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Flashcards in MSK I FA Deck (87)
1

What are the five layers of the epidermis in order from apical to basal?

They all start with stratum: Corneum, Lucidum, Granulosum, Spinosum and Basale. Californians Like Girls in String Bikinis.

2

Which layer of the epidermis sports desmosomes?

Stratum Spinosum

3

Which layer of the epidermis supplies stem cells?

Stratum Basale

4

What are the three types of glands in the epidermis?

Sebaceous, Eccrine and Apocrine

5

What epidermal gland is targeted by acne drugs.

Sebaceous. These glands are are associated with the hair follicle and drugs reduce holocrine secretion of sebum.

6

Starting with glucose, what are all of the glycolytic intermediates as it is broken down to pyruvate?

"German gorillas fight french dandies gloriously by proudly pummeling pretty paris." Gluc, Gluc-6-P, Fru-6-P, Fru-1,6-Bisphosphate, DHA-P and Glyceraldehyde-3-P, 1,3-bisphosphoglycerate, 3-phosphoglycerate, 2-phosphoglycerate, phosphoenolpyruvate, pyruvate 

7

Starting with hexokinase, what are all of the glycolytic enzymes that break down glucose?

"Harry Potter proudly attacks the German Kaiser's monkeys eating people." Hexokinase, Phosphoglucoisomerase, PFK-1, Aldolase, Triose Phosphate Isomerase, Glyceraldehyde-3-Phosphate Dehydrogenase, phosphoglycerate kinase, phosphoglycerate mutase, enolase, pyruvate kinase

8

What is the rate determining enzyme in glycolysis?

PFK-1

9

What regulates the rate-determining enzyme in glycolysis?

POSITIVE REGULATORS: AMP and fructose-2,6-BP NEGATIVE REGULATORS: ATP and citrate

10

How are the molecules necessary for cellular respiration in the heart and liver shuttled into the mitochondrial matrix?

Malate-aspartate shuttle

11

How are the molecules necessary for cellular respiration in the muscle shuttled into the mitochondrial matrix?

Glycerol-3-P shuttle

12

What glycolysis reactions require ATP?

Gluc -> Gluc-6-P by hexokinase and Fructose-6-P -> Fructose-1.6-BP by PFK-1.

13

What glycolysis reactions generate ATP?

1,3-BPG-> 3-PG by phosphoglycerate kinase and PEP -> pyruvate by pyruvate kinase

14

A patient comes to see you with symptoms consistent with rheumatic fever. He reported having a sore throat two weeks ago. What bacteria is likely causing these symptoms and by what mechanism is it doing so?

Streptococcus pyogenes. It produces the Streptolysin O toxin which degrades cell membranes and lyses RBCs. The host produces ASO antibodies against streptolysin O/M protein, which also attack cardiac tissue and cause rheumatic fever.

15

A patient comes to the ED in shock with a rash, vomiting, desqumation and fever. What bacterium may be causing these symptoms and by what mechanism?

Staphylococcus aureus. It produces TSST-1 toxin which is a super-antigen that binds MHC II to CD4 cells and causes overwhelming secretion of IFN-gamma and IL-2. OR Streptococcus pyogenes. It produces Exotoxin A which does the same thing as TSST-1.

16

A parent brings her child to the clinic with scaled skin syndrome. What is causing these symptoms?

Staphylococcus aureus production of exfoliative toxin that disrupts desmosomes in stratum granulosum layer. 

17

The lab runs a gram stain on a sample from a patient and finds gram + cocci. What tests might they run to further specify the bacteria type?

Test for catalase enzyme in H2O2 solution. Staph will be catalase positive and strep will be catalase negative. Staph will also grow in clusters and strep will grow in chains.

18

The lab runs a gram stain on a sample and finds gram +, catalase +, cluster-forming bacteria. What test might they run to further specify the bacteria type?

See if the bacteria is positive for coagulase and will convert fibrinogen to fibrin in serum, manifested by clot formation. Staph aureus will be coagulase positive and staph epidermidis will be coagulase negative.

19

The lab runs a gram stain on a sample and finds gram +, catalase -, chain-forming bacteria. What test might they run to further specify the bacteria type?

But the bacteria on a blood agar plate and test for hemolysis. Group A and B strep will be beta (complete) hemolytic. Viridans strep and strep pneumoniae will be alpha (partial and green) hemolytic. Group D strep and nonenterococcus strep will be non-hemolytic.

20

The lab runs a gram stain on a sample and finds gram +, catalase -, chain forming, beta-hemolytic bacteria. What test might the lab do to further specify the bacteria type?

Ad bacitracin to the plated bacteria to see if they are resistant to the antibiotic. Group A Strep will be bacitracin sensitive and Group B Strep will be resistant.

21

How does staph aureus evade the host immune response?

Protein A binds the Fc region of IgG. This inhibits opsinization for complement activation or phagocytosis.

22

Why is staph aureus so good at making abscesses?

It is coagulase positive and can form a fibrin clot around the area of infection, walling itself off.

23

You are doing an infectious disease rotation at the hospital and you see a patient with a MRSA infection. Why can't you treat this patient with normal antibiotics?

It is resistant to beta-lactams that break up the peptidoglycan wall because it has expressed an altered penicillin binding protein.

24

What bacteria is notorious for infecting dialysis patients?

Stpahylococcus epidermidis. It is great at forming biofilms on IV catheters and prosthetic devices. It is a component of our normal flora.

25

What are the different diseases caused by streptococcus progenies (group A)?

PYOGENIC: pharyngitis, cellulitis and impetigo TOXIGENIC: scarlet fever, toxic shock, necrotizing fasciitis IMMUNOLOGIC: rheumatic fever, acute glomerulonephritis

26

Your neighbor thinks his friend might have rheumatic fever? What symptoms would you check for to see if his suspicion may be correct?

"PENES"- Polyarthritis, endocarditis, nodules, erythema marginatum and Sydenham's chorea.

27

Two patients have secondary infections from the same microbe. One has rheumatic fever and the other glomerulonephritis. What was most likely their primary condition?

Pharyngitis from group A strep (pyogenes)

28

A patient comes to see you with secondary condition of glomerulonephritis. What will be the first primary condition you suspect? The secondary?

Impetigo most often leads to glomerulonephritis then pharyngitis.

29

A female tells you she thinks she has scarlet fever. What do you look for before you make a diagnosis?

Scarlet rash on face, strawberry tongue and scarlet throat

30

A football player has hypopigmented patches on his shoulders upper back and upper chest. KOH prep after a skin scraping shows a spaghetti and meatball appearance. What is his condition and what is causing it?

Tinea versicolor caused my Malassezia furfur. The fungus degrades lipids and produces acids that damage melanocytes and create funky looking pigmentation.

31

A patient has multiple clear vesicular papules near his mouth and keratoconjunctivits. What virus may have infected this patient and what type of virus is it? How is this transmitted?

HSV-1. Double-stranded, enveloped DNA virus. Respiratory droplets and saliva.

32

A patient has multiple clear vesicular papules on his genetilia. What virus may have infected this patient and what type of virus is it? How is this transmitted?

HSV-2. Double-stranded, enveloped DNA virus. Sexual contact and perinatal.

33

What herpesvirus has a vaccine available? How is this virus transmitted?

VZV for chickenpox or shingles. Respiratory droplets

34

What is the most common cause of sporadic encephalitis in the US?

HSV-1 infection

35

Your diagnose a patient with VZV, where will this virus reside in latency?

Dorsal root ganglia or trigeminal ganglia

36

You diagnose a patient with HSV-1. Where will this virus reside in latency?

Trigemminal ganglia

37

You diagnose a patient with HSV-2. Where will this virus reside in latency?

Sacral ganglia

38

How can a lab confirm diagnosis of HSV-1, HSV-2 or VZV?

PCR, Tzanck test (look for syncitial giant cells) and Cowdry A inclusions

39

What drugs target components of fungal cell walls?

Azoles. They inhibit P-450 enzyme conversion of lanosterol to ergosterol

40

You find that a pregnant mother is infected with HSV-2. What drug do you prescribe for prophylaxis of the mother prior to giving birth? How does this drug work?

Acyclovir. It is a guanosine triphosphate analogue. It messes with thymidine kinase because it does not have a 3' OH group for elongation of replication. Replication terminates = virus can't replicate

41

You diagnose a patient with CMV. What drug do you prescribe and how does it work?

Ganciclovir. It is guanosine monophosphate analogue. It mutates viral DNA polymerase.

42

If Ganciclovir fails in helping a patient to CMV, what drug do you turn to? How does it work?

Forscarnet. It is a pyrophosphate analogue that inhibits viral DNA polymerase.

43

How does arsenic work?

It inhibits pyruvate dehydrogenase complex and cellular respiration cannot occur as normal. Apoptosis results.

44

How does bone formation differ in different locations of the head?

The base of the skull is formed through endochondral ossification with a primary chondrocyte framework. The face and skull is formed through membranous ossification where bone is formed without cartilage.

45

A young boy comes to your clinic with muscle rigidity, lockjaw and very dirty wounds on his feet. How would a particular microbe elicit these symptoms?

Clostridium tetani release the toxin tetanospasmin. The toxin acts on the SNARE complex and prevents release of inhibitory neurotransmitters GABA and glycine. This causes muscle spasms in tetanus.

46

A mother brings her 12 year old son in to see you who is having increased difficulty breathing, faccidity and difficulty speaking. Symptoms started shortly after eating some home canned beans. How would a particular microbe elicit these symptoms?

Clostridium botulinum releases the botulinum toxin. The toxin acts on the SNARE complex and prevents release of ACh and inhibits muscle contraction. This is what causes flaccidity.

47

What antibiotics block cell wall synthesis by inhibition of peptidoglycan cross-linking?

Beta lactams = "I PAC MAP" Imipenem, Penicillin, Ampicillin, Cephalosporin, Methicillin, Amoxicillin and Piperacillin

48

What antibiotics block peptidoglycan synthesis?

Bacitracin and Vancomycin

49

What antibiotics block nucleotide synthesis via folic acid pathways?

Sulfonamides and Trimethoprim

50

What antibiotic blocks DNA topisomerase?

Fluoroquinolones

51

What antibiotics block mRNA synthesis?

Rifampin

52

What antibiotics actually damage DNA? How are we unaffected?

Metronidazole. It must be metabolized before it becomes active and our bodies cannot metabolize it.

53

What antibiotics block protein synthesis at the 50S subunit?

Chloramphenicol, macrolides, clindamycin, streptogramins (quinupristin, dalfopristin) and linezolid

54

What antibiotics block protein synthesis at the 30S subunit?

Aminoglycosides and Tetracyclines

55

What is penicillin's mechanism?

It binds PCN-binding proteins (transpeptidases) and inactivates them by blocking peptidoglycan cross-linking.

56

What type of bacteria is penicillin mostly prescribed for?

Gram-positive. It is bactericidal for gram + cocci, gram + rods, gram - cocci and spirochetes.

57

What is the mechanism of penicillinase-resistant penicillins (oxacillin, nafcillin and dicloxacillin)?

Same as penicillin. It is resistance to beta-lactamase because bulky R groups block the enzyme from accessing the beta-lactam ring

58

Why use oxacillin, nafcillin or dicloxacillin over penicillin?

They are resistant to beta-lactamase and have a narrow spectrum targeted at staph…except for MRSA. "Use naf for staph"

59

Why would you use amoxicillin/ampicillin (aminopenicillins) over penicillin?

They have the same mechanism. They just have a wider spectrum: Haemophilus Influenzae, E. Coli, Listeria monocytogenes, proteus mirabilis, salmonella, shigella and enterococci. "HELPSS kill enterococci." They can also be combine with clavulanic acid to protect against beta-lactamase.

60

Why would you us ticarcillin/piperacillin (antipseudomonals) over penicillin?

They are specific for pseudomonas and gram - rods. Use with clavulanic acid because they are susceptible to beta-lactamases.

61

This antibiotic is commonly used in combination with sulfonamides. Why?

Trimethoprim. It inhibits dihydrofolate reductase, which is down the folic acid synthesis line from dihydropteroate synthase where sulfonamides work.

62

What are common infections where you would prescribe trimethoprim?

UTIs. Also with Shigella, Salmonella, Pneumocystis jiroveci pneumonia.

63

What are common infections where you would prescribe sulfonamides?

Gram +, gram -, Nocardia, Chlamydia and UTIs (in combination with Trimethoprim to inhibit folic acid synthesis)

64

Why prescribe cephalosporin over penicillin antibiotics? Why prescribe penicillin antibiotics over cephalosporin?

It is a bactericidal less susceptible to beta-lactamases. Cephalosporins are generally not effective against Lysteria, Atypicals (Chlamydia/Mycoplasma), MRSA and Enterococci. 

65

What is the only cephalosporin that can be used to treat MRSA?

Ceftaroline

66

What are the 1st generation cephalosporins and what do they protect against?

"PEcK her 1st!" Cefazolin and Cephalexin are effective against Proteus mirabilis, E. Coli, Klebsiella pneumoniae.

67

What is typically used for prophylaxis prior to surgery?

Cefazolin for protection against S. aureus wound infection

68

What are the 2nd generation cephalosporins and what do they protect against?

"HEN PEcKS 2nd!" Cefoxitin, Cefaclor and Cefuroxime are effective against Haemophilus influenzae, Enterobacter aerogenes, Neisseria spp, Proteus mirabilis, E. coli, Klebsiella pneumoniae, and Serratia marcesens.

69

What are the 3rd generation cephalosporins and what do they protect against?

Ceftriaxone (meningitis and gonorrhea), Cefotaxime, Ceftazidime (Pseudomnas) are effective against serious gram - infections that are resistant to other beta-lactams. 

70

What is the lone 4th generation cephalosporin and what is it effective against?

Cefepime is effective against Pseudomonas and gram + organisms

71

Why use aztreonam over penicillin?

It is monobactam that is synergistic with amino glycosides and does not have cross-allergy with penicillin drugs. You can only use it against gram + rods.

72

Why use imipenum/cilastatin/meropenum over penicillin?

It is a broad-spectrum carbapenum for use only against life-threatening infections because of toxicity.

73

What is always administered with imipenum?

Cilistatin. This decreases drug deactivation in renal tubules.

74

What drug is effected by a mutation in the D-ala-D-ala linkages in bacterial cell walls?

Vancomycin. It is a bactericidal specific against D-ala-D-ala

75

What antibiotics are your protein synthesis inhibitors?

"Buy AT 30, CCEL at 50." 30S inhibitors: Aminoglycosides (bactericidal) and Tetracyclins (bacteriostatic). 50S inhibitors: Chloramphenicol (bacteriostatic), Clindamycin (bacteriostatic), Erythromycin (macrolide which is bacteriostatic), and Linezolid

76

What clinical signs might you find in someone who has damaged a nerve in a fracture of the surgical neck of the humerus?

Inability to abduct humerus between 15 and 90 degrees. Numbness over deltoid muscle = Axillary Nerve.

77

What clinical signs might you find in someone who has damaged a nerve in a fracture of the midshaft of the humerus?

Weak extensors ("BEST": brachioradialis, extensors of wrist/fingers, supinator and triceps), numbness of dorsal hand and thumb, and wrist drop = Radial Nerve.

78

What clinical signs might you find in someone who has damaged a nerve in a fracture of the supracondylar humerus?

Weak thumb opposition, wrist flexion and lateral finger flexion. "Pope's blessing" or "Ape hand" when asked to make a fist = Median Nerve 

79

What clinical signs might you find in someone who has damaged a nerve in a fracture of the medial epicondyle of the humerus?

Loss of medial lumbrical function and ulnar claw (inability to extend 4th and 5th fingers). = Ulnar Nerve.

80

What clinical signs might you find in someone with carpal tunnel syndrome?

Tingling and numbness down lateral 3.5 fingers. 2nd and 3rd digits are clawed upon extension of fingers.

81

What clinical signs might you find in someone with an upper brachial plexus avulsion versus someone with a lower brachial plexus avulsion?

Upper: waiter's tip. Lower: Klumpe's total claw (loss of forearm flexors from median nerve and loss of finger extensors from radial nerve)

82

A swimmer is having trouble abducting his arm for the 1st 15 degrees. What nerve could be impinged in this patient?

Suprascapular nerve that innervated the infraspinatous rotator cuff muscle

83

A pitcher is having trouble internally/medially rotating his shoulder. What nerve could be damaged?

Subscapular nerve that innervated the subscapularis rotator cuff muscle

84

A weight lifter is having trouble adducting and externally/laterally rotating his arm. What nerves could be damaged?

The teres minor adducts and externally/laterally rotates the humerus and is innervated by the axillary nerve. The infraspinatous also externally/laterally rotates the arm and is innervated by the supra scapular nerve.

85

What causes rigor mortis?

The body is no longer producing ATP. ATP is what releases actin from myosin in muscle contraction. This makes the muscles stiff.

86

What causes malignant hyperthermia?

A hypersensitive ryanodine receptor remains open and Ca continues to flow into the muscle fiber sarcoplasm. This causes continual hydrolysis of ATP and generation of heat.

87

How does Ca allow muscle contraction to proceed?

It binds Troponin C, which moves tropomyosin away from the myosin binding site on actin. This allows myosin to bind to actin and proceed with power-stroking.