Usmle Review Time!

Front 1

Aplasia vs. atrophy

Back 1

Aplasia- never grew
Atrophy- shrunk... from: dec blood supply, disuse, dec hormone stim, denervation.

Front 2

Psoriasis: Hypertrophy or hyperplasia?

Back 2

hyperplasia

Front 3

Hyperplasia predisposes you to:
(what is the one exception)

Back 3

Cancer; BPH

Front 4

Why are AIDS pts often w/ methemoglobinemia?

Back 4

They are TMP-Sulfa prophylaxis for PCP.

Front 5

Which drugs can precipitate hemolytic anemia with G6PD- deficiency? WHY?

Back 5

fava-beans, TMP-sulfa, primaquin (anti-malarial drugs), dapsone (leprosy tx), nitro drugs, sulfa drugs. TB drugs.

These drugs increase H202 (peroxide);
With G6PD-def., there is less NADPH; thus dec reduced glutathione, thus less ability to detox free rads and peroxides. The peroxides damage Hb giving met-hemoglobin; so Hb clumps up, the RBC membrane gets screwed up and intravascular hemolysis occurs.

Front 6

What will you see on a blood smear for G6PD def?
WHY?

Back 6

Heinz bodies- clumped Hb b/c it's met-hemoglobin from getting oxidatively damaged from peroxide that can't be cleared b/c decreased reduced glutathione b/c not enough NADPH because no G6PD.

Bite cells: from phagocytic removal of Heinz bodies from macrophages.

Front 7

Does giving oxygen help for a pt with G6PD def?

Back 7

No, because the Hb is met-hemoglobin and won't bind it; doesn't matter if there is tons of it around or not.

Front 8

Compare the treatment of CO poisoning with G6PD def.

Back 8

CO poison= 100% O2
G6PD= transfusion only... 100% O2 doesn't help b/c the Hb is met-hemoglobin and won't bind O2.

Front 9

What is the number one symptom of CO poisoning?

Back 9

HA

Front 10

Explain the mech of CO poisoning

Back 10

The CO binds the heme instead of O2.
Treatment= 100% O2.

Front 11

Contrast aplasia with hypoplasia with atrophy. Give examples

Back 11

Aplasia- NO development. renal agenesis.
hypoplasia- DEC development. gonads in klinefelter.
atrophy- DEC of size (post normal dev.). muscle loss post having a cast on.

Front 12

Hypoxia vs. hypoxemia

Back 12

Hypoxia- decreased O2 supply
Hypoxemia- dec O2 concentration in arterial blood

Front 13

Five causes of hypoxia:

Back 13

1. ischemia (blood flow obstruction)
2. anemia
3. CO poison
4. Dec. blood flow (dec perfusion)
5. Hypoxemia (i.e. from pulm dz).

Front 14

Describe early characteristics (reversible) of hypoxic cell injury:

Back 14

-Decreased oxidative phosphorylation in the MITOCHONDRIA.
So dec ATP.
Failure of Na/K-ATPase mem pump.
inc intracell Na so cell swelling/organelle swelling (hyropic change, vacuoles in cytoplasm, swelling of ER and mitochondria).
-Ribosome disaggregation (b/c mem changes).
-stimulation of phosphofructokinase: inc glycolysis so inc lactate, dec intracell pH.
-End of early stage= myelin figures (whorl like from mem damage), cell blebs (bad cytoskeleton).

Front 15

Describe late characteristic of hypoxic cell injury:

Back 15

Point of no return:
Calcium influx from membrane damage. (Ca++ATPase pump disrupted so Ca++ goes in and activates everything giving cell death)
calcification of mitochondria.
intracell enzyme/protein release.
(ex. AST, LDH, CK, CK-MB, amylase)

Front 16

Describe the relative vulnerability of the following cells to hypoxia:
neurons, myocytes, skeletal muscle cells

Back 16

neurons die 3-5 min,
myocardial cells (and hepatocytes) die 1-2 hours
skel muscle cells die after many hours.

Front 17

What controls the development of external genital differentiation?

Back 17

Adrenal androgens

Front 18

What occurs with complete androgen insensitivty in a XY karyotype?

Back 18

external female genitalia but internal male genitalia. They appear as females.

Front 19

What occurs with 5-alpha reductase deficiency in a XY karyotype?

Back 19

dec conversion of testosterone to 5-DHT. Thus underdeveloped external male genitalia and prostate. Normal epididymus, ductus deferens, etc.

Front 20

Where does the corticospinal tract cross?

Back 20

Caudal medulla (pyramidal decussation)

Front 21

If you aspirate a peanut while upright it will go where?

Back 21

lower portion of right inferior lobe

Front 22

If you aspirate a peanut while supine where will it go?

Back 22

Superior portion of right inferior lobe

Front 23

What bugs secrete IgA protease?

Back 23

S. pnuemo, H. flu, Neisseria

Front 24

What does IgA protease do?

Back 24

Cleavces IgA, leaving the Fc parts to coat the bacterium. Then the bacterium can bind the Fc receptors on various mucosal celss.

Front 25

What does Protein A do?

Back 25

Binds Fc portion of Ig. Screws up opsonization and phagocytosis.

Front 26

What bacterium has Protein A?

Back 26

Staph A

Front 27

What does M protein do?

Back 27

Helps prevent phagocytosis.

Front 28

What bug has M protein?

Back 28

Strep pyogenes (group A strep)

Front 29

What drug is used to stop M protein?

Back 29

Clindamycin

Front 30

What type of nerve block is used in the second stage of labor?

Back 30

PUDENDAL nerve block which innervates the muscle and skin of perianal area.

Front 31

What landmark is used for a pudendal block?

Back 31

ischial spine

Front 32

What landmark is used for a lumbar puncture?

Back 32

iliac crest

Front 33

Describe what layers are pierced (in order) for a lumbar puncture

Back 33

Skin
Superficial fascia
Deep fascia
Supraspinous ligament
Interspinous ligament
Ligamentum flavum
Interlaminar space (only present in lumbar region)
Epidural space
Dura
Arachnoid
Subarachnoid space (CSF)

** Pia is not Pierced!!!

Front 34

What spinal level is a lumbar puncture at?

Back 34

L4/L5

Front 35

An infarct to what artery causes locked in syndrome?

Back 35

Basilar

Front 36

What does a lesion to the ventral pons result in?

Back 36

Locked-in syndrome: quadriplegia and inability to speak;
patient is aware, awake, and can communicate w/ vertical eye movements and blinks.

Front 37

What is the mechanism of nystatin?

Back 37

Complexes w/ ergosterol and causes cell membrane leakage

Front 38

What other drug has the same mechanism as nystatin?

Back 38

amphotericin B

Front 39

What anti-fungal blocks ergosterol synthesis?

Back 39

Terbinafine

Front 40

What anti-fungal inhibits beta-glucan?

Back 40

Echinocandins (e.g. caspofungin)

Front 41

What anti-fungal messes up mitotic spindle formation?

Back 41

Griseofulvan

Front 42

What is the mechanism of flucytosine?

Back 42

Interferes w/ thymidilate synthetase

Front 43

Define prosopagnosia

Back 43

Inability to recognize faces

Front 44

In severe anemia describe what occurs with the pulse pressure, cardiac output, heart rate and stroke volume

Back 44

They all increase!

Front 45

Describe the changes in LV volumes (diastolic and systolic) after nitroglycerin admin

Back 45

they both will decrease (dec. venous return, dec. TPR)

Front 46

What diseases occur in a HIV pt w/ CD4+ from 200-400

Back 46

Oral thrush, tinea pedic, VZV reactivation, TB reactivation, bacterial infections (h flu, s pneumo, salmonella)

Front 47

What diseases occur in a HIV pt w/ CD4+ from 100-200

Back 47

HSV reactivation, cryptosporidium, isospora, dissem coccidioidomycosis, PCP.

Front 48

What diseases occur in a HIV pt w/ CD4+ from 50-100

Back 48

Candida esophagitis, toxoplasmosis, histoplasmosis

Front 49

What diseases occur in a HIV pt w/ CD4+ from 0-50

Back 49

CMV retinitis/esophagitis, dissem MAC, cryptococcal meningoencephalitis.

Front 50

Where in the brain will herpes simplex encephalitis affect?

Back 50

Frontal and temporal lobes (think that the herpes lesions on the face spread via the nasopharynx)

Front 51

Polyarteritis nodosa is associated with which hepatitis strain?

Back 51

Hep B

Front 52

What hepatitis is associated with essential mixed cryoglobulinemia?

Back 52

Hep C

Front 53

Which two hepatitis viruses can give you a form of vasculitis?

Back 53

Hep B and Hep C

Front 54

SE of Digoxin

Back 54

PSVT, AV node block

Front 55

Is prostatic fluid acidic or basic?

Back 55

acidic

Front 56

What is a marker for prostate gland function?

Back 56

Acid phosphatase in the seminal fluid

Front 57

Compare the viscosity of fluid secreted by the prostate versus the seminal vesicles

Back 57

Seminal vesicles= viscous;
prostate= thin, watery.

Front 58

What is the role of zinc in sperm? Where does it come from?

Back 58

role= stablizes nuclear condensation (i.e. sperm chromatin)
source= prostate gland.

Front 59

Cowpers glands (aka, bulbourethral glands) serve what function?

Back 59

Aid neutralization of seminal fluid-- w/ thick alkaline mucus.

Front 60

What does the epididymus add to seminal fluid?

Back 60

carnitine and acetylcarnitine

Front 61

What accounts for giving the largest constituent of seminal fluid?

Back 61

seminal vesicles.

Front 62

Describe the component of fluid from the seminal vesicles

Back 62

High in fructose concentration, antigens to prevent female immune response (trophoblast lymphocyte cross-reactive antigen)

Front 63

Where does spermatogenesis occur?

Back 63

Seminiferous tubules of testis.

Front 64

What is the mechanism of colchicine?

Back 64

Inhibition of MT formation, to prevent leukocyte migration and phagocytosis; thus less inflammation.

Front 65

The reduviid bug is the vector for what?

Back 65

Chagas dx

Front 66

What is the vector for yersinia pestis? what dz does it cause?

Back 66

Flea, bubonic plague

Front 67

What is the vector for Rickettsia prowazeki? what dz does it cause?

Back 67

Louse; epidemic typhus

Front 68

What is the vector for Arboviruses? what dz does it cause?

Back 68

Mosquite; West nile, st. louis encephalitis.

Front 69

Name two major symptoms of Chagas dz

Back 69

Myocarditis, esophageal achalasia

Front 70

Deficiency of complement factors C6, C7, C8 expose a patient to what infection?

Back 70

Neisseria.

Front 71

Deficiency of complement factor C1q expose a patient to what infection?

Back 71

SLE-like syndrome

Front 72

Deficiency of complement factors C1rs, C1s, C4, C2 expose a patient to what infection?

Back 72

SLE- like and glomerulonephritis

Front 73

Deficiency of complement factors C3 and C5 expose a patient to what infection?

Back 73

pyogenic infections

Front 74

Neutrophil abnormalities will cause what diseases?

Back 74

Pyogenic infections or granulomatous infections.

Front 75

T-cell deficiencies will expose you to what organisms?

Back 75

Opportunistic: Candida, pneumocystis or CMV

Front 76

UV light induces formation of what?

Back 76

Thymidine dimers.

Front 77

Describe xeroderma pigmentosum

Back 77

AR dz, w/ defective excisional repair for elimination of thymidine dimers formed by UV light.
Gives extreme sens to sunlight and inc predisposition to skin cancer

Front 78

What are the fever and rash in scarlet fever due to?

Back 78

Strep pyogenes pyrogenic exotoxin that is phage-encoded

Front 79

What dz gives "strawberry tongue" and "sandpaper rash"

Back 79

Scarlet fever

Front 80

What bugs produce alpha toxin?

Back 80

S. aureus and C. perfringens; it is a cytolysin

Front 81

What bugs have Endotoxin?

Back 81

gram-negs

Front 82

What is the FIRST Ig produced in an immune response?

Back 82

IgM (M for mother!)

Front 83

Are fatty acids gluconeogenic?

Back 83

NO! BUT.... "Fat" can still make some glucose; since the glycerol backbone is glycogenic: The GLYCEROL backbone gives 80% of glucose in dieting obese pts and 20% pf glucose (behind the amino acid pathways) in truly starving pts.

Front 84

Describe GNG precursors for dieting fat people vs. starving pts.

Back 84

FAT: 80% from glycerol backbone of TGs from fat breakdown
STARVING: After glycogen store depletion: 80% from a.a. degradation.

** the other 20% is from the opposite source.

Front 85

What does purine catabolism produce?

Back 85

Uric acid! (waste product- it's excreted in urine)

Front 86

What vessel abnormality will give a beaded appearance of the renal arteries?

Back 86

Fibromuscular dysplasia.

Front 87

The principal cells of the cortical collecting duct do what to K?

Back 87

Secrete it into lumun; the intercalated cells reabsorb potassium.

Front 88

What is the cause of osteoarthritis?

Back 88

repititive joint trauma

Front 89

What benefit does celecoxib have over naproxen? why?

Back 89

Dec GI irritation; Celecoxib is selective for COX-2 inhibition; thus less GI irritation and renal impairment as opposed to traditional NSAIDS that are non-sel COX-1/COX-2 inhibitors

Front 90

Potter's synfroms is caused by a failure of what to develop?

Back 90

Ureteric buds; which form the ureters, renal pelvis, calyces, and collecting tubules.

Front 91

What do the paramesonephic ducts form?

Back 91

Uterine tubes, uterus, and upper 1/3 of vag

Front 92

What does the urogenital sinus form?

Back 92

Urinary bladder in both sexes.
In males= prostatic urethra, prostate, membranous urethra, bulbourethral glands, penile urethra and littre's glands.
In female- most of urethra, urethral glands, paraurethral glands, vestibule of vagina and greater vestibular glands.

Front 93

What does the urorectal septum form?

Back 93

Partitions the cloaca into the urogenital sinus and rectum (and upper anal canal).