Random Review Part 3 Flashcards

1
Q

Observational Studies summary

A

Cross-sectional: Group of people with a disease, lets see if they have a gene present. Can’t establish causality

Case-control (only retrospective): Group of people with COPD. What were the odds they were smokers for each group? Odds ratio

Cohort (pro or retrospective): Group of smokers, what is the risk of getting COPD?

Clinical trials: Is it safe? Does it work? Is it better? Can it stay?”

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2
Q

Select biases/effects

A

Berkson bias - study population selected from hospital

Pygmalion effect - researchers believe in efficacy of treatment which affects the outcome

Hawthorn effect - Participants knowledge of being studied affects outcome

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3
Q

Disease prevention

A
Primary = preventing
Secondary = screening
Tertiary = treating
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4
Q

Lymph node structure

A
Follicle = B cell
Medulla = reticular cells + macrophages
Paracortex = T-cells
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5
Q

Spleen structure

A
Periarteriolar lymphatic sheeth = T cells
Follics = B-cells
Marginal zone (between red and white) = APCs
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6
Q

Cell markers

A

CD16 (binds Fc) or CD56 = NK cells
CD3/CD4/CD25/FOXP3 = Treg
CD14 (recognizes LPS) = macrophages
CD34 = hematopoietic stem cell

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7
Q

Th1 cells activate:

A

Macrophages (IFN-y)

Cytotoxic T-cells (IL-12)

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8
Q

To activate Th1 or Th2 cells:

A

Th1 by IL-12

Th2 by IL-4

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9
Q

Turn down immune response

A

TGF-B, IL-10

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10
Q

Septic shock and cachexia

A

TNF-a

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11
Q

X-linked agammaglobulinemia

A

Manifestations after 6 months due to IgG from mother still in circulation

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12
Q

IL-12 Receptor Deficiency

A

Decreased IFN-y (due to decreased TH1 response). Often presents after BCG vaccine w/disseminated mycobacterial infection. Also fungal infection.

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13
Q

Hyper-IgE syndrome

A

Deficient Th17 cells (STAT3 mutation) –> neutrophils not recruited to sites of infection

FATED: 
Facies (coarse)
Abscesses (staph)
Teeth (retained primary )
IgE
Derm problems (eczema)
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14
Q

SCID causes

A
IL-2R defective (most common, X-linked)
ADA deficiency (AR)
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15
Q

Chediak Higashi Syndrome

A

Lysosomal trafficking regulator gene. Microtubule dysfunction. Partial albinism. Peripheral neuropathy. Giant granules in granulocytes and platelets.

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16
Q

Immunosupressants

A

Cyclosporine –Binds cyclophilin, blocks calcineurin, no NFAT, no IL-2 transcript
Tacrolimus – Binds FKBP, same as above, no IL-2 transcript
Sirolimus (Rapamycin) – Binds FKBP, inhibits mTOR, prevents IL-2 response
Daclizumab, basiliximab – blocks IL-2R
Glucocorticoids – Inhibits NF-kB

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17
Q

Bcl-2 inhibits:

A

BAX/BAK and Apaf-1

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18
Q

CD11/CD18 (LFA-1/Mac-1)

A

Let’s fuck mac daddy, Im 18 now. Integrins on leukocyte. defective in LAD type I (effects tight binding). ICAM, VCAM (POV, vag cam) to film it. The endothelial sites for tight binding.

If you have decreased Sialyl Lewis to initiate the whole process, thats LAD type 2 (effects margination and rolling)

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19
Q

Wound healing factors

A

PDGF - smooth muscle cell migration, fibroblast growth for collagen synthesis
FGF - Stimulates angiogenesis
EGF - Cell growth via tyrosine kinases
TGF-B - angiogenesis, fibrosis, cell cycle arrest

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20
Q

TNF-a

A

Important in maintaining granulomas

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21
Q

Amyloidosis

A

Cardiac atria - ANP
Thyroid - Calcitonin
Pancreatic islets - Islet amyloid polypetitde (Amylin)
Cerebrum - B-amyloid
Pituitary - Prolactin
Old age - transthyretin (esp in myocardium)

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22
Q

Dermatomyosites malignancy

A

Think GU

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23
Q

c-kit

A

GIST

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24
Q

NF1 vs NF2 gene

A

NF1 = Ras GTPase, neurofibromin

NF2 - Merlin (schwannomin) protein

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25
Q

p16

A

Melanoma

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26
Q

VHL

A

Inhibits hypoxia inducible factor 1a

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27
Q

PO2 of umbilical vein

A

pretty low, at 30mmHg

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28
Q

Fetal flow of blood (IVC vs SVC)

A

IVC - FO

SVC - PA to ductus

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29
Q

Remnants

A

allaNtois –> mediaN umbilical vein
umbiLical arteries –> mediaL umbilical ligaments
umbilical vein –> ligamentum teres hepatis inside falciform ligament

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30
Q

Most peripheral resistance is from which vessel:

A

arterioles

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31
Q

When graphing cardiac vs vascular function curves

A

Inotropy changes cardiac function slow
Venous tone changes x intercept
TPR changes both curves at same time, but maintains same meeting point at the x axis (vasopressors, exercise)

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32
Q

Heart sounds summary

A

Systolic - aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD, MVP
Diastolic - aortic/pulmonic regurg, mitral/tricuspid stenosis

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33
Q

Holosystolic murmurs (2 of them)

A

MR/TR vs VSD – high pitched blowing at apex vs harsh-sounding at LSB

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34
Q

Opening snap/S2 length

A

Less = worse because over time LA develops more force and is able to open it quicker.

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35
Q

PDA

A

congenital rubella

36
Q

U wave

A

Hypokalemia

37
Q

Drugs that prolong QT

A

Some risk meds can prolong QT
Sotalol, risperidone, macrolides, chloroquine, protease inhibitors, quinidine, thiazides/TCAs

Also ondansetron and haldol

38
Q

Congenital long QT

A

1) Romano-Ward (AD), most common

2) Jervell and Lange-Nielsen syndrome (AR), +sensorineural deafness [2 names, 2 problems]

39
Q

Rate and rhyhtm control drugs

A

Rate: B-blockers, digoxin, non-dhp Ca2+ blockers
Rhythm: IC or III

40
Q

Nesiritide

A

recombinant BNP (think, nesa has no brain)

41
Q

Baro/chemoreceptors transmit to:

A

solitary nucleus of medulla

42
Q

Free wall rupture due to

A

macrophage mediated structural degradation (days 3-14)

43
Q

All septal leads =

A

Anterior (LAD)

44
Q

I, aVL, V5-V6

A

Lateral (LCX)

45
Q

II, III, aVF

A

Inferior (RCA)

46
Q

Post MI pericarditis

A

Fibrinous - 1-3 days after

Dressler syndrome - autoimmune, 2+wks after

47
Q

Loffler syndrome

A

Endomyocardial fibrosis w/eosinophilic infilitrate

48
Q

heart failure cells

A

pulmonary edema can cause hemosiderin laden macrophages over time

49
Q

endocarditis on heart valve cause

A

s. epidermidis

50
Q

Cardiac tumors

A

Mxyoma most often in left atrium

Rhabdomyomas associated with tuberous sclerosis

51
Q

Kaposi vs bacillary angiomatosis

A

lymphocytic vs neutrophilic infilitrate

52
Q

Polyarteritis nedosa

A

Associated with HBV
Does not involve pulmonary arteries
Immune complex mediated
Transmural inflammation w/fibrinoid necrosis

53
Q

Microscopic polyangiitis

A

Like Wegeners but without the nasopharngeal involvement, no granulomas, and instead p-ANCA mediated

54
Q

Churg-Strauss

A

associated with peripheral neuropathy and wrist/foot drop

55
Q

Nitroprusside caution

A

Cyanide toxicity, tx w/sodium thiosulfate

56
Q

Fenoldopam

A

D1 agonist that decreases BP and increases natriuresis

57
Q

Class I drugs

A

IB is Best post-MI, IC is Contraindicated post-MI (and structural/ischemic disease)

58
Q

Related hormones

A

Alpha subunit: TSH, FSH, LH, hCG
Stim by CRH: ACTH, MSH, B-endorphin
Stim by TRH: TSH, prolactin

59
Q

Cortisol effects

A
  • Upregulates a-1 receptors on arterioles to increase sensitivity to norepi and epi
  • Can find aldo receptors at high levels
  • Decrease osteoblast activity
60
Q

PTH and VitD

A

Very similar, including feedback regulation. Only diff is that VitD stims absorption of both Ca and phos

61
Q

Mg and Ca

A

Decreased Mg increases PTH seceretion, but severely depleted Mg decreases PTH because its needed as a cofactor. Thus patients resistant to Ca correction must first have Mg fixed.`

62
Q

cAMP hormones

A

FLAT ChAMP

FSH, LH, ACTH, TSH, CRH, ADH (V2), MSH, PTH

63
Q

Thyroid hormone functions

A

Increase B1 receptors in heart

Increase Na/K-ATPase activity

64
Q

Riedel thyroiditis

A

Thyroid replaced by fibrous tissue, can mimic anaplastic carcinoma. Related to IgG4 systemic disease (autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis)

65
Q

Increased cAMP in urine

A

PTH

66
Q

cyclists nerve injury

A

Ulnar

67
Q

Denosumab

A

Monoclonal ab against RANK-L

68
Q

Von Gierke

A

Glycogen storage disease (g6phostase) but can also present with excessive uric acid

69
Q

Reactive arthritis after:

A

Post-GI (dysentery causers), or post-chlamydia infections

70
Q

Poly/dermatomyositis histology + immuno

A
Polymositis = CD8 endomysial
Dermatomyositis = CD4 perimysial
71
Q

Lichen planus

A

6Ps: Pruritic, purple, polygoal, planar, papules

Associated w/HCV

72
Q

-dronates

A

bisphosphonates. pryophosphate analogs. bind hydroxyapatite, inibiting osteoclast activity

73
Q

Spinda bifida occulta AFP

A

normal. the other NTD have increased

74
Q

Not protected by BBB

A

Area postreme, OVLT (osmotic sensing), neurohypohysis

75
Q

Phases of sleep

A
Awake (Eyes open)    B
Awake (Eyes closed)  A
N1                                T
N2                                S(sleep spindle/kcomplex)
N3                               D
REM                             B
76
Q

Lateral Medullary Syndrome

A

Nucleus ambiguous effects (specific to this syndrome)
PICA
-Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)

77
Q

Lateral pontine syndrome

A

Facial nucleus effects (specific to this syndrome)

-Facial dronyu op means the AICAs pooped

78
Q

Friedreich ataxia

A

Friedreich is fratastic (frataxin), hes always stumbling around and falling, but he has a big sweet heart. Chromosome 9

79
Q

Cavernous Sinus components

A

Occular movements + V1, V2 (III, IV, V1, V2, VI)

Postganglionic sympathetic pupillary fibers –> horner syndrome

80
Q

Curtain drawn down vision

A

retinal detachment

81
Q

Butorphanol

A

mu partial agonist, kappa agonist –> good for migraie or labor, causes less respiratory depression

82
Q

Tramadol

A

Extremely weak opiod agonist, also blocks 5HT and NE reuptake [tram it all]

Caution: serotonin syndrome

83
Q

Local anesthetics

A

Amides have 2 I’s in the name, esters have 1. Esters more likely to produce allergy. Block inner portion of Na channel

84
Q

Amantadine

A

Used to be used for influenza A, but now used to increase dopamine release and decrease reuptake for parkinsons.

85
Q

Selegiline

A

Preferentially blocks MAO-B, which mostly degrades dopamine and not NE or 5HT