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Step 1 Uworld and Notes > Must Knows and Reminders > Flashcards

Must Knows and Reminders Flashcards

1
Q

AB exotoxin bacteria

ABCDES

A 
Pseudomonas Aeruginosa
Bordetella pertussis
Cholera, Clostridia
Diphtheria
E. coli
Shigella
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2
Q

P. aeruginosa

[Exotoxin, MOA]

A

Exotoxin A.

>Inhibits EF-2 (elongation factor) – inhibits protein synthesis – host cell death, necrosis

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3
Q

B. pertussis

[Exotoxin, MOA]

A

Pertussis toxin.

>Inhibits Gi – overactivates adenylyl cyclase – inc. cAMP – phagocyte dysfxn

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4
Q

V. cholera

[Exotoxin, MOA]

A

Cholera toxin.
>Overactivates adenylate cyclase – inc. cAMP – activates CFTR – inc. Cl- secretion, H20 secretion – “Rice water” diarrhea

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5
Q

C. botulinum

[Exotoxin, MOA]

A

Botulinum toxin.

>Protease that cleaves SNAREs – prevents ACh release into NMJ – flaccid paralysis

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6
Q

C. tetani

[Exotoxin, MOA]

A

Tetanospasmin.

>Protease that cleaves SNAREs – prevents GABA/glycine release into spinal cord – spastic paralysis

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7
Q

C. diphtheriae

[Exotoxin, MOA]

A

Diphtheria toxin.

>Inhibits EF-2 (elongation factor) – inhibits protein synthesis – pseudomembranous pharyngitis

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8
Q

Enterotoxic E. coli (ETEC)

[Exotoxin, MOA]

A

Labile toxin.
>Overactivates adenylyl cyclase – inc. cAMP – activates CFTR – inc. Cl- secretion, H2O secretion – watery diarrhea.
>Similar to cholera

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9
Q

Enterohemorrhagic E. coli (EHEC)

[Exotoxin, MOA]

A

Shigella-like toxin (SLT; verotoxin).
>Inhibits 60s ribosomal subunit – inhibits protein synthesis, inc. cytokine release – bloody diarrhea (HUS).
>Similar to Shigella, but doesn’t invade host cell

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10
Q

Shigella

[Exotoxin, MOA]

A

Shigella toxin.
>Inhibits 60s ribosomal subunit – inhibits protein synthesis, inc. cytokine release – damages gut epithelium – bloody diarrhea (HUS)

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11
Q

ABC carboxylase (3)

A

ATP, Biotin, CO2.
>Pyruvate carboxylase (gluconeogenesis).
>Acetyl-CoA carboxylase (FA synthesis).
>Propionyl-CoA carboxylase.

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12
Q

TLCFN dehydrogenase (3)

A

Thiamine, Lipoic acid, CoA, FAD+, NAD+.
>Pyruvate dehydrogenase.
>a-ketoglutarate dehydrogenase.
>Branched chain ketoacid dehydrogenase.

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13
Q

Intracellular organisms

A

Rickettsia, Chlamydia

Listeria, Legionella, Mycobacteria, Salmonella, Neisseria

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14
Q

Catalase (+)

Cats Need PLACESS

A

Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, Staphylococcus, Serratia

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15
Q

Encapsulated organisms (polysaccharide capsule)

A

S. pneumonia, H. influenzae type B, N. meningitidis, E. coli, Salmonella, Klebsiella pneumoniae, GBS

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16
Q

Aerobic bacteria

A

Mycobacteria
Pseudomonas
Nocardia
(have superoxide dismutase)

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17
Q

Anaerobic bacteria

A

Actinomyces
Bacteroides
Clostridium
Fusobacterium

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18
Q

Chocolate agar.

Selective for what organism?

A

H. influenzae type B

Has Factor V (NAD+) and X (hematin)

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19
Q

Sabouraud agar.

Selective for what organism?

A

Fungi

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20
Q

Thayer-Martin agar.

Selective for what organism?

A

Neisseria

Vancomycin, Trimethoprim, Colistin, Nystatin

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21
Q

Charcoal yeast extract (w/ Cysteine + iron).

For what organism?

A

Legionella

needs Cysteine

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22
Q

Loffler agar.

For what organism?

A

C. diphtheriae

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23
Q

Regan-Lowe agar.

For what organism?

A

B. pertussis

Charcoal, blood, antibiotics

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24
Q

Lowenstein-Jensen agar.

For what organism?

A

Mycobacteria

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25
Q

Eaton agar.

For what organism?

A

Mycoplasma

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26
Q

Tellurite agar.

For what organism?

A

C. diphtheriae

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27
Q

Bordet-Gengou agar.

For what organism?

A

B. pertussis

Potato

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28
Q

MacConkey agar.

For what organisms?

A 
Lactose fermenters (pink)
E. coli, Klebsiella
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29
Q

Poor gram staining bugs

A 
Treponemia
Mycobactera
Mycoplasma
Legionella
Rickettsia
Chlamydia
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30
Q

Biofilm producers

A

S. epidermidis – prosthetic devices, IV catheters
Viridans strep – dental carries, endocarditis
P. aeruginosa – Pneumonia, CF, contacts
H. influenzae – otitis media, other mucosal infxns

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31
Q

DNA viruses

HHAPPPPy

A 
Hepadna
Herpes
Adeno
Pox
Parvo
Papilloma
Polyoma
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32
Q

DNA virus properties

A

> dsDNA (except Parvo – ssDNA).
Linear (except Papilloma, Polyoma, hepadna – circular).
Icosahedral (except Pox).
Replicates in nucleus (except Pox).

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33
Q

Naked viruses

A

> DNA: Parvo, Adeno, Papilloma, Polyoma

>RNA: Calici, Picorna, Reovirus, Hepevirus

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34
Q

(+) RNA viruses

A

Calici, Corona
Retro, Toga
Flavi, Hepe, Picorna

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35
Q

(-) RNA viruses

Always Bring Polymerase Or Fail Replication

A

Arena, Bunya
Paramyxo, Orthomyxo
Filo, Rhabdo

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36
Q

Segmented RNA viruses

ROBA parts

A

Reovirus
Orthomyxo
Bunya
Arena

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37
Q

Reoviruses

A

Rotavirus (fatal diarrhea in kids)

Coltivirus

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38
Q

Picornaviruses

A 
>Poliovirus (Sabin, Salk)
>Echovirus - aseptic meningitis
>Rhinovirus - common cold
>Coxsackievirus - hand-foot-mouth dse, aseptic meningitis.
>HAV
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39
Q

Hepevirus

A

HEV

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40
Q

Calicivirus

A

Norovirus - viral gastroenteritis

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41
Q

Flaviviruses

A 
HCV
Yellow fever
Dengue
West nile virus
St. Louis encephalitis
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42
Q

Togavirus

A

Rubella

Easter/Western equine encephalitis

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43
Q

Retroviruses

A

HIV - AIDs (lentivirus)
HTLV - T cell leukemia (oncovirus)
Have reverse transcriptase

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44
Q

Coronavirus

A

Coronavirus - common cold

SARS

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45
Q

Orthomyxoviruses

A

Influenza virus

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46
Q

Paramyxoviruses

A

> Parainfluenza - croup
RSV - bronchiolitis in babies
Measles, Mumps

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47
Q

Rhabdovirus

A

Rabies

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48
Q

Filoviruses

A

Ebola/Marburg hemorrhagic fever

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49
Q

Arenaviruses

A

> LCMV - lymphocytic choriomeningitis virus

>Lassa fever encephalitis

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50
Q

Bunyavirus

A

> California encephalitis
Sandfly/Rift Valley fevers
Crimean-Congo hemorrhagic fever
Hantavirus - hemorrhagic fever, pneumonia

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51
Q

Delta virus

A

Defective virus – needs HBV to replicate

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52
Q

IL-1

A

Secreted by macrophages.
Acute inflammation.
Fever.
Recruits WBCs.

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53
Q

IL-6

A

Secreted by macrophages.

Acute phase reactant prodn.

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54
Q

IL-8

A

Secreted by macrophages.

Neutrophil chemotactic.

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55
Q

IL-12

A

Secreted by macrophages.
Th1 differentiation.
Activated NK cells.

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56
Q

TNF-alpha

A

Secreted by macrophages.
Mediates septic shock.
WBC recruitment, vascular leak.

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57
Q

IL-2

A

Secreted by T cells.

T cell growth.

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58
Q

IL-3

A

Secreted by T cells.

Growth and differentiation of BM stem cells.

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59
Q

IFN-gamma

A

Secreted by Th1 cells.
Stimulates macrophages to kill.
Activated NK cells to kill.

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60
Q

IL-4

A

Secreted by Th2 cells.
Th2 differentiation.
B cell growth – IgE, IgG.

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61
Q

IL-5

A

Secreted by Th2 cells.
B cell diff – IgA.
Eosinophils.

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62
Q

IL-10

A

Secreted by Th2 cells.
Attenuates immune response, inflammation.
Inhibits macrophages and dendritic cells.

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63
Q

TCR.

What cells? Binds to?

A

T cells.

Binds Ag-MHC complex

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64
Q

CD28.

What cell? Binds to?

A

T cells.

Binds to B7 on APCs

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65
Q

CD40L.

What cell? Binds to?

A

Helper T cells.

Binds to CD40 of B cells

66
Q

CD21.

What cell? Binds to?

A

B cells.

Receptor for EBV

67
Q

CD40.

What cell? Binds to?

A

B cells.

Binds to CD40L of Helper T cells

68
Q

MHC II.

What cell? Binds to?

A

APCs (B cells, macrophages).

Binds to TCR of CD4+ T cells

69
Q

B7.

What cell? Binds to?

A

APCs.

Binds to CD28 on T cells

70
Q

Fc and C3b receptors.

What cell? Function?

A

Macrophages.

To enhance phagocytosis

71
Q

CD4.

What cell?

A

Helper T cells

72
Q

CD8.

What cell?

A

Cytotoxic T cells

73
Q

CD16.

What cell? Binds to?

A

NK cells.

Binds to Fc of IgG, for antibody-dependent cell-mediated cytotoxicity.

74
Q

CD56.

What cell?

A

Unique marker for NK cells

75
Q

BCR-ABL.

Tumor?

A

CML, ALL

76
Q

BCL-2.

Tumor?

A

Follicullar lymphoma, undifferentiated lymphoma

77
Q

BRAF.

Tumor?

A

Melanoma

Non-hodgkin lymphoma

78
Q

C-myc.

Tumor?

A

Burkitt lymphoma

79
Q

HER2/neu (c-erbB2).

Tumors?

A

Breast, ovarian, gastric CA

80
Q

L-myc.

Tumor?

A

Lung tumor

81
Q

N-myc.

Tumor?

A

Neuroblastoma

82
Q

RAS.

Tumors?

A

Colon, lung, pancreatic cancer

83
Q

RET.

Tumors?

A

MEN 2a, 2b

Medullary thyroid cancer

84
Q

APC.

Tumor?

A

Colorectal cancer (FAP)

85
Q

BRCA1/BRCA2.

Tumor?

A

Breast, ovarian cancer

86
Q

NF1, NF2.

Tumors?

A

Neurofibromatosis type 1 (neurofibromin)

Neurofibromatosis type 2 (Merlin/schwannomin)

87
Q

p16.

Tumor?

A

Melanoma

88
Q

p53.

Tumors?

A

Most human cancers, Li-Fraumeni

89
Q

PTEN.

Tumors?

A

Breast, prostate, endometrial cancers

90
Q

Rb.

Tumor?

A

Retinoblastoma, osteocarcinoma

91
Q

VHL.

Tumor?

A

Von Hippel-Lindau dse

Renal cell carinoma

92
Q

TSC1, 2.

Tumor?

A

Tuberous sclerosis (hamartin; tuberin)

93
Q

DCC.

Tumor?

A

Colon cancer

94
Q

DPC4/SMAD4.

Tumor?

A

Pancreatic cancer

95
Q

Cancer screening.

How many cell divisions for early ssx? Purpose of screening? Examples?

A

At least 30 divisions of a single mutated cell will result in early ssx. Each division has inc. mutations, so poor prognosis if cancer detected late.
>Purpose: 1) detect dysplasia before CA, 2) detect CA before clinical sx arise.
>Examples: pap smear, mammogram, colonoscopy

96
Q

Psammoma bodies.

Found in what diseases?

A 
>Laminated, concentric spherules w/ dystrophic calcification.
>Papillary CA of thyroid.
>Serous papillary cystadenoCA of ovary.
>Meningioma.
>Malignant mesothelioma.
97
Q

Cholinesterase inhibitor poisoning. (organophosphates: Echothiophate, Malathion, Parathion; Nerve gas Sarin)
DUMBBEELSS

A

> Irreversibly inhibit AChE.
Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle/CNS, Lacrimation, Sweating, Salivation.
Tx: Atropine + Pralidoxime (regenerates AChE if given early).

98
Q

Atropine

[Action, SE, Tx]

A

Muscarinic antagonist; Blocks DUMBBEELSS
>Mydriasis, cycloplegia; Dec. airway secretions; Dec. gastric acid secretion, Dec. peristalsis; Dec. urinary urgency
>SE: inc. body temp (dec. sweating), dry mouth, flushed skin, cycloplegia, disorientation
>Tx: Physostigmine (Neostigmine, Edrophonium)

99
Q

CYP450 Inducers

Chronic alcohol and Gritty Carbs NevR Stop Phen-Phen

A 
Chronic alcohol use
St. John's wort
Phenytoin
Phenobarbital
Rifampin
Griseofulvin
Carbamazepine
Nevirapine
100
Q

CYP450 Inhibitors

Alcohol abuse and Grapefruit juice RACK QuIMs

A 
Acute alcohol abuse
Ritonavir (-avirs)
Amiodarone
Cimetidine
Ketoconazole
Sulfonamides
INH
Grapefruit juice
Quinidine
Macrolide's (except azithromycin)
101
Q

CYP450 substrates

A

Anti-epileptics
Warfarin
Theophylline
OCPs

102
Q

Sulfa drugs

[Drug names, ssx of sulfa allergies]

A

Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamides, Sulfasalazine, Sulfonylureas
Sulfa allergies: fever, UTI, SJS, hemolytic anemia, thrombocytopenia, agranulocytosis, urticaria

103
Q

CAMP factor.

Which bacteria? Function?

A

> Produced by S. agalactiae (GBS). Enlarges the area of hemolysis formed by S. aureus.
Arrowhead clearing at junction of the 2 organisms)

104
Q

Culture tests for C. perfringens

A

> “Stormy fermentation” on milk media.
Double zone of hemolysis.
Nagler reaction on egg yolk agar (opalescence around colonies)

105
Q

Whipple Triad (of insulinoma)

A

> Low Blood glucose
Ssx of Hypoglycemia
Ssx disappear w/ normalization of glucose levels

106
Q

Cushing reflex is the body’s way of maintaining cerebral perfusion in the setting of inc. ICP (brain injury). What are the roles of the chemoreceptors and baroreceptors in this reflex?

A

> Inc ICP compresses cerebral arteries – cerebral ischemia, inc. PCO2 – chemoreceptors send signals to vasomotor center to inc. peripheral vasoconstriction – inc. CO, inc. MAP (HTN) – more blood to brain, better cerebral perfusion
Reflex Bradycardia due to stimulation of peripheral baroreceptors from increased stretch – signals sent to VMC to dec. HR

107
Q

What is the cause of decreased, irregular respiration (respiratory depression) in Cushing reflex?

A

> Reduced perfusion of brainstem from swelling or possible brain herniation (due to inc. ICP) – occurs if condition is not caught early enough. (Central chemoreceptors in medulla oblongata detect pCO2 in brain CSF).
Cushing triad: HTN, bradycardia, respiratory depression

108
Q

Diagnostic tests for MI

A

> Gold standard for first 6 hrs: ECG.
Troponin I: rises after 4 hrs, elevated for 7-10 days, specific.
CK-MB: rises after 6-12 hrs, normal after 48 hrs; diagnose reinfarction, nonspecific (skeletal muscle).

109
Q

Duke’s criteria for Bacterial endocarditis

A

B.E.F.E.V.R (2 major / 1 major, 3 minor/ 5 minor)
>Major: (+) Blood culture, (+) Endocardial involvement on Echo.
>Minor: Fever > 38C, Vascular phenomenon (Janeway lesions, emboli, infarct), Evidence of micro/immuno findings (Osler nodes, Roth spots), Risk factors.

110
Q

Jones criteria for Rheumatic Fever

A 
J.O.N.E.S (2 major / 1 major, 2 minor)
Joints (migratory polyarthritis)
❤️ (pancarditis)
Nodules (Subcutaneous)
Erythema marginatum
Sydenham chorea
>Minor: Fever, arthralgia, inc. acute phase reactants
111
Q

Aortic stenosis murmur

A

> Systolic murmur, Crescendo-decrescendo w/ peak mid-systole.
Inc. LV pressure&raquo_space; aortic pressure
“Pluses parvus et trades”: pulses weak w/ delayed peak.
Syncope, Angina, Dyspnea (SAD).
Due to age-related calcification or early-onset calcification of bicuspid aortic valve

112
Q

Mitral/Tricuspid regurgitation murmur

A

> Holosystolic, high-pitched “blowing” murmur.
Mitral - apex radiating to axilla, IHD (post-MI), doesn’t usually intensify w/ inspiration.
Tricuspid - tricuspid area radiating to right sternal border, intensifies w/ inspiration
Assctd w/ RF and infective endocarditis.

113
Q

Mitral valve prolapse murmur

A

> Late systole; crescendo w/ midsystolic click.
Most frequent valve lesion.
Loudest just before S2, apex.
Predisposes to infective endocarditis.
Caused by myxomatous degeneration, RF, chord rupture.

114
Q

VSD murmur

A

Holosystolic, harsh-sounding.

Loudest at tricuspid area.

115
Q

Aortic regurgitation murmur

A

> Early diastolic murmur, high-pitched “blowing” murmur.
Hyper dynamic pulse when severe and chronic (head bobbing, bounding pulses).
Due to aortic root dilation, bicuspid aortic valve, endocarditis, RF.
Can progress to left HF

116
Q

Mitral stenosis murmur

A

> Diastolic murmur; opening snap ff. by rumbling.
Inc. LA pressure&raquo_space; LV pressure.
Due to RF; Can lead to LA dilatation.

117
Q

PDA murmur

A

> Continuous, machine-like.
Loudest at S2, left infraclavicular area.
Due to congenital rubella, prematurity.

118
Q

High anion gap metabolic acidosis (MUDPILES)

A 
Methanol (formic acid)
Uremia
DKA
Propylene glycol
Iron tablets, Isoniazid
Lactic acid
Ethylene glycol (antifreeze)
Salicylates
119
Q

Normal anion gap metabolic acidosis (HARD-ASS)

A 
Hyperalimentation
Addison disease (dec. aldosterone)
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
120
Q

Acute PSGN (LM, IF, EM)

A

> LM: enlarged, hypercellular glomeruli.
IF: “starry sky” granular appearance (Ig, IgM, C3).
EM: sub epithelial IC humps

121
Q

RPGN (LM, IF)

A

> LM, IF: crescentic moon shape filled w/ fibrin and plasma proteins

122
Q

DPGN (LM, EM, IF)

A

> LM: “wire looping” of capillaries.
EM: subendothelial IgG-based IC deposits.
IF: granular.

123
Q

IgA nephropathy (LM, EM, IF)

A

> LM: mesangial proliferation.
EM: mesangial IC deposits.
IF: IgA-based IC deposits in mesangium

124
Q

Alport syndrome (LM, EM)

A

LM, EM: thinning and splitting of GBM

125
Q

MPGN type I (EM, IF, PAS, H and E)

A

> EM: subendothelial deposits.
IF: granular.
PAS, H and E stains: “tram-track” due to GBM splitting caused by mesangial ingrowth.

126
Q

MPGN type II (EM findings)

A

EM: intramembranous deposits, “dense deposits”

127
Q

FSGS (LM, IF, EM)

A

> LM: segmental sclerosis, hyalinosis
IF: nonspecific for focal deposits of IgM, C3, C1.
EM: effaced foot processes

128
Q

MCD (LM, IF, EM)

A

> LM: normal glomeruli (maybe lipid in PCT cells).
IF: nonspecific deposits.
EM: effaced foot processes

129
Q

Membranous nephropathy (LM, IF, EM)

A

> LM: diffuse capillary and GBM thickening.
IF: granular.
EM: “spike and dome” w/ sub epithelial deposits

130
Q

Amyloidosis nephrotic syndrome (LM findings)

A

LM: Apple-green birefringence under polarized light w/ congo red stain

131
Q

Diabetic glomerulonephropathy (LM findings)

A

LM: GBM thickening, mesangial expansion, Kimmelstiel-Wilson lesions (eosinophilic nodular glomerulosclerosis)

132
Q

External carotid branches (SALFOPMS, from bottom up)

A 
Superior thyroid artery
Ascending pharyngeal artery
Lingual artery
Facial artery
Occipital artery
Posterior auricular artery
Maxillary artery (terminating branch)
Superficial temporal artery (terminating branch)
133
Q

Process of Ammoniagenesis in PCT cells

A

> Site for RECLAIMING HCO3 that’s been filtered.
Intracellular CA combines CO2 and H20 into H2CO3 –> dissolves into H+ and HCO3 –> HCO3- reabsorbed while H+ secreted into urine (Na/H antiporter) –> H+ combines w/ urine HCO3 to become H2CO3 –> CA dissolves H2CO3 into CO2 and Water, w/c diffuse back into cell to continue cycle.

134
Q

HCO3- regenerated and reabsorbed in Collecting ducts

A

CO2 from renal interstitium diffuses into cell and combines w/ H2O via CA to become H2CO3 –> dissolves into H+ and HCO3- –> HCO3 reabsorbed while H+ secreted (H-ATPase) –> H+ combines w/ acid buffers to be secreted (NH3, PO4).

135
Q

Renal collecting duct is the primary sign for K+ excretion (Na/K-ATPase) and excretion of excess H+ (H/K-ATPase). How are these channels affected by Aldosterone?

A

> In principal cells, aldosterone enhances action of ENaC (Na reabsorbed), epithelial K channels (K loss), and N/K pump –> K+ excretion.
In alpha-intercalated cells, aldosterone enhances H/K pump to secrete H+ in exchange for K+. H+ is excreted w/ HPO3 and NH3 as H2PO4 and NH4+.

136
Q

Pathogenesis of RTA type 1 (distal)

A

> Inability to regenerate HCO3- due to dysfunctional H/K-ATPase (H out, K in) in collecting tubules – Severe Hypokalemia.
Urine pH > 5.5 (alkaline, dec. titratable acid in urine).
Dec. HCO3, H+ combines w/ Cl- in blood –> Normal anion gab metabolic acidosis.
Causes: amphora, lithium, Sickle cell trait/dse

137
Q

Pathogenesis of RTA type 2 (proximal)

A

> Inability of PCT to reclaim HCO3.
Urine is initially at pH > 5.5 (alkaline), but when serum HCO3 finally equals the lowered renal threshold for HCO3 reclamation, the PCT can go back to reclaiming HCO3 and urine pH

138
Q

Pathogenesis of RTA type 4 (Hyperkalemic)

A

MC RTA in adults.
>No aldosterone – Na loss, K retention – Hyperkalemia, w/c inhibits ammoniagenesis in PCT – transcellular switch b/w H+ and K+, so K+ enters cell while H+ exits – intracellular alkalosis inhibits ammonia synthesis from glutamine, no generation of HCO3.
>Normal anion gap Metabolic Acidosis.
>Causes: dec. Aldosterone prod (ACEi, ARBs), aldosterone resistance (K-sparing diuretics, nephropathy due to obstruction)

139
Q

Structures found at vertebral levels T4, T8, T10, T12

A

> T4: sternal angle of Louis, begin and end of aortic arch, end of superior mediastinum, trachea bifurcates.
T8: IVC.
T10: esophagus, CN X.
T12: aorta, thoracic duct, azygous vein.

140
Q

What is the mechanism of gastric H+ secretion by gastric parietal cells?

A

After a meal, CO2 is extracted from the blood and converted, w/ H20, by CA into H+ and HCO3. Activation of parietal cell by Histamine, Gastrin, and ACh stimulates the H/K-pump to secrete the H+ in exchange for K+. The HCO3 is absorbed into bloodstream (“alkaline tide” of venous blood) in exchange for Cl-. Cl- maintains (-) potential of stomach lumen, and Cl- is also secreted w/ H+ to form HCl.

141
Q

Only monosaccharides are absorbed by enterocytes. What is the transporter for Glucose and Galactose? For Fructose? What transports all monosaccharides in the blood?

A

> Glucose, Galactose: SGLT1 (Na dependent).
Fructose: GLUT5.
Blood transporter: GLUT2.

142
Q

What is the D-xylose absorption test? Where is it useful?

A

D-xylose is a monosaccharide that doesn’t need pancreatic enzymes for digestion before absorption, but requires only intact mucosa. Differentiates GI musoca damage from other causes of malabsorption.
In pancreatic insufficiency, the test has normal absorption w/ normal urinary excretion. If there is an intestinal mucosal defect or bacterial overgrowth, there is dec. excretion due to a problem w/ absorption.

143
Q

Opioid intoxication ssx

A 
Respi/CNS depression
Pupillary constriction (pinpoint pupils)
Seizures (overdose)
144
Q

Opioid withdrawal ssx

A

Sweating
Dilated pupils
Piloerection
Flu-like ssx (diarrhea, nausea, rhinorrhea, fever)

145
Q

Amphetamine intoxication ssx

A 
Euphoria, grandiosity
Pipillary dilation
Prolonged wakefulness and attention
HTN, tachycardia
Severe: cardiac arrest, seizure
146
Q

Amphetamine withdrawal ssx

A

Anhedonia
Hypersomnolence
Existential crisis

147
Q

Cocaine intoxication ssx

A 
Impaired judgment
Pupillary dilation
Hallucinations (tactile)
Combative, uncooperative
Sudden cardiac death (potent vasoconstrictor)
148
Q

Cociaine withdrawal ssx

A

Hypersomnolence
Psychological craving
Depression/suicidality

149
Q

Barbiturate intoxication ssx

A

Low safety margin

Marked respi depression

150
Q

Barbiturate withdrawal ssx

A

Life-threatening cardiovascular collapse

Delirium

151
Q

BZD intoxication ssx

A

Greater safety margin vs Barbs
Minor respi depression
Ataxia

152
Q

BZD withdrawal ssx

A

Rebound anxiety
Depression
Sleep disturbance

153
Q

PCP intoxication ssx

A 
Belligerence
Impulsivity
Homocidality (violent behavior)
Psychosis
Delirium
Nystagmus
154
Q

LSD intoxication ssx

A

Perceptual distortion (visual, auditory)
Depersonalization
Possible flashbacks

155
Q

Marijuana (cannabinoid) intoxication ssx

A

Euphoria, Paranoid delusions
Perception of slowed time
Conjunctival injection
Hallucinations

156
Q

Marijuana withdrawal ssx

[peak, detectability]

A

Depression, Insomnia, Nausea, Anorexia.
Peaks in 48 hours, lasts 5-7 days.
Detectable in urine up to 1 month (stored in lipophilic tissues, slowly released).

157
Q

What is the antibiotic of choice for treating Lung abscesses?

A

Clindamycin can cover a combination of anaerobic oral flora (Bacteroides, Fusobacterium, Peptostreptococcus) and aerobic bacteria.

158
Q

C.R.A.B. of Multiple myeloma

A

> C: Hypercalcemia (GI ssx).
R: Renal involvement (thirst).
A: Anemia (fatigue, pallor), thrombocytopenia.
B: Bone lytic lesions, Back pain (fractures).

159
Q

Chromosomal translocations: Burkitt lymphoma, CML, Mantle cell lymphoma, Follicular lymphoma, AML-M3

A

> Burkitt lymphoma: t(8;14), c-myc activation.
CML: t(9;22) Philadelphia chromosome, BCR-ABL hybrid.
Mantle cell lymphoma: t(11;14), cyclin D1 activation.
Follicular lymphoma: t(14;18), Bcl-2 activation.
AML-M3: t(15;17)

160
Q

Dermatomes: C2, C3, C4, T4, T7, T10, L1, L4

A 
>C2: posterior skull
>C3: neck (turtleneck)
>C4: low collar
>T4: nipple line
>T7: xiphoid
>T10: umbilicus
>L1: inguinal ligament
>L4: kneecap
161
Q

Clinical reflexes: biceps, triceps, patella, achilles, anal wink, cremaster

A 
>Achilles: S1, S2
>Patella: L3, L4
>Biceps: C5, C6
>Triceps: C7, C8
>Anal wink: S3, S4
>Cremaster: L1, L2
162
Q

Describe the regulation of iron absorption.

A

> Dec. iron stores: upregulate DMT, ferroportin; dec. liver hepcidin secretion – DMT absorbs Fe from gut lumen, ferroportin releases Fe into blood – transferrin transports Fe to liver and marrow.
Inc. iron stores: DMT downregulated, liver releases hepcidin w/c degrades ferroportin.

Step 1 Uworld and Notes (64 decks)

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