Qbank Wrong, Rapid Review

Front 1

whats the MoA of a TB drug w/ visual problems as SE

Back 1

Ethambutol

MoA: inhibit Carbohydrate Polymerization
-inhibits Arabinosyl Transferase → Arabinogalactan, for MYCOLIC CELL WALL

Front 2

SE of only TB drug to directly inhibit synthesis of Mycolic Acids

Back 2

Isoniazid
SE: neurotoxicity & hepatoxicity (Pyridoxine, B6) can prevent the Neurotoxicity
**INH can also → drug-induced SLE

Front 3

Space Constant in Multiple Sclerosis

Back 3

demyelination in MS → decr Space Constant
-this means more charge dissipation along axon

Front 4

how calculate Case-Fatality Rate

Back 4

Case-Fatility Rate = #dead / #diseased

Front 5

in a patient who passes out in garage w/ car on, what happens to PaO2, CaO2

Back 5

PaO2 does NOT change
-what changes is the formation of Carboxyhemoglobin (this is CO poisoning) → decr O2 binding to Hgb → decr CaO2 since less O2 bound

Front 6

in a patient who went walking thru the woods yesturday and now has a rash along her legs and distal arms, what was the first type of cell to mediate this rxn?

Back 6

T Lymphocytes
-this is Contact Dermatitis, a Type IV Hypersensitivity rxn
-all Type IV Hypersensitivity rxn's occur by T Lymphocytes invading → release lymphokines → attract macrophages

Front 7

which gastric or intestinal hormone would →parietal cell proliferation and hyperplasia

Back 7

Gastrin
-its trophic to gastric mucosa

TGFα → mucosal cell growth, but NOT Parietal

Front 8

to avoid the development of pt's hip dipping to R when lift R foot, which gluteal quadrant would injection go? (assuming on the side that would cause this defect)

Back 8

inject in Superolateral Quadrant
-Sciatic n is in Inferomedial quadrant, and Superior Gluteal n is in Superiormedial quadrant
-thus, injection in Superolateral quadrant would miss these
-L side Sup Gluteal n lesion would → Trendelenburg on R (hip dips to R w/ R leg raise)

Front 9

heart murmur w/ Diastolic Opening Snap followed by rumbling vs Systolic Click followed by crescendo

Back 9

Diastolic Opening Snap followed by Rumbling:
MV stenosis

Systolic Click followed by Crescendo
MV Prolapse

Front 10

biochemical change to → Gout

Back 10

anything that'd incr Purine production
-incr Vmax of PRPP or HGPRT, etc

Front 11

cell responsible for inflamm of gout

Back 11

Neutrophils
-they phagocytose Monosodium Urate Crystals (that give (-) birefringence → inflamm of Gout
-Colchicine is useful b/c it inhibits the immigration of Neutrophils

Front 12

1 hematologic way to tell the difference btw Primary Hyperaldosteronism and Secondary

Back 12

Hyperaldosteronism

Primary = LOW Renin
-aldosterone-secreting tumor → high Na & H2O reabsorption that inhibits renin release due to Vol overload

Secondary = HIGH Renin
-something causing incr Renin like Juxtaglomerular Cell Neoplasm, etc

Front 13

Conn's would affect this zone of adrenal, and Cushing's would affect _ zone of adrenal

Back 13

Conn's = Primary Hyperaldost
-this would affect the Zona Glomerulosa (produces Alosterone)

Cushing's (Hypercortisolism)
-this would affect Zona Fasciculata (produces Cortisol)

Front 14

short-acting vs long-acting insulin

Back 14

Short Acting Insulin
-Lispro, Aspart, Regular
-Lispro & Aspart best for post-prandial hyperglycemia
-Regular best for IV admin (DKA)

Long-Acting:
-Glargine, Detemmir

Front 15

after surgery goes well, pt develops incr ALT, incr AST, confusion, what could be happening

Back 15

all inhaled anesthetics have potential for Hepatotoxicity, but esp Halothane

Front 16

m/c n lesion to → visual difficulties walking down the stairs

Back 16

Vertical Diplopia

-most noticeable when looking towards nose, as in reading newspaper or walking down starts
-m/c n lesioned = CN IV

Front 17

gastrinoma would be part of MEN1, MEN2A, MEN 2B, von-Hippel Lindau?

Back 17

MEN1
-Parathyroid tumors, Pituitary tumors, Pancreatic endocrine tumors (Zollinger-Ellison syndrome, Insulinoma, VIPomas, glucagonomas)

Front 18

cells involved in forming Granuloma

Back 18

Th1 cells secrete IL-2 & IFNγ

IFNγ stim's macrophages, granuloma formation

Front 19

how activate/inactivate Rb protein, and what is this protein, and what does it do?

Back 19

Rb = Tumor Suppressor Protein
-Rb-PO4 = INactive; Rb = active

-when cell in quiescent state, dephosphorylated Rb is active and prevents cell cycle progression
-when cell ready to enter S phase, Cyclin-depend. Kinases Phosphorylate Rb to inactivate it, and allow cycle progression

Front 20

m/c location of Crohn's lesions

Back 20

Terminal Ileum....& colon

Front 21

Th1 & Th2 for which (Crohn's, UC)

Back 21

Crohn's a/w abnrl Th1 response

UC a/w abnrl Th2 response

Front 22

Hyperacute transplant rejection vs Acute rejection (which involves what type of immune respones)

Back 22

Hyperacute Rejection
-w/ in minutes of transplant; Ab-med'd (Type II)

Acute Rejection
-cell-med'd, usually Cytotoxic T lymphocytes
-weeks after transplant

Front 23

IM in young patient
-which virus if agglutinate sheep RBCs, and if DON'T agglutinate sheep RBCs (and what is this sheep RBC test)

Back 23

sheep RBC test is Heterophile Ab test (Monospot test)

agglutinate sheep RBCs = Heterophile (+) c/w EBV meningitis

do NOT agglutinate RBCs, (-) for EBV, instead, CMV

Front 24

in addn to main SE of TCA's, what are some lesser known

Back 24

main 3 = Tri-C's = Convulsions, Coma, Cardiotoxicity
-also Confusion & hallucinations
***anti-cholinergic SEs

Front 25

what type of bias does blinding prevent?

Back 25

observer bias

Front 26

following trauma, pt develops severe pain in leg, x-ray shows gas production in leg. what's the main toxin producing it, what can this bug cause in GI tract, & whats the Tx

Back 26

alpha toxin (Lecithinase, a Phospholipase) of Clostridium perfringes

-can also cause late-onset food poisoning w/ watery-diarrhea

Tx: PCN, Clindamycin

Front 27

MoA of terbinafine vs azoles

Back 27

Terbinafine: inhibits Squalene Epoxidase (1st step in Ergosterol synthesis)

azoles block production of Ergosterol

Front 28

what drug would be used for Aspergillosis Tx, and what's its MoA?

Back 28

use cASPofungin

-inhibits cell wall synthesis by inhibiting synthesis of beta-glucan

Front 29

a slow ESR is due to which of the following substances:
Bradykinin, LTB4, EPO, IL-6, PAF, TXA2

Back 29

IL-6
-IL-1, -6, TNFalpha are 'acute phase reactants' that lead to secretion of many other substances
-1 is fibrinogen, that causes Rouleaux formation, that causes ESR incr

Front 30

recurrent Giardia infections can mean a pt has what deficiency, & Tx?

Back 30

IgA production

-secretory IgA helps prevent & clear infection by binding the Trophozoite (2 nuclei & 4 flagella) form

Giardia Tx = Metronidazole

Front 31

2 parts of Tx for CN poisoning

Back 31

Nitrites & Thiosulfate

Front 32

of the following choices, which would cause a decr in L ventricular compliance: viral myocarditis, alcoholic cardiomyopathy, amyloidosis, diphtheritic myocarditis, high-dose doxorubicin

Back 32

amyloidosis

Front 33

this compound is req'd in the trasamination rxn's (what's the chemical name for it)

Back 33

Pyridoxine (B6)

Front 34

alpha-ketoglutarate dehydrogenase req's this cofactor

Back 34

Thiamine (B1)

Front 35

pyruvate carboxylase, acetyl CoA carboxylase, propionyl CoA carboxylase, & 3-methylcrotonyl-CoA-carboxyase all req what cofactor

Back 35

Biotin (Vit B7)

Front 36

enzyme deficit if have benign inability to metabolize fructose

Back 36

Fructokinase

-fructose is easily excreted in urine, so if fructose builds up (fructokinase defic), no problem

-in contrast to Aldolase B defic will cause accumulation of Frc-1-PO4 that will then → decr PO4 available for glycogenolysis, gluconeogenesis, etc → hypoglycemia, jaundice, cirrhosis, V, lethargy

Front 37

if infant begins eating solids & fruit juices, turns hypoglycemic, jaundiced, cirrhotic, what is wrong

Back 37

Fructose Intolerance
-defic of Aldolase B

-Frc-1-PO4 builds up, inhibits glycogenolysis & gluconeogenesis → hypoglycemia, jaundice, cirrhosis, V, lethargic

Front 38

difference btw true hydrocephalus & hydrocephalus ex vacuo

Back 38

True Hydrocephalus is caused by either a) incr CSF production, b) abnrl CSF circulation, or c) d/o of CSF absorption

Hydrocephalus ex vacuo occurs due to atrophy of brain making a CT appear that CSF is pushing on brain structures, when actually CSF P is nrl

Front 39

quadrad of Sx of Kartagener's syndrome

Back 39

infertility, situs inversus, recurrent sinusitis/otitis, bronchiectasis

Front 40

liver w/ finely granular ("ground-glass") appearance vs lymphoid aggregates w/in the portal tracts and focal areas of macrovesicular steatosis

Back 40

finely granular "ground-glass" cytoplasm in liver = Hep B

lymphoid aggregates w/in portal tracts & focal areas of macrovesicular steatosis = Hep C

Front 41

rise in JVD w/ inspiration

Back 41

Kussmaul's sign

-in constrictive pericarditis due to restriction of R heart filling that occurs w/ the nrl incr drive to fill the heart in inspiration

Front 42

why would a slight drop in CaO2 occur in L atrium after blood being oxygenated

Back 42

bronchial artery blood causing decr O2 tension

Front 43

difference btw aortic body receptors and central chemoreceptors

Back 43

aortic body receptors mainly respond to hypoxia

central chemoreceptors respond to decr pH to stimulate Medullary Respiratory center

Front 44

what change in blood drives incr ventilation?

Back 44

PaCO2 is main stim of respiratory drive
-CO2 diffuses easily past BBB to form H+ ions, these activate Medullary Respiratory Center

-PaO2 is sensed by chemoreceptors in Carotid & Aortic Bodies
-when PaO2 >70, O2 does NOT have big effect on respiratory drive
-when PaO2 < 70, O2 DOES have main stim on respiratory drive

Front 45

pt w/ long-standing COPD comes into ED w/ severe dyspnea, given O2, later loses respiratory drive, what happened?

Back 45

in pt's w/ long-standing COPD, the chronic & profound hypercapnia (high CO2) stops driving respiration
-hypoxia becomes only stimulant of respiratory drive
-if give rapid & high amnts of O2, may lose only respiratory stimulus

Front 46

important parts to C diphtheriae Tx?

Back 46

FIRST is Antitoxin to neutralize remaining exotoxin not yet entered into cardiac/neural cells

-SECOND is PCN or Erythromycin

-Third is DTaP vaccine

Front 47

mom c/o symmetric swelling & pain in PIP, wrist, & knees. 5 y.o son just had bout of facial rash & fever. Tx'd w/ NSAIDS, how sponataneously healed, what is?

Back 47

Parvovirus B19

-in kids → fever, malaise, erythema nodosum

-in adults, mimicks RA, but resolves spontaneously

Front 48

23 y.o M to ED w/ 2d Hx of fever, HA, confusion; pt slips into coma & dies several d after admission; autopsy shows intense bilateral hemorrhagic necrosis of inferior & medial temporal lobes

Back 48

Herpesvirus

-HSV-1 affects teens & young adults, & is m/c cause of sporadic encephalitis
***Temporal Lobe involvement is characteristic***
-m/c early Sx are HA & fever
-then mental status change, cranial nerve deficits, seizures
-specific Herpes lesions → aphasia (speech areas), olfactory hallucinations (olfactory cortex), personality changes (amygdala)
-eosinophilic Cowdry inclusions on Bx, multinuclear giant cells on Tzank smear

Front 49

30 y.o w/ ADPKD to ED w/ sudden severe HA & confusion, neuro exam nrl but CT shows subarachnoid blood. 5th day after admit, pt c/o weakness in R arm & leg, which Rx could have helped?

Back 49

Ca chnnl blocker

-cerebral vasospasm is common >3d after SAH, Nimodipine is effective at preventing this

Front 50

marker of activity of Osteoblasts?

Back 50

serum bone-specific Alkaline Phosphatase
-ALP is released as Osteoblasts synth bone matrix

-liver also makes, so must differentiate (1 way is heating- bone ALP is more heat-sensitive (bone = boils))

Front 51

28 y.o F to ED w/ severe RLQ & abdominal pain, vaginal bleeding. 7wks LMP, Hx of PID, BP is now 80/40, HR 130; endometrial curettage would m/l show

Back 51

Decidualized Endometrium

-stromal decidualization is nrl pregnancy change
-no embryonic tissue or chorionic villi

Front 52

contents of nucleolus, and whats its function

Back 52

proteins, rDNA (DNA coding rRNA), rRNA

-functions to make ribosomes!

Front 53

difference btw SVC syndrome and R Brachiocephalic obstruction

Back 53

R Brachiocephalic syndrome
-R-sided face & arm swelling, engorgement of subcu veins on R side of neck
-R brachiocephalic v also drains lymph from R UE, R face & neck, R hemithorax, RUQ of abdomen

SVC syndrome is BILATERAL

Front 54

why are host Ab ineffective against Hep C?

Back 54

HCV is constantly making new envelope proteins due to high error-prone genetic copying

Front 55

which antiarrhythmic Rx has more affinity for ischemic myocardium

Back 55

Lidocaine

*though, Amiodarone has replaced this Rx
-Ischemic Myocardium is Depolarized tissue, and Lidocaine likes rapidly depolarizing/depolarized cells

Front 56

main users of NADPH, and where is this NADPH from?

Back 56

NADPH from HMP Shunt (Pentose Phosphate Pathway)

-2 NADPH produced by Oxidative steps of pathway used for: cholesterol & FA biosynthesis, drug metabolism, steroid biosynth

Front 57

Etoposide inhibits _?

Back 57

DNA Topoisomerase II

-Topoisomerase II → double strand breaks that → cell death

-Topoisomerase I → single-strand breaks in DNA to relieve negative coiling, II induces double strand breaks to relieve + & - coiling; w/ Etoposide present, II can't close those cuts it made

Front 58

important step in workup of pt w/ PaCO2 49, pH 7.59

Back 58

PaCO2 49, pH 7.59 is c/w metabolic alkalosis

-important step is checking urine Cl

-can help ID cause: V will → hyopCl and low Cl; loop & thiazide diuretics will → incr urine Cl; Conn → incr Cl

Front 59

difference btw Tumor Suppressor vs Proto-oncogene mechanism of causing cancer

Back 59

Tumor Suppressor gene nrl'ly inhibits cellular proliferation
-thus takes an inactivating mutation of Tumor Suppressor gene to → neoplasm

-Proto-oncogene stim's cell proliferation
-thus, overexpression or amplification of proto-oncogene → incr cell proliferation & neoplastic growth

Front 60

difference btw ras, N-myc, ERB-B1 & -2, abl, BRCA-1 & -2, NF-1, APC, p53, RB, WT-1

Back 60

ras, N-myc, ERB-B1 & -B2, abl, are all Protooncogenes
-thus, req activating mutation of these to → neoplasm

BRCA-1 & -2, NF-1, APC, p53, RB, WT-1 are all Tumor Suppressor genes
-this, takes inactivating mutation of these to → neoplasm

Front 61

heteroplasmy

Back 61

different organellar genomes w/in a single cell

-ex: mitochondrial disease in family, relatives affected at different ages, different severity, etc b/c depends on how much in single cells

Front 62

this cytokine can cause cachexia in cancer pt

Back 62

TNF-alpha

-can influence hypothalamus to → appetite suppression

Front 63

common area of spine to be damaged in pt w/ loss of sensation in UE, diminished pinprick sensation in upper back, shoulders, UE, nrl position & vibration sense, nrl LE

Back 63

this is Syringomyelia

-form CSF-filled cavities (syrinx) in cervical region of spinal cord usually, and they enlarge & destroy Ventral White Commissure & Ventral Horn usually

Front 64

hypertension, low plasma renin

Back 64

Primary Hyperaldosteronism

-hypoK, ~nrl Na, incr pH

Front 65

difference btw Conn's, Addison, Cushing's

Back 65

Conn's = Primary Hyperaldosteronism
-low plasma renin w/ HTN, hypoK, incr pH
-2ndary = high plasma renin

Addison's = Primary Adrenal Insufficiency
-hypoBP, incr K, hypoNa, eosinophilia, incr ACTH

Cushing's = hypercortisolism