhea. What caused this? What is the mechanism of action?
20. Atropine is not effective in reversal of organophosphate poisoning. What drug would best help this patient?
21. Which of the muscarinic antagonists discussed could be used to improve FEV1 in a patient [MXL'34(#
%]IEVSPHWGLM^STLVIRMGQERRS[LEWYVMREV]VIXIRXMSRHYIXSLMWRIYVSPITXMG;LEXdo you treat it with?
23. In the dark, both pupils are dilated. (see image) In the light, the control pupil is miotic while the pupil given drug X remains mydriatic. What is drug X?
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3 QUESTION WARM-UP1. What are the symptoms of organophosphate poisoning? What are the symptoms of
atropine overdose? (FA11 p238-239) (FA12 p265-266)
2. What are the 3 different G proteins and what are their downstream effects? Which receptors use these G proteins? (FA11 p236) (FA12 p263)
3. What regulates prolactin secretion from the pituitary? (FA11 p290) (FA12 p317)
SYMPATHETIC AGENTSGG: Chapter 12
Sympathomimetics (FA11 p240) (FA12 p266-267) (GG p277)Sympathoplegics (FA11 p241) (FA12 p267) (GG p295)
4. Label the following spinal cord representation seen at levels T1 L3
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QUICK QUIZ5. Which receptors are stimulated by the following sympathomimetics? (FA11 p240-241)
(FA12 p266-267)ClonidineDopaminePhenylephrineAlbuterolNorepinephrine IsoproterenolEpinephrineDobutamineTerbutaline
6. Which sympathomimetic matches the following statement? (FA11 p240) (FA12 p266-267)Given as a nebulizer for asthmaDrug of choice for anaphylaxis1SWXGSQQSRVWXPMRIEKIRXJSVTEXMIRXWMRGEVHMSKIRMGWLSGO1SWXGSQQSRVWXPMRIEKIRXJSVTEXMIRXWMRWITXMGWLSGOGiven subQ for asthmaUsed by ENT to vasoconstrict nasal vesselsUsed to treat ADHD
;LEXHVYKW[SYPHFIQSWXETTVSTVMEXIMRETEXMIRXMRWLSGOFIGEYWIXLI]QEMRXEMRVIREPFPSSHS[#
SYMPATHETIC BLOCKERSGG: Chapter 12
Alpha-blockers (FA11 p241) (FA12 p268) (GG p304)Beta-blockers (FA11 p242) (FA12 p269) (GG p310)
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PHA
RM
BA
SIC
S 3
Sy
mpa
thet
ics
END OF SESSION QUIZ8. How does blood pressure response to phenylephrine administration change if an
FPSGOIVMWEHQMRMWXIVIHFIJSVILERH#;L]MWXLMWHMJJIVIRXXLERXLIGLERKIWIIR[LIRepinephrine is used rather than phenylephrine? (FA11 p241) (FA12 p268)
9. What are the common side effects of FPSGOIVW#;LMGLTEXMIRXTSTYPEXMSRWWLSYPHYWIGEYXMSR[LIRXEOMRKFPSGOIVW#*%T*%T
10. What are the various clinical uses for the following sympathomimetics? (FA11 p240) (FA12 p266-267)DopamineClonidineAmphetamineTerbutalineEpinephrine
;LEXEVIXLIZEVMSYWGPMRMGEPETTPMGEXMSRWSJFIXEFPSGOIVW#*%T*%T
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 1
Upper Extremity Axilla and Brachial Plexus
Before beginning this video lecture, review the following structures in your anatomy atlas. The Lippincott Williams & Wilkins Atlas of Anatomy plate references are given for comparable reference.
2-15, 2-09, 2-53 2-14 Blood Vessels Thoracoacromial artery Anterior circumflex humeral artery Posterior circumflex humeral artery Subscapular artery Circumflex scapular artery Brachial artery Thoracodorsal artery Subclavian artery Superior thoracic artery Axillary vein Brachial vein Cephalic vein
Nerves Dorsal scapular nerve Suprascapular nerve Nerve to the subclavius muscle Medial pectoral nerve Medial brachial cutaneous nerve Medial antebrachial cutaneous nerve Lateral pectoral nerve Upper subscapular nerve Thoracodorsal nerve Lower subscapular nerve Ulnar nerve Radial nerve Musculocutaneous Axillary Median nerve
Borders of the Axilla 1. What structures make up the following borders of the axilla?
Posterior Subscapularis muscle, teres major, latissimus dorsi
Medial Serratus anterior, 1st-4thribs and the associated intercostal muscles
Lateral
Anterior Pectoralis major, pectoralis minor
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 2
Blood Supply
2. When does the subclavian artery become the axillary artery?
3. When does the axillary artery become the brachial artery?
4. What are the 6 branches of the axillary artery? Clinical Correlation 5. What is the arrangement of the axillary lymph nodes?
6. What is the common side effect that can occur after removing the axillary lymph nodes?
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 3
Brachial Plexus
7. What ventral rami form the brachial plexus?
8. Label the divisions of the brachial plexus:
9. What is the name of the structure that enters the axilla through the cervicoaxillary canal bound to the axillary
blood vessels?
10. What is the mnemonic used for the branches of the posterior cord? U and L
T R
A
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 4
Clinical Correlation
11. Label the following diagram of the brachial plexus:
1. 2. 3. 4. 5. 6.
7. 8. 9. 10. 11.
12. What type of palsy is caused by an injury to the superior part of the brachial plexus, and what is the associated clinical picture?
13. What type of palsy is caused by an injury to the inferior part of the brachial plexus, and what is the associated clinical picture?
Dr.KuriMC
Dr.KuriLP
Dr.KuriRADIAL
Dr.KuriTD
Dr.Kuri
Dr.Kuri -
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 5
End of Session Quiz 1. What are the 6 branches of the axillary artery?
2. What are the branches of the subscapular artery?
3. What are the 3 branches of the lateral cord of the brachial plexus? 4. What are the 5 branches of the medial cord of the brachial plexus?
5. What are the 5 branches of the posterior cord of the brachial plexus?
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Copyright 2012, Doctors In Training.com LLC. All rights reserved. Images from Lippincott Williams & Wilkins Atlas of Anatomy
Solid Anatomy 2008 Wolters Kluwer Health, Inc. All rights reserved. 6
Mock Practical
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[ 33 ]Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
NEU
RO 9 Basal G
anglia
BASAL GANGLIA AND HYPOKINESISPhys: Chapter 56H: Chapter 372
Basal ganglia (FA11 p400) (FA12 p438) (Phys p690)Parkinson disease (FA11 p401) (FA12 p438) (R p1319) (Phys p693) (H p3317)Parkinson medications
- Parkinson disease drugs (FA11 p435) (FA12 p478) (H p3321) (GG p614) - L-dopa (levodopa)-carbidopa (FA11 p435) (FA12 p478) (H p3321) (GG p614) - Selegiline (FA11 p436) (FA12 p478) (GG p618)
(MJJIVIRXMEPHMEKRSWMWSJL]TSVII\ME
4. Basal Ganglia
3 QUESTION WARM-UP1. What is the rate-limiting step in heme synthesis? (FA11 p354) (FA12 p386)
2. What is the structure of HbH? What disease results in HbH production? What is the structure of Hb Barts? What disease results in Hb Barts production? (FA11 p349) (FA12 p380)
3. What excitatory neurotransmitter is involved in pain?
-
[ 34 ] Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
NEU
RO 9
B
asal
Gan
glia
HYPERKINESISR: Chapter 28H: Chapter 372
Hemiballismus (FA11 p401) (FA12 p439) (H p3332)Huntington disease (FA11 p401) (FA12 p439) (R p1322) (H p3330)Huntington drugs (FA11 p436) (FA12 p479) (GG p622)Types of hyperkinesis and dyskinesis
- Chorea (FA11 p401) (FA12 p439) - Athetosis (FA11 p401) (FA12 p439) - Myoclonus (FA11 p401) (FA12 p439) - Dystonia (FA11 p401) (FA12 p439) (H p3328)
(MJJIVIRXMEPHMEKRSWMWSJL]TIVVII\ME
QUICK QUIZ5. What are the cardinal features of Parkinson disease? (FA11 p401) (FA12 p438)
6. 28-year-old chemist presents with MPTP exposure. What neurotransmitter is depleted?
7. How do the following structures normally impact movement: globus pallidus internal segment, subthalamic nucleus, and substantia nigra pars compacta?
END OF SESSION QUIZ8. A man in his 40s begins to develop early dementia and uncontrollable movements of his
upper extremities. In what portion of the brain do you expect to see atrophy?
%QEPITEXMIRXTVIWIRXW[MXLMRZSPYRXEV]EMPMRKSJSRIEVQ;LIVIMWXLIPIWMSR#
10. What are the Cs of Huntington disease? (FA11 p401) (FA12 p439)
11. What neurotransmitters are altered in Huntington disease? (FA11 p401) (FA12 p439)
-
[ 21 ]Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
3 QUESTION WARM-UP ;LEXMWXLIVIWYPXSJEKP]GSP]XMGIR^]QIHIGMIRG]#*%T*%T;LEXMWXLI
VIWYPXSJEHIGMIRG]MRT]VYZEXIHIL]HVSKIREWI#*%T*%T
;LMGLWYFWXERGIWWIVZIEWGLIQSXEGXMGEKIRXWJSVPIYOSG]XIW#*%T*%T
;LMGLGVERMEPRIVZIWMRRIVZEXIQYWGPIWHIVMZIHJVSQXLIFVERGLMEPEVGLIW# *%T*%T
QUICK QUIZ -HIRXMJ]XLILITEXMXMW&WXEXYWSJXLIJSPPS[MRKTEXMIRXWFEWIHSRXLIMVLITEXMXMW&WIVSPSKMG
QEVOIVWHepBsAg HepBsAb HepBcAb Status2IKEXMZI 4SWMXMZI 4SWMXMZI2IKEXMZI 2IKEXMZI 4SWMXMZI4SWMXMZI 2IKEXMZI 4SWMXMZI-K14SWMXMZI 2IKEXMZI 4SWMXMZI-K+2IKEXMZI 4SWMXMZI 2IKEXMZI
;LEXQIHMGEXMSRWEVIYWIHMRXLIXVIEXQIRXSJGLVSRMGLITEXMXMW&ERH'#*%T*%T*%T*%T
;LMGLERXMFSHMIWGERFIYWIHXSLIPTQEOIXLIHMEKRSWMWSJEYXSMQQYRILITEXMXMW#
+-0MZIV4EXLSPSK]
HEPATITISR: Chapter 18H: Chapters 304-306
Viral Hepatitis (FA11 p171) (FA12 p190)Hepatitis serologic markers (FA11 p172) (FA12 p191)Autoimmune hepatitis Protozoal liver disease
- Entamoeba histolytica (FA11 p160) (FA12 p175) - Leishmania donovani (FA11 p161) (FA12 p177)
%YXSMQQYRI,ITEXMXMW%2%%RXMWQSSXLQYWGPIERXMFSH]%RXMPMZIVOMHRI]QMGVSWSQEPERXMFSH]%RXMQMXSGLSRHVMEPERXMFSH]
-
[ 22 ] Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
+-
0MZI
V4EXLS
PSK]
END OF SESSION QUIZ %]SYRKQERTVIWIRXW[MXLEXE\MEERHXVIQSVW,ILEWFVS[RTMKQIRXEXMSRMREVMRK
EVSYRHXLITIVMTLIV]SJLMWGSVRIE;LEXXVIEXQIRXWLSYPHLIVIGIMZI#
%R]IEVSPH[SQERGSQIWXS]SYVGPMRMGFIGEYWILIVJEQMP]MWGSRGIVRIHEFSYXLIV]IPPS[MRKWOMR)\EQVIZIEPW]IPPS[MRKSJXLIWOMRMRGPYHMRKXLITEPQWERHWSPIWFYXRSWGPIVEPMGXIVYW;LEXUYIWXMSRGSYPH]SYXSEWOXLITEXMIRXXLEX[SYPHQSWXPMOIP]MHIRXMJ]XLIGEYWISJ]IPPS[MRK#
;LEXMWXLIYRHIVP]MRKTVSFPIQMR;MPWSRHMWIEWI#;LEXEVIXLIGLEVEGXIVMWXMGWSJ;MPWSRHMWIEWI#;LEXMWXLIXVIEXQIRXJSV;MPWSRHMWIEWI#*%T*%T
;LEXMWXLIGPEWWMGXVMEHSJW]QTXSQWMRLIQSGLVSQEXSWMW#;LEXPEFXIWXWEVIYWIHXSHMEKRSWILIQSGLVSQEXSWMW#;LEXMWXLIXVIEXQIRXJSVLIQSGLVSQEXSWMW#*%T*%T
;LEXEVIXLIVMWOJEGXSVWJSVXLIHIZIPSTQIRXSJLITEXSGIPPYPEVGEVGMRSQE#*%T*%T
ADDITIONAL LIVER DISEASESH: Chapters 92, 309
Wilson disease (FA11 p333) (FA12 p364)Hemochromatosis (FA11 p334) (FA12 p364)1%RXMXV]TWMRHIGMIRG]*%T*%TLiver tumors
- Hepatic adenoma - Hepatic angiosarcoma - Hepatocellular carcinoma (FA11 p331) (FA12 p361)
,ITEXMG%HIRSQE1SWXSJXIRMRJIQEPIW3'4]IEVW 6MWO*EGXSVW3'4YWIEREFSPMGWXIVSMHWKP]GSKIRWXSVEKIHMWIEWIX]TIW-ERH--- 7\695TEMRFYXYWYEPP]XLIVIEVIRSW]QTXSQWFIGEYWIMXMWSJXIRERMRGMHIRXEPRHMRKSRMQEKMRK1EPMKRERXXVERWJSVQEXMSRMRSJTEXMIRXW 6\('XLI3'4WIVMEPMQEKMRKERH%*4VIWIGXMSRIWTMJ"GQ
,ITEXMG%RKMSWEVGSQE1EPMKRERXIRHSXLIPMEPRISTPEWQMRPMZIV6MWO*EGXSVWZMR]PGLPSVMHIEVWIRMG
-
[ 10 ] Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
END
OC
RIN
E 4
Pa
ncre
as
ENDOCRINE PANCREAS AND DMPhys: Chapter 78H: Chapter 344
Endocrine pancreas cell types (FA11 p289) (FA12 p315) (R p1130) (Phys p939)Glucagon (FA12 p316) (R p1132) (Phys p947)Insulin (FA11 p289) (FA12 p315) (Phys p939)Insulin-dependent organs (FA11 p289) (FA12 p316)Diabetes mellitus (FA11 p301) (FA12 p329) (R p1131)Sorbitol (FA11p104) (FA12 p109)Type 1 vs. type 2 DM (FA11 p301) (FA12 p330) (R p1134)
3 QUESTION WARM-UP1. What are the tumor markers for pancreatic cancer? (FA11 p336) (FA12 p367)
;LIVI[SYPH]SYI\TIGXXSRH&GIPPWERH8GIPPWMRXLIWTPIIR#-RXLIP]QTLRSHIW#*%p200) (FA12 p222)
3. What drug category has the following ending? (FA11 p247) (FA12 p274) -ane -azine -tidine -tropin -chol -bendazole
QUICK QUIZ4. How is hemoglobin glycosylated in DM to form HgbA1c?
;LMGLX]TISJHMEFIXIWQIPPMXYWXWXLIJSPPS[MRKHIWGVMTXMSRW#*%T*%TAssociated with obesityMay cause ketoacidosis Strong genetic predispositionAssociated with HLA DR3 & DR4
-R[LMGLXMWWYIW[MPP]SYRH+098VIGITXSVW#*%T*%T
;LMGLXMWWYIWHITIRHSRMRWYPMRJSVKPYGSWIYTXEOI#*%T*%T
;LMGLXMWWYIWEVIEPPS[IHXSYTXEOIKPYGSWIIZIRMRXLIEFWIRGISJMRWYPMRFIGEYWIXLI]YWIE+098VIGITXSV#*%T*%T
-azepam -conazole -triptyline -zosin -stigmine -dipine
-
[ 11 ]Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
END
OC
RIN
E 4 PancreasDKA AND DM MEDICATIONSH: Chapter 344GG: Chapter 43
Diabetic ketoacidosis (FA11 p302) (FA12 p330) (H p2976)Diabetes drugs (FA11 p304) (FA12 p333) (GG p1248, 1255) (H p2996)
'SQQSRGEYWIWSJ(/%(Almost always related to a state of excess glucagon, catecholamines, or corticosteroids)
-RJIGXMSRTRIYQSRMEKEWXVSIRXIVMXMW98-Diabetic medication reduction or omission 7IZIVIQIHMGEPMPPRIWW1-':%XVEYQE9RHMEKRSWIH(1DehydrationAlcohol or drug abuse (especially stimulants)Corticosteroids
10. Newer DM Agents 7MXEKPMTXMR.ERYZMEERH7E\EKPMTXMR3RKP]^E
- -RLMFMXSVWSJHMTITXMH]PTITXMHEWI-:(44-:[LMGLEJJIGXWKPYGEKSRPMOITITXMHI+04EQSRKother hormones
- Prolongs incretin actions, which decreases glucagon secretion and increases insulin secretion, delays gastric emptying
)\IREXMHI&]IXXEERH0MVEKPYXMHI:MGXS^E - )\IREXMHIMWEREREPSKSJI\IRHMRELSVQSRIHIVMZIHJVSQ+MPEQSRWXIVWEPMZE[MXLEGXMSRWWMQMPEVXS+04
- 0MVEKPYXMHIMWEW]RXLIXMGEREPSKSJLYQER+04 - Mimic the actions of incretins, which decrease glucagon secretion and increase insulin secretion, delay
gastric emptying. - 2SXETTVSZIHJSVYWI[LMPISRMRWYPMRXLIVET] - SE: possibly increased risk of acute pancreatitis.
Pramlintide (Symlin) - Amylin analog, normally secreted with insulin, decreases glucagon secretion and gastric emptying - 9WIHSRP]MRTEXMIRXWXEOMRKMRWYPMRFYXMRIMXLIVX]TISVX]TI(1TEXMIRXW
-
[ 12 ] Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
END
OC
RIN
E 4
Pa
ncre
asEND OF SESSION QUIZ11. Which of the oral agents used in the control of type II diabetes has the following
characteristics? (FA11 p304) (FA12 p333)
Lactic acidosis is a rare but worrisome side effectMost common side effect is hypoglycemiaOften used in combination with any of the other oral agents%PWSLIPTPS[IVXVMKP]GIVMHIWERH0(0GLSPIWXIVSPPIZIPWNot safe in settings of hepatic dysfunction or CHF7LSYPHRSXFIYWIHMRTEXMIRXW[MXLIPIZEXIHWIVYQGVIEXMRMRI7LSYPHRSXFIYWIHMRTEXMIRXW[MXLPMZIVGMVVLSWMWIPIZEXIHWIVYQGVIEXMRMRISVMREQQEXSV]FS[IPHMWIEWI,ITEXMGWIVYQXVERWEQMREWIPIZIPWWLSYPHFIGEVIJYPP]monitored when using these agents2SXEWWSGMEXIH[MXL[IMKLXKEMRSJXIRYWIHMRSZIV[IMKLXdiabetics1IXEFSPM^IHF]PMZIVI\GIPPIRXGLSMGIMRTEXMIRXW[MXLVIREPdisease
Primarily effects postprandial hyperglycemia
13%GPSWIW/GLERRIPSR cells depolarization 'EMRY\ insulin releaseMOA: inhibits -glucosidase at intestinal brush borderMOA: agonist at PPAR receptors MQTVSZIHXEVKIXGIPPresponse to insulin
%]IEVSPHQEPIGSQIWXSXLIIQIVKIRG]VSSQJSVXLIXVIEXQIRXSJ(/% ,MWX]TIHMEFIXIWMWRSVQEPP][IPPGSRXVSPPIHERHLIHSIWRXORS[[L]LMW(/%HIZIPSTIHXLMWXMQI;LEXMWXLIHMJJIVIRXMEPHMEKRSWMWJSVXLIHIZIPSTQIRXSJLMW(/%#(FA11 p302) (FA12 p330)
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-1
27 - Estrogens and Hormone Replacement Therapy (HRT) Estrogen Basics
1. What are the three different physiologic estrogens and where are they produced?
x (E1) produced by peripheral conversion x (E2) produced by x (E3) produced by placenta
2. What enzyme is essential for the generation of estrogen?
3. Pause the video and complete the following chart:
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-2
4. Complete the following hypothalamic-pituitary-gonadal (ovary) axis diagram.
5. How do the hypothalamus and anterior pituitary regulate estrogen production? 6. What is the action of estrogens at the nuclear receptor?
Alter RNA and protein synthesis Direct intracellular
7. What are the effects of estrogen?
Female sexual maturation breast and female fat distribution
Genital development growth development Feedback inhibition of LH and FSH
Maintains healthy skin and teeth Maintains bone strength Maintains blood vessels Improves cholesterol lower LDL and higher
HDL
Estrogens
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-3
8. Outline the general hormone sequence of the female reproductive cycle.
FSH o Follicle maturation o Production of estradiol o Production of LH surge o Ovulation o Corpus luteum o Progesterone (with Estradiol) o Maintenance of endometrial lining & inhibition of FSH and LH production o Decline of corpus luteum o Shedding of endometrial lining (No production of estradiol and progesterone) o Loss of FSH inhibition o Increase in FSH o (repeat step 1)
9. What are some of the common uses of estrogen?
Hypogonadism Contraception Hormone replacement therapy
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-4
Estrogen Supplementation 10.What were the first natural estrogens? 11.What are examples of two synthetic estrogens? 12.How are synthetic estrogens an improvement upon equine estrogen?
They are synthetically altered to decrease first-pass metabolism which results in a longer and increase (lower dose is required).
13.What are methods of exogenous estrogen delivery?
Pills Creams Gels
Foams Transdermal patches
14.What disadvantage does oral estrogen administration have over other routes of administration?
Detrimental effects of stimulating the
-
Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-5
Quick Review 1
1. Which hormones are made by the aromatase enzyme?
2. How do the effects of estrogen relate to its therapeutic uses?
Effects of Estrogen Common uses for estrogen Female sexual maturation and genital development
Endometrial lining growth and follicle development
Feedback inhibition of LH and FSH
Maintains healthy skin and teeth
Maintains bone strength
Maintains blood vessels
Improves cholesterol Higher HDL and lower LDL
3. What are some of the more testable causes of hypogonadism?
Hypergonadotropic (high LH and high FSH) = ovarian dysfunction Hypogonadotropic (low LH, low FSH) = hypothalamic or pituitary dysfunction
4. What stimulates the ovarian follicle to produce estradiol? 5. What effect do high levels of estrogen and progesterone have on LH and FSH? 6. Which is a more potent manner to dose estrogen: oral pill or transdermal patch? 7. What is the relationship between estrogen, progesterone, OCPs, and HRT?
OCPs: estrogen and progesterone HRT: estrogen
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-6
Menopause and HRT 1. What is the average age of menopause?
2. What are the classic signs and symptoms of menopause? Sleep disturbance Urogenital
- Dyspareunia - UTIs - Urinary
Skin and teeth changes
loss Osteoporosis Lipid changes
- total cholesterol - -
Loss of 3. What are the benefits of hormone replacement therapy in postmenopausal women?
Helps Helps sleep Helps Helps urinary incontinence Helps symptoms
4. What is the most influential study to date that has elucidated the effects of postmenopausal hormone replacement therapy?
5. What did the WHI teach us about the dosage, timing, and indication of hormone replacement therapy? Dosage prescribe the dose needed to treat symptoms Timing start right away and stop Indication best for and
6. What are some of the non-estrogen treatments for menopausal vasomotor symptoms (hot flashes)?
- Venlafaxine - Desvenlafaxine
Clonidine Gabapentin
7. What are the common methods of administering estrogen hormone replacement? 8. In a woman with urogenital atrophy, what is the preferred method of dosing hormone replacement?
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-7
9. What problems can arise when giving postmenopausal estrogen replacement without coadministration of
progesterone (AKA unopposed estrogen)? Unopposed estrogen
10.What are some of the adverse effects of estrogen replacement? Strokes and heart disease Endometrial cancer Breast cancer
11.Which populations are at higher risk of venous thromboembolism including deep venous thrombosis (DVT)
and pulmonary embolism when prescribed estrogen? Those with hereditary Smokers Increase in risk after age
12.What are the absolute contraindications to estrogen?
Severe cardiac disease Stroke History of blood clots Smokers over age 35 endometrial
or breast cancer
Liver cancer Known >5 years after menopause Migraines with Undiagnosed uterine bleeding
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-8
Quick Review #2
1. What is the precursor pathology to uterine cancer?
2. What is the biggest risk factor for uterine cancer? Polycystic ovarian syndrome (PCOS) Obesity Sertoli-Leydig cell tumor of the ovary HRT
3. What are the most common hereditary thrombophilias that can increase ones risk for DVT and PE when
estrogen is given? mutation Prothrombin gene mutation Protein C Deficiency/Protein S Deficiency Antithrombin deficiency
4. Is hormone replacement therapy contraindicated in smokers over age 35?
5. A 55-year-old female comes to her physician to discuss menopause because all of her friends are complaining about it. She is not having menopausal symptoms and is still having monthly cycles. She continues to take the combination oral contraception pill that she has taken since age 35. What would the physician do for this patient? She should be switched More conservative option: and determine if she has any uncomfortable
menopausal symptoms that would necessitate HRT
6. How should the clinical use of OCPs and HRT be adjusted with respect to breast cancer risk? Do not use OCPs in patients with HRT may the risk of invasive breast cancer but does not increase the risk of
noninvasive breast cancer Do not use HRT in a patient with
7. A 50-year-old female comes to the clinic for treatment of menopausal symptoms. During the history she states she has been having some vaginal spotting about every 2 weeks for the last few months. What work-up needs to be done prior to being prescribed HRT?
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-9
Selective Estrogen-Receptor Modulators (SERMs) 1. Complete and study the following table of selective estrogen-receptor modulators. (LP p302-303)
SERM MECHANISM OF ACTION THERAPEUTIC USE ADVERSE EFFECT Tamoxifen Antagonist in
Partial agonist in uterine tissue
Estrogen-receptor positive breast cancer
Nausea Abnormal bleeding
Toremifene
Antagonist in breast tissue Estrogen receptor-positive breast cancer
Cannot use for tamoxifen-resistant breast cancer
Same as tamoxifen
Raloxifene
in bone Antagonist in breast tissue
Restricted to osteoporosis Hot flashes Joint pain Nausea
Clomiphene
Partial agonist in
Ovulation induction Nausea Headache Hot flashes
Other Anti-Estrogen Drugs 2. What medication is a pure estrogen-receptor antagonist that is used in the treatment of breast cancer that
have developed resistance to tamoxifen?
3. What medications inhibit the aromatase enzyme and what are the uses of these medications? x Reversible , letrozole x Irreversible -
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-10
GnRH Agonists 4. How does hypothalamic GnRH secretion cause different effects than continuous administration of a GnRH
agonist? Hypothalamus secretes GnRH in a manner and the pituitary secretes FSH
and LH Continuous administration leads to a drop in estrogen to levels
5. What are the different GnRH agonists? 6. In a premenopausal woman taking leuprolide, if the side effects of the medication become problematic, what
can be given to provide relief? 7. What are the therapeutic uses for GnRH agonists such as leuprolide?
Fibroids Endometriosis cancer Prostate cancer
-
Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-11
Quick Review 3
1. A 40-year-old black female with menorrhagia due to uterine fibroids is placed on leuprolide. She comes to the
clinic complaining of severe hot flashes. What is the treatment for this patient?
2. A 72-year-old thin, white female is being treated with a bisphosphonate and raloxifene. What is she at increased risk for because of the raloxifene?
3. In treating a female for osteoporosis with an estrogenic agent, what are the advantages of using raloxifene rather than conjugated estrogen? Reduces the risk of cancer Raloxifene will not increase the risk of cancer
4. What is the drug of choice for infertility treatment due to anovulatory cycles?
5. How exactly does clomiphene work? Partial estrogen agonist at the Results in negative feedback inhibition by endogenous estrogen
6. A 40-year-old female undergoes surgery for the resection of breast cancer. Pathologic analysis of the tumor reveals that is an estrogen-receptor positive tumor. What medication will this patient probably have to take?
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Solid Pharmacology Copyright 2010, Doctors In Training.com LLC, All Rights Reserved 27-12
End of Session Quiz 1. Why is a patients past surgical history an important consideration when determining post-menopausal
hormone replacement therapy needs? (LP p301)
2. For what duration is tamoxifen dosing limited due to increased risk of uterine cancer? (LP p302)
3. What SERM used to prevent breast cancer may not increase the risk of endometrial cancer? (LP p302) 4. What enzyme is essential for the generation of estrogen?
5. What is the therapeutic use of each of the following agents?
Drug Therapeutic use Leuprolide
Clomiphene
Tamoxifen
Ethinyl estradiol
6. What are the signs and symptoms that HRT aims to alleviate? (LP p300-301) 7. What are the adverse effects associated with estrogen therapy? (LP p301-302)
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8. Which drugs are classified as selective estrogen-receptor modulators? How do they work? (LP p302-303)
SERM Mechanism of action Tamoxifen
Raloxifene
Toremifene
Clomiphene
9. What changes are seen in serum estrogen, LH, and FSH after the onset of menopause? 10.How does the body synthesize estradiol from cholesterol?
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BIOC
HEM
6 - HM
P Shunt and Other Sugars
3 QUESTION WARM-UP1. What are the features of Plummer-Vinson syndrome? (FA11 p322) (FA12 p351)
2. Explain why methanol is such a toxic substance. (FA11 p246) (FA12 p100, 270)
3. A woman commonly develops intense muscle cramps and darkening of her urine after exercise. What is her diagnosis?
QUICK QUIZ4. What is the rate-limiting step of the pentose phosphate pathway? (FA11 p95) (FA12 p101)
5. Which tissues of the body use the pentose phosphate pathway? (FA11 p102) (FA12 p107)
)\TPEMR[L]EHIGMIRG]SJXLIIR^]QIXLEXMWXLIVEXIPMQMXIVJSVXLI,14WLYRXGERresult in hemolytic anemia? (FA11 p102) (FA12 p107)
HMP SHUNTPhys: Chapter 67
HMP shunt (pentose phosphate pathway) (FA11 p101) (FA12 p107) (Phys 816)Respiratory burst (oxidative burst) (FA11 p102) (FA12 p107)+PYGSWITLSWTLEXIHIL]HVSKIREWIHIGMIRG]*%T*%T
FRUCTOSE, GALACTOSE, AND LACTOSEPhys: Chapter 67, 84
Disorders of fructose metabolism (FA11 p103) (FA12 p108)Disorders of galactose metabolism (FA11 p103) (FA12 p108)0EGXEWIHIGMIRG]*%T*%T6TLactate (Phys p1033)
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BIO
CH
EM 6
- H
MP
Shun
t an
d O
ther
Sug
ars
END OF SESSION QUIZ7. What are the symptoms of classic galactosemia? (FA11 p103) (FA12 p109)
;LEXIR^]QIGSRZIVXWKPYGSWIXSWSVFMXSP#*%T*%T
;LEXHMWSVHIVMWGEYWIHF]EHIGMIRG]SJXLIJSPPS[MRKIR^]QI# (FA11 p103) (FA12 p108, 109)GalactokinaseAldolase B LactaseGalactose-1-phosphate uridyltransferase Fructokinase
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CA
RD
IOVA
SCU
LAR
7 - Heart M
urmurs
3 QUESTION WARM-UP1. What protozoal/helminth matches the following statement?
(FA11 p160-163) (FA12 p175-176) (R p336) 'SRXVEGXIHF]IEXMRKYRHIVGSSOIHWLERHGEYWIWERMREQQEXMSRSJXLIFMPMEV]XVEGXMost common protozoal infection in USCause of Chagas diseaseMost common helminthic infection in the US Snail host, swimmers itchDiarrhea in campers and hikersTransmitted in raw meat or infected cat feces
2. What effect does stress have on adipocytes? (Phys p929)
3. What are the 4 obligate aerobic bacteria? (FA11 p138) (FA12 p149)
SYSTOLIC MURMURSH: Chapter 227Phys: Chapter 23
Auscultation of the heart (FA11 p258) (FA12 p284) (Phys p265, Fig. 23-2, 23-3)Heart murmurs (FA11 p259) (FA12 p285) (Phys p267)
4. What heart sounds are considered benign when there is no evidence of disease? Split S1 Split S2 on inspiration S3 heart sound in a patient
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CA
RD
IOVA
SCU
LAR
7 -
Hea
rt M
urm
urs
DIASTOLIC MURMURS H: Chapter 227Phys: Chapter 23
Heart murmurs (FA11 p259) (FA12 p285) (H p1828)
QUICK QUIZ6. Which heart murmur is associated with weak pulses? (FA11 p259) (FA12 p285)
7. What are the systolic heart murmurs? (FA11 p259) (FA12 p285)
8. What are the most common causes of aortic stenosis?
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END OF SESSION QUIZ9. What defect is associated with the following type of murmur?
Crescendo-decrescendo systolic murmur best heard in the 2nd-3rd right interspace close to the sternum
Early diastolic decrescendo murmur heard best along the left side of the sternum
Late diastolic decrescendo murmur heard best along the left side of the sternum
Pansystolic (AKA holosystolic or uniform) murmur best heard at the apex and often radiates to the left axilla
Late systolic murmur usually preceded by a mid-systolic click
Crescendo-decrescendo systolic murmur best heard in the 2nd-3rd left interspaces close to the sternum
Pansystolic (AKA holosystolic or uniform) murmur best heard along the left lower sternal border and generally radiates to the right lower sternal border
Rumbling late diastolic murmur with an opening snap
Continuous machine-like murmur (in systole and diastole)
High-pitched diastolic murmur associated with a widened pulse pressure
10. Know the classic descriptions of heart murmurs. What is the murmur heard best in left lateral decubitus position?
11. An 80-year-old man presents with a systolic crescendo-decrescendo murmur. What is the most likely cause?
CA
RD
IOVA
SCU
LAR
7 - Heart M
urmurs
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17 - Heart Failure Drugs
Physiology of CHF 1. What is the most common type of cardiomyopathy? (LP p183) 2. What other diseases can cause congestive heart failure? (LP p183)
Viral heart disease Hypertensive heart disease
3. What are the features of left ventricular heart failure?
blood pressure Decreased tissue perfusion Decreased tolerance Cardiomegaly
4. What are the features of right ventricular heart failure? Poor Jugular venous distention (JVD) Hepatic congestion and ascites
5. What is the difference between diastolic and systolic heart failure?
Diastolic failure: impaired of the heart Systolic failure: impaired from the heart
6. Why does ventricular hypertrophy lead to diastolic heart failure? The thickened left ventricle cannot because it has lost 7. What term is used to describe a patient with depressed left ventricular ejection fraction (LVEF) but no signs or
symptoms of overt heart failure? (LP p187) heart failure
8. What two physiologic systems are activated to compensate for heart failure and contribute to cardiac
remodeling? (LP p183)
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9. What hormone do the kidneys release in response to underperfusion? (LP p187) 10.What are the two actions of angiotensin II? (LP p187)
Potent increased peripheral resistance increased afterload Increased secretion retention of Na+ and H2O increased blood
volume 11.What is the bodys response to decreased cardiac output and decreased blood pressure? (LP p186) 12.What are the two main effects of increased sympathetic activation on the cardiovascular system? (LP p186)
Peripheral 1 receptors Cardiac 1 receptors heart rate and
force of contraction 13.How do we target the compensatory mechanism in the treatment of heart failure? (LP p187)
Block Block
14.What are the microscopic and macroscopic changes associated with cardiac remodeling? (LP p183, 187)
Microscopic - of myocytes - of myocytes - Fibrosis
Macroscopic - Chambers become - Heart becomes more - - Globular heart
15.What are the goals of pharmacological intervention in heart failure? (LP p183)
Alleviate Slow disease progression Improve Reduce
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16.What are the ACC/AHA stages of heart failure (HF)?
Stage A: Patients at high risk for developing HF in the but no functional or structural disorder
Stage B: Structural heart disorder but no at any stage Stage C: Previous or current in the context of an underlying
structural heart problem, but managed with medical treatment Stage D: Advanced disease requiring , heart transplant, or palliative
care 17.What is the New York Heart Association (NYHA) Functional Classification of Heart Failure?
Class I: ; no symptoms from ordinary activities Class II: of activity; the patient is comfortable at rest or with mild
exertion Class III: Marked limitation of ; the patient is comfortable only at rest Class IV: physical activity brings on discomfort and symptoms
occur 18.List five non-pharmacological interventions in the treatment of heart failure. (LP p187)
Reduction of Reduce intake Treat (HTN, ischemic heart disease) Avoid drugs that CHF (CRT)
19.What percentage of patients do not have synchronous movement of the two sides of the left ventricle, and
thus may benefit from cardiac resynchronization therapy?
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Quick Review 1 1. What are the differences between left ventricular and right ventricular heart failure?
Left ventricular heart failure - Decreased blood pressure, tissue perfusion and exercise tolerance - - Cardiomegaly
Right ventricular heart failure - Poor oxygenation - Jugular venous distention (JVD) - Hepatic congestion and ascites -
2. Match the following abnormalities with their causes.
Jugular venous distention RV failure increase venous pressure fluid transudation Orthopnea Right heart failure increase in venous pressure Ankle, sacral edema Increase venous return in supine position exacerbates pulmonary vascular congestion Dyspnea on exertion Increase in central venous pressure increase in resistance to portal flow Hepatomegaly Failure of LV output to increase during exercise
3. What is the most likely cause of right ventricular heart failure?
4. A 63-year-old male has been diagnosed with congestive heart failure. On examination this patient shows no symptoms, no JVD or edema. His left ventricular ejection fraction is slightly low. This patient overall looks fine and as mentioned before is showing no symptoms. How would you describe what is going on with this patient?
5. A decrease in renal blood flow will cause what changes in renin, angiotensin II, and aldosterone? (LP p187)
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6. What is the New York Heart Association (NYHA) Functional Classification of heart failure? Class I: ; no symptoms from ordinary activities Class II: Slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion Class III: of any activity; the patient is comfortable only at rest Class IV: Any physical activity brings on discomfort and
7. What is cardiac resynchronization therapy (CRT)? Pacing of the and the simultaneously
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Inhibitors of the Renin-Angiotensin System Angiotensin Converting Enzyme (ACE) Inhibitors Captopril Enalapril Fosinopril Lisinopril Quinapril Ramipril 1. What two stimuli cause the juxtaglomerular cells to release renin? (LP p188)
Decreased due to low blood pressure stimulation
2. What suffix is common to the ACE inhibitors? 3. What are the actions of ACE inhibitors? (LP p188)
Decreased vascular resistance and decreased venous tone - Less angiotensin II less vasoconstriction - Diminished bradykinin inactivation more vasodilation
Lower vascular resistance Less angiotensin II less Decreased in heart failure patients
4. In what types of CHF patients might ACE inhibitors be used as monotherapy? (LP p188)
Patients with mild dyspnea and Asymptomatic patients with very low left ventricular ejection fraction (LVEF)
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7. What is the cause of ACE-induced angioedema? (LP p189) 8. What is the treatment for angioedema?
Stop the offending drug Antihistamine Steroids
Angiotensin-Receptor Blockers (ARBs) Losartan Candesartan Valsartan Telmisartan Olmesartan Irbesartan 9. What suffix is common to the ARBs? 10.What is the mechanism of action of ARBs? (LP p189)
Competitive antagonist of More complete blockade of angiotensin action than with No effect on
11.Which ARBs have clearly demonstrated efficacy in treating CHF? (LP p189)
12.Which ARB undergoes first pass hepatic metabolism to an active metabolite? (LP p189) 13.What are the adverse effects of ARBs? (LP p189)
Low risk of Hypotension Potential for angioedema Contraindicated in pregnancy
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-Blockers 14.Which two -blockers are used for CHF? (LP p190) 15.What are the actions of -blockers, in terms of treating CHF? (LP p190)
effects Reduce Reduce the intensity of cardiac contraction
16.Which patients with heart disease should not be on a -blocker? (LP p190)
Patients at high risk but who have no symptoms may show Patients in heart failure
17.What are the adverse effects of -blockers? (LP p190)
Hypotension Dizziness, lightheadedness, near-syncope
18.What side effects are seen with high doses of metoprolol, due to non-selective blockade of 2 receptors? (LP p190) Reflex peripheral Sodium retention
Diuretics 19.What three classes of diuretics are most commonly used to treat volume overload in heart failure? (LP p190)
(furosemide, torsemide, bumetanide) (hydrochlorothiazide, metolazone)
20.What are the actions of diuretics in patients with CHF? (LP p190)
Relieving Relieving
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21.What is orthopnea? 22.What is paroxysmal nocturnal dyspnea (PND)?
Shortness of breath in the , relieved gradually by to breathe
Direct Vasodilators 23.What direct vasodilators are used for CHF? (LP p190)
- Isosorbide dinitrate - Sodium nitroprusside
24.By what mechanism do nitrates cause vasodilation? (LP p190)
Nitrates are converted to nitrite, then to Nitric oxide leads smooth muscle relaxation
25.What types of vessels does hydralazine dilate? (LP p190) 26.Cardiac myocytes secrete brain natriuretic peptide (BNP) in response to what stimulus?
, due to increased blood volume 27.How is BNP used diagnostically?
High BNP is associated with 28.What is the mechanism of action of nesiritide?
Increased in smooth muscle reduces vascular tone in
29.How do vasodilators help in treating CHF? (LP p190)
Dilate veins cardiac preload by venous capacitance
Dilate arteries systemic arteriolar resistance afterload
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Quick Review 2 1. ACE inhibitors decrease circulating levels of angiotensin II. What effects are seen with a decrease in
angiotensin II? (LP p188) Output of sympathetic nervous system is Increase in of vascular smooth muscle Decrease in aldosterone production Increase in Retention of sodium and water is decreased
2. A 58-year-old male presents to your office complaining of a persistent dry cough. While getting a complete history and physical exam the patient mentions he just started on a new medication for his high blood pressure, but cant remember the name. What class of antihypertensive drugs is likely to be causing his cough? (LP p189)
3. What are some therapeutic uses for ARBs? (LP p189)
Hypertension Post-MI Patients who are intolerant of
4. What two E-blockers have been FDA approved for the treatment of congestive heart failure? (LP p190) 5. How is carvedilol different from metoprolol? (LP p190)
6. What are some adverse effects of E-blockers? Hypotension Dizziness, lightheadedness Erectile dysfunction
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7. How do diuretics help CHF? (LP p190)
Decreases decreased venous return to the heart Decreases cardiac workload and demand Decreases by reducing plasma volume decrease in blood
pressure 8. List the vessels that are dilated when using the following medications. (arteries, veins, or both)
Hydralazine Nesiritide Nitrates
9. A patient comes into the ER complaining of severe shortness of breath and palpitations. Physical exam
reveals swelling in their legs, ankles and feet. You suspect acute heart failure. What lab test should you order to help confirm your suspicion?
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Inotropic Drugs Digitalis, Digoxin Dobutamine Amirinone Milrinone 1. What is the basic action of inotropic drugs? (LP p190)
Enhance cardiac muscle contractility cardiac output Increase cytosolic concentrations
2. The force of myocardial contraction is directly related to the intracellular concentration of what ion?
(LP p184) 3. What are two basic mechanisms to remove calcium from the intracellular space? (LP p184-186)
Calcium is taken up by the ion exchanger (antiporter)
Digitalis 4. Which membrane transporter is inhibited by digitalis? (LP p191) 5. Because of its large volume of distribution, how do you start patients on digitalis? (LP p193) 6. What are the adverse effects associated with digitalis? (LP p193)
Cardiac: (bradycardia, AV block, PVCs, ventricular tachycardia/fibrillation, atrial arrhythmias)
GI: , anorexia CNS: fatigue, (altered color vision, blurred vision, scotomas, blindness)
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7. What factors predispose to digitalis toxicity? (LP p193) Electrolyte disturbances
- - Hypercalcemia - Hypomagnesemia
Drugs - displace digitalis from protein binding
sites and compete for renal excretion - Potassium-depleting diuretics lower - Corticosteroids lower
Diseases - - Renal failure - Hypoxemia -
8. What drug is used in emergency treatment of digitalis toxicity? Dobutamine 9. What is the mechanism of action of dobutamine? (LP p194)
-adrenergic agonist Increases cAMP activates protein kinases, which slow Ca2+
channels Increased influx high levels of calcium increased contractility
10.What affect does dobutamine have on heart rate? (LP p194) Phosphodiesterase Inhibitors 11.How are amrinone and milrinone used in treating CHF? (LP p194)
Used short term in patients with Long term use associated with increased
Spironolactone 12.What are the therapeutic uses of spironolactone? (LP p195)
heart failure (in cirrhosis, and to avoid hypokalemia from K+-depleting
diuretics)
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13.What are the adverse effects of spironolactone? (LP p195) GI: gastritis, peptic ulcers, nausea Endocrine: , menstrual irregularities, decreased libido Lethargy/confusion
Order of Therapy
14.What is the usual order of therapy in patients with symptomatic heart failure? (LP p195)
after optimizing diuretic therapy improvement in morbidity and mortality if symptoms persist despite other therapies Spironolactone Vasodilators Biventricular pacing or cardiac transplant
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Quick Review 3 1. Contractility of cardiac muscle is directly related to what ion? (LP p184) 2. Describe the mechanism of action for digitalis and how it leads to an increase in cardiac output. (LP p191)
increases intracellular concentration of sodium Sodium-calcium antiporter will not pump Na+ into the cell or Ca2+ out of the cell Increases intracellular increase in
increase in cardiac output 3. Digitalis in not indicated for patients with what type of heart failure? (LP p192)
Right-sided heart failure
4. How do medications such as quinidine, verapamil, and amiodarone cause digitalis toxicity when used concurrently? (LP p193) By displacing from tissue protein binding sites Competing with digoxin for renal excretion Digoxin plasma levels
5. What are the adverse effects of dobutamine?
Anxiety Headaches Tremors
6. Spironolactone is a direct antagonist of aldosterone and will thereby prevent what 3 things? (LP p195)
Salt retention Hypokalemia
7. What are the adverse effects of spironolactone? (LP p195)
GI: gastritis, peptic ulcers, nausea Endocrine: , menstrual irregularities, decreased libido Lethargy/confusion
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8. What are the common EKG changes seen with digitalis treatment?
QT interval shortening Scooped ST segments with ST depression in the lateral leads
9. What is the mechanism of action and clinical use of eplerenone? (similar to spironolactone) Used mostly in patients with severe CHF with low LVEF after a myocardial infarction
10.What are the signs and symptoms of digitalis toxicity? (LP p193) Electrolyte abnormalities: (in chronic toxicity, hypokalemia is of
greater concern because it increases the patients susceptibility to the toxic effects of digoxin) GI effects: nausea, vomiting, and abdominal pain Neurological: confusion, weakness Visual changes may include altered color vision ( ), scotomas (seeing dark
spots), blindness (bradycardia, AV block, PVCs, ventricular tachycardia and
fibrillation, atrial arrhythmias)
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End of Session Quiz 1. Match the drug or drug class to its mechanism of action or major effect. (LP p187-195)
a. ACE inhibitors
b. ARBs
c. -blockers
d. Diuretics
e. Direct vasodilators
f. Digitalis
g. Phosphodiesterase inhibitors
h. Spironolactone
Increased venous capacitance reduced cardiac preload Counteract compensatory sympathetic stimulation Block enzyme that cleaves angiotensin I to angiotensin II
Block angiotensin type 2 receptor
Relieve volume overload Inhibits Na+/K+ ATPase reduces ability of Na+/Ca2+exchanger to move Ca2+ out of the cell increases cardiac contractility Antagonizes aldosterone
Increase intracellular cAMP increases intracellular Ca2+increases cardiac contractility
2. Match the following clinical descriptions with the most appropriate therapeutic agent.
Choices: metoprolol, spironolactone, digitalis, losartan a. An 85-year-old woman newly diagnosed with CHF who got a cough from her ACE inhibitor b. A 71-year-old man with advanced CHF, significant peripheral edema, and myocardial hypertrophy already
on a diuretic, ARB, and -blocker c. A 64-year-old woman with atrial fibrillation and CHF d. A 59-year-old man with stable CHF and HTN already on an ACE inhibitor and diuretic
3. Which heart failure drug can cause hyperkalemia, gynecomastia, and menstrual irregularities? (LP p195) 4. Which drug for CHF should never be given in an episode of acute CHF exacerbation? (LP p190) 5. Classify the following drugs as vasodilators of primarily arteries, veins, or both: (LP p190)
a. Sodium nitroprusside b. Nesiritide c. Hydralazine
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6. Which -Blocker used for CHF also antagonizes 1 receptors? (LP p190) 7. Do diuretics reduce cardiac preload or afterload? (LP p 190) 8. How should digitalis overdose be managed? (LP p193)
9. Match the drug with its category.
Lisinopril Angiotensin receptor blocker Metoprolol Aldosterone receptor blocker Losartan Loop diuretic Spironolactone Direct vasodilator Furosemide Angiotensin converting enzyme inhibitor Isosorbide dinitrate - blocker
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Cardiology 7 Arrhythmias Lecture Outline I. Antiarrhythmic Drugs A. Class I (Na+ channel-blockers) B. Class II (-blockers) C. Class III (K+ channel-blockers) D. Class IV (Ca2+ channel-blockers) II. Bradycardia A. Sinus bradycardia/Sick Sinus Syndrome B. AV nodal block 1. 1st degree AV block 2. 2nd degree AV block 3. 3rd degree AV block III. Supraventricular arrhythmias A. Atrial fibrillation B. Atrial flutter C. Paroxysmal supraventricular tachycardia IV. Ventricular arrhythmias A. Premature ventricular contractions (PVCs)
B. Ventricular tachycardia (VTach) C. Torsades de Pointes Antiarrhythmic Drugs 1. What are the 4 basic classes of antiarrhythmic drugs?
Class I Class II Class III Class IV
2. List examples of each class of antiarrhythmic drugs.
Class IA
Class IB
Class IC
Class II
Class III
Class IV
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Bradycardia 3. What medications and medical disorders can cause bradycardia?
4. What are the EKG characteristics of each type of AV block?
1st degree AV block
2nd degree AV block
Mobitz 1
Mobitz 2
3rd degree AV block
5. Which types of AV block require a pacemaker? Atrial Fibrillation/Flutter 6. What are the EKG characteristics of atrial fibrillation? 7. What tests should always be performed when looking for underlying causes of new-onset atrial fib? 8. What classes of drugs are typically used for rate control in atrial fibrillation? 9. What are the two main concerns in the chronic treatment of atrial fibrillation? 10.What is the risk of stroke associated with atrial fibrillation? 11.What drug is used to reduce the risk of stroke in patients with atrial fibrillation? 12.What are the EKG characteristics of atrial flutter?
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Quick Review 13.Classify the following antiarrhythmic drugs (Class IA, IB, IC, II, III, or IV).
Amiodarone
Quinidine
Diltiazem
Flecainide
Procainamide
Metoprolol
Sotalol
Lidocaine
Verapamil
Digoxin
14.What drugs are most commonly used to control the heart rate in acute atrial fibrillation with rapid ventricular
response? 15.A 66-year-old man with a history of hypertension and diabetes presents to your office with a complaint of
palpitations for 1 week. EKG reveals atrial fibrillation with a resting HR of 72. After discussing treatment options, he decides that he would prefer a trial of electrical cardioversion in order to avoid lifelong anticoagulation. What preliminary steps would need to be undertaken before cardioversion?
16.Amiodarone is sometimes used to help maintain sinus rhythm in patients with atrial fibrillation. What studies are commonly followed in patients taking amiodarone, to monitor for toxicity?
Paroxysmal Supraventricular Tachycardia 17.What are the two most common causes of paroxysmal supraventricular tachycardia (pSVT)? 18.What vagal maneuvers can be used to slow or break pSVT?
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19.What drug can be used to break or slow pSVT? Ventricular Arrhythmias
20.What does a premature ventricular contraction (PVC) look like?
21.What do we call >3 PVCs in a row?
22.What are the EKG characteristics of ventricular tachycardia (VTach)?
23. If untreated, into what rhythm will VTach often degenerate?
24.How is VTach managed? Complete the chart below.
Is the VTach sustained?
Non-sustained VTach Sustained VTach: Is the patient hemodynamically stable?
Stable VTach
Unstable VTach: Does the patient have a pulse?
Pulseless VTach
Unstable VTach with Pulse
NOO
YES
NOO
YES
NOO
YES
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End of Session Quiz
1. Wolff-Parkinson-White (WPW) syndrome is caused by an abnormal connection between atria and ventricles through an accessory bypass tract. What is the most common accessory bypass tract causing WPW syndrome?
2. What rhythm is classically described as being irregularly irregular?
3. What rhythm is classically described as having a saw tooth pattern on the baseline?
4. A 68-year-old man with a history of coronary artery disease (CAD) presents to the ER with a complaint of chest pain and is subsequently admitted to the telemetry unit for monitoring. Overnight, the nurse calls you to the bedside because of tachycardia. His heart rate has been 160 beats per minute for the last 3 minutes. You race to the bedside, only to find the patient sitting up comfortably. He denies any pain or dyspnea, and says he feels fine. His BP is 114/72, but the telemetry monitor shows a wide-complex rhythm with a rate of 156, and you diagnose ventricular tachycardia. What are your next steps?
5. While you are waiting for your orders from the previous question to be carried out, the patient begins to
complain of feeling woozy. You check his blood pressure, and discover that it has fallen to 82/60. The tele monitor still shows ventricular tachycardia with a rate in the 150s-160s. What are your next steps?
6. What type of heart block is described by the following statements?
PR interval prolonged more than 0.2msec (5 small boxes)
No relationship between P waves and QRS
PR interval becomes progressively longer until a beat is blocked
PR interval fixed, but with occasional dropped beats
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7. A nurse calls the on-call intern in the middle of the night because a patient has developed tachycardia, with rate of 140. The blood pressure is 90/50. The intern orders a stat EKG, then hurries to the floor to examine the patient. She interprets the wide-complex tachycardia on EKG as ventricular tachycardia, but since the patient has a pulse she calls her resident for assistance before initiating therapy. The resident studies the EKG and pronounces this to be supraventricular tachycardia with aberrant conduction. The intern politely but adamantly disagrees. How should the team proceed?
8. What basic EKG rhythm matches the following statements?
Narrow QRS without P waves, rate 50
Chaotic, erratic, wide QRS
Wide QRS not associated with P waves, rate >40 but 100
Wide QRS, not associated with P waves, rate 20-40
Wide QRS, not associated with P waves, rate >100
Narrow QRS not associated with P waves, rate >60 but
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3 QUESTION WARM-UP1. What agents can be used to treat osteoporosis? (FA11 p379) (FA12 p414)
2. A child exhibits proximal muscle weakness and enlarged calves. What is the disease and how is it inherited? (FA11 p87) (FA12 p91)
3. What are 4 types of epithelial cell junctions? What are 4 proteins involved in non-epithelial adhesion mechanisms? (FA11 p370) (FA12 p404)
NEPHRON PHYSIOLOGYPhys: Chapters 27-28GG: Chapter 25
Nephron physiology (FA11 p461) (FA12 p508)Proximal tubuleRelative concentrations along proximal tubule (FA11 p462) (FA12 p509)Thin descending loop of HenleThick ascending loop of HenleEarly distal convoluted tubuleCollecting tubule
4VS\MQEP8YFYPIVWXLEPJ
REN
AL
2 -
Nep
hron
and
Diu
retic
s
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REN
AL 2 - N
ephron and Diuretics
5. Proximal Tubule (second half)
6. Proximal Tubule (anions and cations)
7. Thick Ascending Limb (TAL)
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[ 6 ] Copyright 2012, Doctors In Training.com, LLC. All Rights Reserved.
REN
AL
2 -
Nep
hron
and
Diu
retic
s8. What class of drugs inhibits the Na+/2Cl-/K+ symporter in the thick ascending limb? (FA11 p473)
9. Early Distal Tubule
10. What determines how much water is reabsorbed in the distal tubules and the collecting ducts?
11. What two types of cells compose the collecting duct and the last segment of the distal tubule? What do they do?Principal cells - Intercalated cells -
12. What are the two types of intercalated cells?
13. What class of diuretic directly affects principal cells?
14. What affect does aldosterone have on the intercalated cells and principal cells of the collecting duct? Intercalated cells- Principal cells-
15. What drugs antagonize aldosterones action on the principal cells of the collecting duct, thereby promoting Na+ excretion and inhibiting K+ excretion?
16. What are the critical steps involved in excreting dilute urine?DilYXMSRSJYMHMRXLIXLMGOEWGIRHMRKWIKQI