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studying random facts Flashcards

1
Q

important features of gram + and gram -

A

gram + –> lipoteichoic acid and cell wall/membrane are what triggers immune response

gram - –> lipopolysaccharide (Protein A is MAJOR virulence leading to sepsis) and outer membrane

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2
Q

sex pilli

A

direct connection for conjugation (exchange of material from one bacteria to another)

seen in e. coli and neisseria

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3
Q

components of a spore (3)

A
  1. coat (keratin-like protein that is impermeable to abx and chemicals)
  2. cortex/core wall (innermost, made of peptidoglycans)
  3. dipicolinic acid (large amounts inside spore, help with heat resistance)
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4
Q

giemsa stain

A

Stains INSIDE CELLS

chlamydia

ricketsia

borellia burgdorferi

plasmodium

trypanosomes

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5
Q
A
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6
Q

silver stains

A

H. Pylori

Legionella

Pneumocystis

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7
Q

Pigments:

yellow/golden

blue-green

red

A

yellow –> S. aureus

yellow/green –> pseudamonas (pyocyanin)

red –> serratia

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8
Q

agar for e. coli O157:H7

A

Sorbitol MacConkey agar

think O in sorbitol for O157

o157 CANNOT ferment sorbitol

other e.coli are PINK, o157 is colorless

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9
Q
A
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10
Q

obligate aerobes possess what

A

superoxide dismutase to get rid of O2 free radicals

ex are pseudamonas, bacilis, nocardia, TB

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11
Q

abx that is ineffective against anaerobes

A

aminoglycosides (require O2)

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12
Q

abx:

anaerobic infections ABOVE the diaphragm

anaerobic infections BELOW the diaphragm

A

ABOVE –> clindamycin

BELOW –> metronidazole

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13
Q

Protein A

A

This is major virulence for S. Aureus

Binds Fc portion of IgG

so not able to activate complement and phagocytosis

avoids immune system

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14
Q

endotoxin triggers

A

IL-1 and TNF

cause fever, shock

generate weak Ab response

*these are released by gram - bacteria

they are heat stable

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15
Q

e. coli vs shigella on invasion

A

both shiga toxins, both bloody diarrhea

e. coli–> o157 does NOT invade

shigella DOES invade into mucosa (toxin less important)

both lead to HUS

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16
Q

bacterial transformation

A

take up DNA from environment and incorporate into self

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17
Q

bacterial conjugaiton

A

transfer of one cell to another via sex PILUS

transferred via plasmid (small DNA molecule that is physcially separated from chromosomal DNA)

can replicate independently

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18
Q

scalded skin syndrome skin layer affected

A

affects the stratum GRANULOSUM

causes a + nikolsky sign

happens to newborns at age 3-7 days old

The damage is intraepithelial so it heals with NO SCARS

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19
Q

two uti bacteria that are neg nitrites

A

staph saprophiticus, enterococcus

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20
Q

chloroquine mechanism

A

blocks heme polymerase

see retinopothy with long term use

…also can be used in RA and SLE in addition to malaria

remember to test for G6PD before primaquine and quinidine use

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21
Q

macrolide mechanism

A

block tRNA movment to P site

block 50s

gram + cocci

concentrated INSIDE macrophages (atypicals)

mycoplasma, chlamydia, MAC, H. Pylori, Bartonella

erythro –> bind GI (also reason for GI side effects)

clarithro –> part of triple therapy

PROLONG QT, CHOLESTATIC HEPATITIS

P450 enzyme INHIBITORS

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22
Q

aminoglycoside mechanism

A

block 30s

block initiation of protein synthesis (get misreading of code)

used in combo with B-lactams (synnergistic)

BACTERIOCIDAL

mechanism of resistance is phosphorylation, methylation, adenylation

OTOTOXIC, Nephrotoxic

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23
Q

tetracyclines

A

prevent attachment of tRNA to 30s

atypical bacterias

zoonoses

acne vulgaris

impaired absorption with milk, Ca (chelate drug)

increase efflux mechanism of resistance

PHOTOSENSITIVITY, GI distress, DISCOLORATION OF TEETH (children), TERATOGEN

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24
Q

demeclocycline

A

NOT used as an antibiotic

given in SIADH

ADH antagonist

CAUSES a nephrogenic DI

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25
Q

chloramphenicol

A

inhibits peptidyl transferase 50s

RMSF, meningitis (neisseria)

Grey Baby (baby lack UDP gluc, this is necessary for this abx)

aplastic anemia

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26
Q

clindamycin

A

binds 50s subunit

methylation

anaerobes** above diaphragm

(resistnace by B. Fragilis)

Gardenella, Acne, PID

Treat perfringins but cause C.Diff

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27
Q

Linezolid

A

Bind 50s subunit, bacteriostatic

used in VRE, nosocomial infections

weak MAO inhibitor (serotonin syndrome)

optic neuritis, peripheral neuritis

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28
Q

all protein synthesis inhibitors are cidal/static…except

A

all are bacterioSTATIC

except aminoglycosides which are bacterioCIDAL

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29
Q

PCN mechanism of action

A

binds to transpeptidases

“PCN binding proteins”

mimic alanine (D-ala D-ala) residue and inactivate enzymes

wall breakdown > wall synthesis –> autolysis

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30
Q

probenacid

A

a gout drug that can be used to boost PCN via inhibiton of secretion of PCN in kidney

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31
Q

beta lactamase inhibitors

A

clavulonic acid, sulbactam, tazobactam

(prevent degredation of beta lactam abx)

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32
Q

difference between steven johnson and toxic epidermal necrolysis

A

TEN is severe form of SJS that covers >30% of total body surface area

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33
Q

PCN causing interstitial nephritis presentation

A

classic presentation is fever, oliguria, increased BUN/Cr, Eosinophils in urine, white cells and WBC casts (sterile pyuria)

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34
Q

amoxicillin/ampicillin

A

penetrate porin channel of gram - bacteria

sensitive to Beta lactamase enzymes

Amox: H. Infleunza, strep throat, otitis media, strep pneumo, H. Pylori, lymes (early)

Amp: enterococcus, anaerobes, listeria, prophylaxis post splenectomy and dental proccedures

commonly used with Beta lactamase inhibitors such as clavulonic acid, sulbactam, tazobactam

cause SJS, liver injury

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35
Q

antipseudamonal PCNS

A

Piperacillin, Ticarcillin

Greater porin channel penetration

given with B-lactamase inhibitor

Tic-Clav

Pip-Tazo

These are broad spectrum abx now

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36
Q

floroquinolone mechanism

A

inhibit DNA gyrase (induce ds break, repair break), and Topoisomerase IV (get rid supercoils)

Bacteriocidal

resistance alter gyrase, topoisomerase

Pyelonephritis, acute prostatitis, walking pneumonia, abd infections, bacteroides anthracis

Cipro has most pseudamonas coverage (swimmer ear)

GI upset, neuro side effect, PROLONG QT –> Torsades

Tendonitis, not use in children, not take with Ca,Mg

MSK side effects

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37
Q

Vancomycin

A

binds D-ala D-ala, prevent crosslinking (different from beta lactams that inhibit transpeptidases)

bacteriocidal

Resistance is D-ala D-lac

TOO large to pass outer membrane so only Gram +

nephrotoxicity, ototoxicity, Red Man Syndrome –> histamine release (not hypersensitivity) just need to give slower

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38
Q

Metronidazole

A

needs to be reduced by anaerobic bacteria

when activated, generate free radicals that lead to DNA breaks

BELOW the diaphragm infections

Giardia, Entamebas, Trichamonas, Gardrenella, Aerobes (c. diff, bacteroides), H. Pylori

GET GAP

Disulfuram like rxn

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39
Q

Nitrofurantoin

A

use in UTI (concentrate in urine)

safe pregnancy

ppt hemolysis in pts with 6GPD

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40
Q

most common cause of impetigo and second most common cause

A
  1. S. Aureus
  2. Strep pyogenes
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41
Q

neurocysticercosis

A

ingestion of tenia solium (pork tapeworm) eggs excreted in feces of HUMAN carriers

clinically present with seizures

see eosinophilia, cysts in brain

tx albendazole

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42
Q

how does body fight Listeria infection

A

cell mediated immunity –> T-cells

(Ab are useless)

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43
Q

what TB drug causes loss of acid-fastness

A

Isoniazid (inhibits mycolic acid synthesis)

Without their mycolic acids, mycobacteria lose their acid-fastness and become unable to synthesize new bacteria or multiply

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44
Q

subacute endocarditis caused by? and attacks what valves and how adhere?

A

caused by strep viridans (usually dental procdure) attacks previously damaged valves.

The dextrans attach to fibrin

There is fibrin and platelets at the site of endothelial trauma providing a site for bacterial adherence and colonization

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45
Q

treatment of diptheria

A

passive immunization (diptheria ANTITOXIN)

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46
Q

latex agglutination test for yeast

A

this is indicative of cryptococcus

think thick polysaccharide capsule on india ink and methanamine, muciarmine stain of tissue

think BUDDING YEAST

opporunistic infection

can cause meningioencephalitis (soap bubble lesions in brain), pneumonia

tx amphotericin B and flucytosine then maintenance with fluconazole

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47
Q

clue cells

A

epithelial cells covered with gram-variable rods seen on wet mount

indicative of gardrenella vaginosis (BV)

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48
Q

salmonella virulence factor

A

special capsule called Vi antigen that protects it from opsonization and phagocytosis

remember that salmonella is most common cause of osteomyelitis in Sickle Cell pts

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49
Q

Hepatitis D

A

Considered replicative defective. Must have Hep B present in order to be infective

The hep B surface antigen coats the Hep D antigen before it can infect hepatocytes

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50
Q

what is the effect of a agonist plus a competitive antagonist

A

this shifts the curve to the right

compete for same binding site but if increase dose enough, can overcome

This decreases potency but does NOT change efficacy

Diazepam + Flumazenil (competitive antagonist on GABA)

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51
Q

what is the effect of adding a noncompetitive antagonist

A

this shifts the efficacy DOWN but does NOT change the potency

Essentially you are binding at an allosteric site and removing receptors from the system. This cannot be overcome by adding substrate concentration

ex: NE + phenozybenzamine (noncompetative antagonist on alpha receptor)

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52
Q

effect of partial agonist on dose response curve

A

this lowesrs the efficacy (potency is an independent variable.

Here you are acting at the same site as the full agonist but with LOWER max effect

Morphine + Buprinorphine (parial agonist at mu opioid receptor)

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53
Q

cerebellar lesions present on which side of the body?

A

these are ipsilateral lesions that present as lack of coordination/dysmetria

Think falling towards side of lesion

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54
Q

TCA mechanism

A

inhibit reuptake of both NE and 5HT

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55
Q

turner girls kidney problems

A

prone to UTIs from horshoe kidney

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56
Q

uncomplicated community pneumonia treatment

A

azithromycin

clarithromycin

doxycycline

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57
Q

causes of ARDS

A

Sepsis

Pancreatitis

Aspiration

R Uremia

Truama

Amniotic Fluid Embolism

Shock

SPARTAS

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58
Q

L:S ratio

A

same until week 35ish then L>S 2:1

suggests lungs are mature

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59
Q

betamethasone

A

used to stimulate surfactant production in the lungs

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60
Q

complications of Neonatal Resp Distress Syndrome (3)

A
  1. broncopulmonary dysplasia
  2. PDA
  3. Retinopathy of prematurity (too much o2 causing detatchment of retina –> blindness) via free radicals
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61
Q

Pulm artery and bronchus relationship

A

L pulm artery goes SUPERIOR to L bronchus

R pulm artery goes ANTERIOR to R bronchus

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62
Q

perfusion limited gases

vs

diffusion limited gases

A

perfusion --> O2 (normal healthy), CO2, NO (freely crosses membrane, limited by how quickly the blood is flowing by to take the gas away)

Diffusion –> O2 (emphysema, fibrosis) CO (the problem is the gas crossing the membrane quickly enough, NOT the rate at which blood takes it away)

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63
Q

treatment of primary pulm htn

A
  1. epoprostenol
  2. bosentan
  3. silfenafil

This usually arises from an inactivating BMPR2 gene mutation that results in decreased NO and increased endothelin

Results in smooth muscle proliferation

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64
Q

Loud P2

A

Pulmonary HTN

normal pulm artery pressure is 10-14

pulm HTN is >25

Results in arteriolosclerosis, medial hypertrophy, intimal fibrosis of pulm arteries

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65
Q

4 causes of hypoxia

A

hypoxia = decreased O2 delivery to tissue

  1. decrease CO
  2. hypoxemia (decreased PaO2)
  3. anemia
  4. CO poisoning
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66
Q

Hypoxemia

A

low PaO2 (arterial)

Normal A-a gradient

  1. High Altitiude
  2. Hypoventilation

Increased A-a gradient

  1. V/Q mismatch
  2. Diffusion limitation (fibrosis)
  3. Right to left shunt
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67
Q

Some sort of V/Q mismatch

What happens when give 100% O2

A

Shunt –> 100% O2 does NOT improve PaO2 (think airway obstruction, can get rid of CO2 as blood flows by but the blood is fully saturated with CO2)

Dead space (PE), V/Q mismatch (pulm edema) –> 100% O2 improves PaO2 (think PE, there is an area that cannot be perfused, but if give more O2, can fully oxygenate still)

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68
Q

erythema nodosum

A

sarcoidosis

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69
Q

lecithinase

A

virulence factor for clostridium perfringes

(alpha toxin)

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70
Q

ciliated mucosal epithelium line what parts of resp tract?

A

Ciliary mucosal epithelium line from the traceha to the proximal portions of the respiratory bronchioles

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71
Q

virulence factor of H. Influenza

A

polysaccharide capsule, which is composed of polyribosylribitol phosphate (PRP)

The PRP capsule binds factor H, a circulating complement control protein that prevents complement depositon on host cells

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72
Q

train of four stimulation

A

used during anesthesia to determine the degree of paralysis induced by neuromuscular junction blocking agents

-A peripheral nerve is stimulated 4 times in quick succession and the nerve impulse is recorded

A nondepolarizing agent would result in decreased initial reading that fades away (vecuronium)

A depolarizing agent (succinylcholine) shows initial decrease in all 4 phases, but then during a second trial would show fading.

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73
Q

varenicline

A

partial agonist of a4b2 nicotinic ACh receptor in CNS

because it is a partial agonist, it helps to decrease the symptoms of withdrawl by mildly stimulating the receptor

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74
Q

V/Q at base and apex of lung

A
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75
Q

zones of the lung

A

zone 1: does not occur in the lung under normal physiologic conditions, but would be found at the apex. alveolar pressure > arterial pressure > venous pressure. The arterial pressure is low becuse the heart must pump blood uphil to get here

zone 2: here arterial > alveolar > venous. Blood flows through this section in pulsatile fashion

zone 3: arterial > venous > alveolar so blood flows continuously through this section

*note, in a supine position, the blood flow is entirely in zone 3

76
Q

what does CFTR actually do?

  1. lungs/gi
  2. sweat glands
A
  1. lungs –> secretes Cl (via ATP) so that it pulls water with it to hydrate the mucosal surface
  2. In sweat glands –> pulls NaCl out of sweat to make it hypotonic
77
Q

fun facts about CF

A

AR, CFTR gene, chr 7, delta F508. Abnormal folding of protein

CFTR secrete Cl in gi/lungs and reabsorb Cl in sweat glands

Dx: Cl >60, present hypokalemia, increase immunoreactive trypsinogen (newborn screen)

get bronchiectasis, bronchitis, steatorea, meconium ileus, biliary cirrhosis, pancreatitis, absence vas deferens (problem with transport not spermatogenesis)

tx: albuterol, dornase alfa, hypertonic saline, N-acetylcystine, pancreatic enzyms, abx

78
Q

S1Q3T3

A

S wave in 1

Q wave in 3

Inverted T wave in 3

This is indicative of right heart strain –> Pulmonary Embolism

79
Q

Triad of:

immune dysfunction

low platelets

eczema

A

Wiskott-Aldrich Syndrome

X-linked disorder of WAS gene

80
Q

ITP

A

platelts do not live as long as they should in the plasma

antibodies against the IIb/IIIa receptor

cleared by splenic macrophages –> splenomegaly

tx: ivig, steroids, splenectomy

ITP ab against TwoP~B

81
Q

TTP

A

disorder of small vessel thrombus formation

consume platelts –> thrombocytopenia

decrease activity of vWF cleaving protein ADAMTS13 (which normally breaks down multimers of vWF)

usually an acquired Ab to ADAMST13

DANGEROUS CONDITION

82
Q

Microangiopathic hemolytic anemia

A

produce shistocytes

seen in: HUS, TTP, DIC

83
Q

uremia in context of bleeding disorder

A

renal dysfunction –> bleeding

poor aggregation and adhesion of platelets

caused by uremic toxins in the plasma

see prolonged BLEEDING TIME

normal platelet count

normal coag testing

84
Q

borderline personality disorder

A

persistent pattern of unstable relationships, mood lability, and impulsivity

85
Q

paranoid personality disorder

A

think mistrust and suspicion

86
Q

osteocytes are connected by

A

gap junctions

87
Q

antihistone antibodies

A

drug induced lupus

procainamide, hydralizine, INH

88
Q

zidovudine

A

nucleoside reverse transcriptase inhibitor used in HIV

competitively binds to reverse transcriptase and is encorporated into the viral genome as a thymidine analog

lack 3’ OH group

The 3’ –> 5’ phosphodiester bond formation is inhibited

89
Q

pure red cell aplasia

A

seen in Parvovirus B19, thymoma, lymphocytic leukemias

(see normal granulopoiesis and thrombopoeiosis)

90
Q

12th rib fx

A

kidney laceration possible

*spleen above kidney

SKI (spleen, kidney, intestine)

91
Q

diptheria vaccine

A

stimulates production of neutralizing antibodies against the binding component of the diptheria exotoxin

(IgG against circulating proteins)

92
Q

transient myocardial ischemia causes what to fail

A

Na/K atpase and Ca pump

results in higher Na in cell and higher Ca in cell –> cellular swelling

93
Q

anti-histadyl-tRNA synthase

A

polymyositis

proximal muscle weakness

also see anti-jo antibodies

often underlying adenocarcinoma possible

94
Q

intense itching after hot shower

A

polycythemia vera

95
Q

treatment of polycythemia vera

A

hydroxyurea

phlebotomy

96
Q

myelofibrosis

A

obliteration of bone marrow with fibrosis

increased fibroblast activity

teardrop cells = dacrocyte

MASSIVE SPLEEN

start to see extramedullary hematopoeisis

PDGF and TGF-B –> activate fibroblasts

97
Q

congenital torticollis

A

typically develos 2-4 weeks of age. Caused by birth trauma or malposition in utero resulting in SCM injury and fibrosis

baby presents with only wanting to look to one side with pain upon moving head to other side

98
Q

disopyramide

A

class 1a antiarrhythmic

slow phase 0

prolong phase 3

99
Q

cidofovir

A

broad spectrum antiviral nucleotide analog that does not depend on the presence of a virally encoded kinase

100
Q

med used in hypertensive emergency that acts at the kidney to improve perfusion

A

fenoldopam

D1 agonist causes arterial vasodilation, increased renal perfusion and promotes naturesis

101
Q

NNRTIs (3) think action!

A

These do NOT NEeD phosphorylation to be active

nevirapine (inducer)

efavirenz

delaviridine

102
Q

most common type of Ehler’s Danlos

A

procollagen peptidase deficiency

(hyperextensible skin)

103
Q

use inulin to measure

use PAH to measure

A

inulin –> GFR

PAH –> renal plasma flow

104
Q

PAH kidney

A

nearly 100% that enters the kidney leaves in the urine, therefore, we use this to measure Renal Plasma Flow.

105
Q

Renal blood flow calculation

A

RBF=RPF/(1-Hct)

remember that plasma =1-hct

106
Q

GFR calculation

A

GFR=(Uinulin x V)/(Pinulin)

107
Q

If they give you inulin clearance, what have they given you?

A

GFR

108
Q

excreted =

A

filtered + secreted - reabsorbed

remember, for inulin, filtration = excreted (no reabsorption, no secretion)

109
Q

negative urine anion gap in acidosis

positive urine anion gap in acidosis

A

neg gap –> GI cause

positive gap –> Renal Tubular Acidosis (type 1)

110
Q

Quick facts about Renal Tubular Acidosis

A

Type 1: DISTAL, Bicarb <10, bilateral kidney stones, HIGH urine pH. Think Sjorgen, RA, Amphotericin B

Type 2: PROXIMAL, mild acidosis, fanconi

Type 4: hyperkalemia, diabetics, renal failure, decreased aldosterone response/production. can be caused by TMP-SMX

111
Q

RBC casts

A

glomerulonephritis, malignant HTN

112
Q

WBC casts (3)

A

acute pyelonephritis, transplant rejection, tubulointerstitial inflam (acute interstitial nephritis)

113
Q

Fatty casts

A

nephrotic syndrome

114
Q

Granular (muddy brown) casts

A

acute tubular necrosis

115
Q

Waxy casts

A

end stage renal disease/chronic renal failure

(think Wax near end of alphabet, near end of kidney life)

116
Q
A
117
Q

JG cells

A

modified smooth muscle of afferent arteriole

118
Q

nephrotoxic antibiotics

A

aminoglycosides (made even worse when combined with cephalosporins) and vancomycin

119
Q

B blocker in a diabetic

A

need to be cautious because they mask the effects of hypoglycemia

–> hypoglycemia unawareness

120
Q

furosemide cause metabolic acid/alk?

A

causes metabolic alkalosis due to loss of volume leading to activation of RAAS. The aldo then acts in the collecting duct to dump K and H and bring in Na and HCO3. This leads to a metabolic alkalosis

121
Q

what metal are alcoholics deficient in?

A

magnesium (alcohol causes increased excretion, also dietary intake is less)

122
Q

most common cause of staghorn calculus

A

proteus

causes struvite stone (ammonium, mg, phosphate)

radiopaque, coffin lid appearance

(can also be saphrophiticus and klebsiella)

123
Q

electrolyte derrangements of renal failure *serum*

A

increased K

increased phosphate (stop responding PTH)

decreased Ca (stop activating vit D)

metabolic acidosis (stop producing bicarb)

124
Q

renal tubular defects

A

fanconi (F=first) = PCT

barter (thick ascending loop)

gitelman (DCT)

little (collecting tubule)

125
Q

causes of ATN (acute tubular necrosis)

A
  1. ischemic –> hypotension, shock, sepsis
  2. nephrotoxic –> rhabdo (myobogin), aminoglycosides, contrast dye, ethylene glycol
126
Q

things that give you intrinsic renal failure

A

acute tubular necrosis

RPGN

HUS

acute interstitial nephritis

Would see:

FENa >2%

serum BUN/Cr <15 (see a decrease in both of these)

127
Q

normal anion gap metabolic acidosis

A

anion gap 8-12

H: hyperalimentation

A: addisons (adrenal insufficiency)

R: renal tubular acidosis

D: diarrhea

A: acetazolamide

S: spironolactone

S: saline infusion

128
Q

prerenal azotemia

A

urine osmoles > 500

urine sodium < 20 (trying to conseve volume)

FeNa <1

serum BUN/CR >20 (BUN is reabsorbed, creatinine is NOT..think of less fluid decreasing the GFR so it is moving slower and has more time to reabsorb the BUN as well as the Na)

129
Q

PSGN where da humps at?

A

subepithelial humps

130
Q

granular subendothelial deposits think?

A

SLE

diffuse proliferative

membranoproliferative

131
Q

ADPKD chromsome

A

16

132
Q

allantois –> urachus

umbulical arteries

A

median umbilical ligament (pee out of belly button)

umbilical arteries –> medial umbilical ligaments

133
Q

cyclosporine

A

blocks IL-2 production and its receptor

IL-2 is necessary for differentiation and activation of ALL T-lymphocytes

134
Q

Ang II actions on PCT

A

acts to increase Na/H exchanger to pump more H into the lumen. This is then combined to eventually increase BICARB REABSORPTION

NO net change in H+

Net Bicarb resorption

135
Q

hepatorenal syndrome

A

declining hepatic function leads to decreased GFR leads to progressive functional renal failure

characterized by splanchnic vasodilation and vascoconstrction of the renal vascular beds

RAAS activation

pre-renal azotemia

**kidney looks normal**

136
Q

HIV pt kidney manifestation

A

focal segmental glomerulosclerosis

presents as nephrotic syndrome

shows IgM in AFFECTED glomeruli

137
Q

alkaptonuria urine findings

A

black

homogentisic acid

(due to defiency in homogentisic acid oxidase)

these pts have problems with arthritis and their fingers are black-ish

138
Q

MUDPILES

A

Methylene Glycol

Uremia

DKA

Propylene glycol

INH, IRON

Lactic Acidosis

Ethylene Glycol

Salicylates

139
Q

where dem kidneys at?

A

T12-L3

Left is higher than right

Retroperitoneal

140
Q

low levels of DA effect on kidney

A

dilate afferent and efferent and increase renal blood flow

at higher levels, it would be alpha-1 agonist (vasoconstrict, give in shock)

141
Q

ASA overdose

A

sodium bicarb (used to alkalinize both the urine and plasma)

see tinitis, n/v lethargy

142
Q

PCT glucose reabsorption cutoff numbers

A

200-375 glucose is seen in the urine

>375 glucose reabsorption is saturated and everything past this will be in urine

143
Q

abx safe for UTI in preg

A

cephalosporin 1st gen

144
Q

fibromuscular dysplasia

A

non-atherosclerotic, non-inflammatory disease of the blood vessels

most commonly affects the renal and carotids

main sx is HTN with bruit over renal artery

145
Q

Hartnup

A

cannot bring in neutral AA (except for proline) in enterocytes and prox renal tubules.

decreased tryprophan so no niacin so get pellagra

146
Q

tetracycline tox

A

can cause nephrogenic DI

also tooth discoloration, hepatotox, renal tox

147
Q

tumor lysis syndrome prevention/tx

A

allopurinol and hydration

inhibits production of uric acid, prevents renal failure

148
Q

chronic kidney disease- mineral bone disease

A

due to loss of ability to excrete phosphate, leads to increase in PTH –> increased bone reabsorption –> increase fracture risk

The increased phosphate also binds free calcium, which can lead ot hypocalcemia, which in turn leads to increased PTH production (secondary hyperparathyroidism)

Decreased renal production of Vit D

149
Q

intternuclear opthalmoplegia

A

side that cannot go medial is the side with the MLF lesion

**cannot move L eye medially, due to L MLF lesion**

150
Q

eye trying to move medially but cannot vs eye trying to move laterally but cannot

A

medially but cannot –> INO (MLF lesion)

laterally but cannot –> CN 6 palsy (no lateral rectus)

151
Q

cachexia, weight loss in cancer (1 main thing, 4 total)

A

TNF-alpha

INF-y

IL-1

IL-6

152
Q
A
153
Q

high BUN/Cr

A

prerenal azotemia

less blood flowing to kidney, allows more time for the BUN to be reabsorbed because the GFR is less.

*remember, BUN is reabsorbed, Cr is NOT*

154
Q

decreased BUN/Cr ratio

A

This implies intrinsic renal failure (acute tubular necrosis, PSGN, HUS)

Get a decrease in GFR due to debris and necrotic tissue blocking the lumen

The BUN reabsorption is impaired

155
Q

Side effects

pyramidal

extrapyrimadal

A

pyrimadal –> corticospinal tract, see WEAKNESS

extrapyrimidal –> basal ganglia nuclei. MOVEMENT DISORDERS

156
Q

onset of extrapyramidal side effects of antipsychotics

A

ADAPT (much more common with high potency –> haloperidol)

AD: Acute Dystonia –> hours to days, muscle spasm, stiffness

Akathisia –> days/months (restlessness, urge to move)

Parkinsonism (bradykinesia)

Tardive Dyskinesia –> months/years (irreversible, chorea, snake-like movements)

157
Q

what is lewy body

Lewy body found in cortex –>

Lewy body found in basal ganglia –>

A

lewy body = alpha-synuclein

cortex –> Lewy Body Dementia

Basal ganglia –> Parkinson

158
Q

hemangioblastoma what need to know

A

can produce EPO –> polycythemia vera

Associated with Von-Hippel-Lindau Syndrome (chr 3, renal cell carcinoma)

159
Q

Pineal tumor

A

cause perinaud syndrome and hydrocephalus

(cannot look up via compression of tectum and compress cerebral aqueduct)

160
Q

Brain tumor that expresses Estrogen Receptors

A

Meningioma

Common primary benign brain tumor. Occurs near surface of the brain “extra-axial”

+Psammoma bodies

161
Q

cause of Tetrology of Fallot

A

anterior and cephalad deviation of the infundibular septum during embyologic development resulting in a malgaligned VSD with an overriding aorta

162
Q

PCWP in ARDS

A

normal, this is considered a noncardiogenic pulmonary edema that can be caused by SPARTA

An elevated PCWP would be more indicative of cardiogenic pulm edema

163
Q

absent CD18

A

leukocyte adhesion deficiency

(recurrent skin and mucosal bacterial infections with NO pus, umbilical cord stay attached for >21 days)

164
Q

what produces elastase?

A

alveolar macrophages

165
Q

staph scalded skin syndrome caused by?

A

exotoxin mediated skin damage

*Think exo for exfoliate (+ nikolski sign)*

166
Q

PO2 in CO and Cyanide poisoning

A

NORMAL as this is a meausre of the oxygen dissolved in plasma and unrelated to hemoglobin fxn

167
Q

how treat exopthalmos of Graves

A

High dose glucocorticoids such as prednisone help to decrease the severity of inflammation and decrease extraocular volume

*Note the normal antithyroid drugs do NOT improve opthalmopathy

168
Q

Concern for pts taking PTU and Methimazole for hyperthyroidism

A

If they came in with something like sore throat you would be concerned about agranulocytosis caused by these drugs

169
Q

what shows up in blood of infant infected with HBv infection in utero?

A

HBeAg and viral load can be detectable

170
Q

what levels of GI tract are the plexus’

A

Submucosa –> Meissner = submucosal nerve plexus (control secretions)

Muscularis externa –> Auerbach = Myenteric plexus (control GI motility)

171
Q

Alk phos > AST/ALT –>

AST/ALT > Alk Phos –>

A

Alk phos > AST/ALT –> chestatic pattern (bile duct problem)

AST/ALT > Alk Phos –> hepatocellular pattern (hepatocyte problem)

172
Q

cofactor for transamination reactions

A

B6

173
Q

med to avoid in HOCM pts

A

Isosorbide Dinitrite

Diuretics (decrease preload)

Vasodilators in general (CCB, NO, ACE-I) all lead to decreased afterload

174
Q

weber test localizes to

A

weber localizes to affected ear with conductive hearing loss

WAC

weber localizes to unaffected sensorineural side

WUS

175
Q

restless leg syndrome tx

A

Dopamine Agonist (pramipexole)

176
Q

Hepatitis B with viral HBsAg and HBcAg stimulate what in host?

A

stimulate cytotoxic CD8 T cells to destroy infected hepatocytes

177
Q

St. John inducer/inhibitor

A

inducer (st john’s island induce bliss)

178
Q
A
179
Q

PAH at PCT how does it move across membranes

A

carrier mediated secretion

(remember, it is filtered and then secreted)

The secreted part of this is the RLS in how much PAH can be secreted into urine

180
Q

one drug that increases osteoblast activity

A

teriperatide

(remember that bisphosphonates decrease osteoclast activity by binding hydroxyapetite)

181
Q

xanthogranulomatous pyelonephritis

A

widespread kidney damage due to granulomatous tissue containing foamy macrophages.

A result of having chronic pyelonephritis

182
Q

Filgrastrin (med)

A

G-CSF (use to recover bone marrow)

increase entire myeloid lineage

183
Q

big platelets

A

ITP

(anti GP IIb/IIIa antibodies –> splenic consumption of platelet-antibody complex. Commonly due to viral illness)

184
Q

malonyl coA inhibits

A

inhibits fatty acid oxidation

required for synthesis

185
Q

gancyclovir side effect

A

bone marrow suppression

renal tox

use in CMV (guanosine analog)

186
Q

foscarnet side effect

A

nephrotoxicity

electrolyte abnormalities that can lead to seizures

STEP COPY (36 decks)

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