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Multisystems > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

Diffuse scleroderma has a early and significant incidence of? (list 2 organ systems involved)

A

Renal and interstitial lung disease

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2
Q

Ab assoc w/ diffuse scleroderma

-what is the Ab against?

A

Anti-Scl 70 -> anti-DNA Topoisomerase I

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3
Q

Skin involvement w/ lmtd scleroderma

A

Hands, face, feet and forearms (Acral distribution)

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4
Q

Pulm HTN and renal disease incidence in lmtd scleroderma

A

Late incidence PHTN -> 10-15%

Renal disease RARELY occurs

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5
Q

Ab seen w/ lmtd scleroderma

At which stage of the cell cycle does it attack?

A

Anticentromere Ab (ACA)

metaphase

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6
Q

Define CREST

A

Calcinosis -> dystrophic calcification of subcutaneous tissue

Raynaud’s phenomenon

Esophageal dysmotility

Sclerodactyly -> tight skin

Telangiectasia -> punctate blood vessel dilations

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7
Q

Difference b/w raynaud’s phenomenon and disease with regards to finger involvement

A

Disease -> healthy people
-symmetric involvement of fingers; usually all

Phenomenon -> 2ndary to disease
-asymmetric involvement of fingers

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8
Q

PHTN etiology in systemic vs lmtd scleroderma

A

Systemic -> 2ndary to ILD

Lmtd -> vaso-occlusive

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9
Q

Imaging of intestines in scleroderma patients with GI involvement

A

Stacked coin pattern w/ pseudodiverticula (doesn’t go through the muscle)

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10
Q

Scleroderma renal crisis often confused with what? when is this confusion increased?

A

TTP/HUS -> both have microangiopathic hemolysis and thrombocytopenia

If patient w/ renal crisis and no HTN -> confusion inc

DO NOT GIVE STEROIDS IF SCLERODERMA

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11
Q

MCTD contains clinical features of which disorders?

A

SLE, Scleroderma, polymyositis

Occasionally Sjogren’s and RA

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12
Q

High titer of which Ab in MCTD?

A

Anti-U1RNP Abs = HALLMARK

antibodies against a U1 ribonucleoprotein complex

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13
Q

Early clinical manifestations of MCTD

A

generalized malaise
arthralgias
low-grade fever

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14
Q

List 4 signs/sxs suggestive of MCTD

  • hands
  • renal and CNS disease
  • arthritis
  • PHTN
A

Raynaud’s w/ swollen hands and puffy fingers
-more impressive than scleroderma

Absence of severe renal and CNS disease

More severe arthritis than expected in CT disease

Insidious onset PHTN -> not always related to interstitial lung disease
-very bad news

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15
Q

Jaccoud’s arthropathy

A

deforming non erosive arthropathy characterised by ulnar deviation of the second to 5th fingers with MCP subluxation.

IMPORTANT -> correctable!
-b/c problem with ligaments

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16
Q

Confirmatory dx for Sjogren’s

A

Labial salivary gland bx

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17
Q

Key histologic feature of Sjogren’s

A

Focal collection or collections of LYMPHOCYTES

foci -> 50+ lymphocytes/4mm^2

Positive test > 1 foci aggregate per 4mm^2

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18
Q

Abs seen w/ Sjogren’s

A

Anti-Ro and/or SS-B (anti-La)

Also RF

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19
Q

Define Sjogren’s. Which type of HSR?

A

Autoimmune destruction of exocrine glands
-lacrimal and salivary are top 2

TYPE IV HSR

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20
Q

Define fibromyalgia

  • criteria for dx
  • proposed cause
  • factors involved in the etiology
A
  1. Chronic widespread pain and tenderness (>/= 3 months)
  2. Due to abnormal responsiveness or function of CNS
  3. Familial, environmental and genetic factors involved
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21
Q

Hallmark clinical features of fibromyalgia (list 8)

A
  1. chronic widespread pain
  2. sleep disturbance
  3. fatigue
  4. tenderness
  5. stiffness
  6. mood disturbances (anxiety, depression)
  7. Cognitive difficulties (dec concentration, forgetfulness, disorganization)
  8. Fxal impairment
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22
Q

Central pain disorders respond which type of pharmacologic tx?

A

neuroactive compounds

DESCENDING PATHWAY TARGETS

  • serotonin
  • NE

ASCENDING PATHWAY

  • glutamate
  • substance P
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23
Q

List 7 clinical characteristics of central pain disorders

A
  • multifocal pain and diffuse tenderness
  • higher current and lifetime hx of pain
  • multiple other somatic sxs (fatigue, memory, sleep issues etc.)
  • Sensitivity to multiple sensory stimuli (light, sound etc)
  • more common in WOMEN
  • strong familial/genetic underpinnings
  • triggered or exacerbated by stressors
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24
Q

Mech of pregabalin (lyrica)

  • ascending or descending pathway?
  • MC side effect reported?
A

Binds to alpha-2-delta subunit of VG Ca++ channels or neurons -> reduces Ca++ influx at nerve terminals -> inhibited release of GLUTAMATE and SUBSTANCE P

Works on the ASCENDING PATHWAY

MC side effect -> Dizziness

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25
Q

Duloxetine (cymbalta) and milnacipran (savella) MoA

  • ascending or descending pathway?
  • MC side effect reported?
A

SNRIs -> inhibit serotonin and NE reuptake

  • DESCENDING pathway
  • Nausea and headache
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26
Q

Non-pharm tx approaches for management of FM (list 4)

A
  1. Exercise
    - aerobic
    - 30-60 min of low to moderate intensity >/= 2 to 3x per week
  2. CBT
  3. PT
  4. Lifestyle and diet mods
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27
Q

Match the appropriate drug choice for FM with the following presentations:

  • pain, fatigue, depressed mood
  • pain, sleep disturbance, anxiety
A
  • pain, fatigue, depressed mood -> use SNRI (duloxetine, milnacipran)
  • pain, sleep disturbance, anxiety -> pregabalin (alpha-2-delta ligand)
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28
Q

5 components of metabolic syndrome

A
  • high fasting glucose
  • high TG
  • low HDL
  • high BP
  • high waist circumference
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29
Q

Impaired fasting glucose / impaired glucose tolerance

A

IFG -> 100-125

IGT -> 140-199

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30
Q

Diabetes criteria based on fasting plasma glucose and OGTT

A

FPG >/= 126

OGTT (2 hr post glucose load) >/= 200

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31
Q

General HbA1c target range

Post and pre prandial glucose?

A

HbA1c < 7.0% (individualize to the patient)

Pre-prend< 130 mg/dL
Post-prandial PG <180 mg/dL

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32
Q

Biguanides (metformin)

  • MoA
  • side effects
A

MECH

  • Activates AMP-kinase
  • dec hepatic glucose production

SE

  • Gastrointestinal
  • Lactic acidosis -> rare but 50% mortality
  • B-12 deficiency
  • Contraindications -> renal failure
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33
Q

Sulfonylureas/meglitinides

  • MoA
  • side effects
A

MECH
-Closes KATP channels -> Insulin secretion

SE

  • Hypoglycemia
  • Weight gain
  • Low durability

Meglitinides are NON-sulfonylurea secretagogues

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34
Q

Thiazolidinediones (pioglitazone)

  • MoA
  • side effects
A

MECH
Binds to PPAR-gamma nuclear transcription regulator -> inc insulin sensitivity in peripheral tissues

SE

  • weight gain
  • edema
  • hepatotoxicity
  • heart failure
  • bone fractures
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35
Q

DPP-4 inhibitors

  • linagliptin
  • saxagliptin
  • sitagliptin
A

inhibits breakdown of incretins (GLP-1 and GIP) -> DEC glucagon release and INC insulin release

SE

  • only modest dec in A1c
  • maybe pancreatitis
  • urticaria
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36
Q

Alpha-glucosidase inhibitors

A
  • Inhibits α- glucosidase
  • Slows carbohydrate absorption -> dec postprandial hyperglycemia

Basically medically induced lactose intolerance

SE
-GI -> osmotic diarrhea, gas

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37
Q

Insulin independent glucose uptake

A

BRICK L

  • Brain
  • RBCs
  • Intestine
  • Cornea
  • Kidney
  • Liver
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38
Q

human health hazard =

A

(Inherent toxicity) x (exposure)

Exposure = (dose) x (time)

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39
Q

How do people get poisoned?

1) 1-5 years
2) 5 - 18
3) Adult

A

1-5 -> accidental

5-18 -> accidental but increasingly intentional

Adults

  • intentional -> OD, suicide
  • accidental -> occupational exposure or incorrect dosing (elderly)
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40
Q

Opioid Toxidrome

-antidote?

A

Classic triad -> opioid OD until proven otherwise

  • coma
  • resp depression
  • miosis

Also

  • hypoTN
  • bradycardia

Antidote -> Naloxone

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41
Q

Cholinergic toxidrome (use mnemonic)

antidote

A 
D - defecation/diarrhea 
U - urination 
M - miosis
B - bradycardia 
B - bronchospasms/bronchorrhea 
E - emesis/excitation of skeletal muscles 
L - lacrimation 
S - sweating / salivation

Antidote -> atropine (competitive inhibitor) or pralidoxime (regenerates AChE if given early)

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42
Q

Sympathomimetic toxidrome

  • think?
  • some drugs
  • treatment?
A

Think withdrawal (alcohol, benzos) along with the sympathomimetic drugs

HTN -> stroke, MI, aortic rupture 
Tachy -> arrhythmia 
Hyperpyrexia -> heat stroke 
Mydriasis
Anxiety/delirium 
Diaphoresis

Drugs

  • caffeine
  • ephedrine
  • cocaine
  • ritalin (methylphenidate)
  • amphetamines

Tx -> BENZOS: depress release of catecholamines from the CNS

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43
Q

Anticholinergic toxidromes

A

Think opposite of DUMBBeLSS

Hot as a hare 
Dry as a bone 
Red as a beet 
Blind as a bat 
Mad as a hatter
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44
Q

How can you distinguish b/w parasympatholytic and sympathomimetic syndromes?

A

DIAPHORESIS -> only with sympathomimetic syndrome!

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45
Q

Life threats to muscarinic and nicotinic systems

A

Muscarinic -> bradycardia, bronchorrhea, seizures

Nicotoinic -> resp failure

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46
Q

Tx for organophosphate poisoning vs. carbamates

A

Organophosphates require OXIME in addition to ATROPINE

Oximes (e.g. pralidoxime) -> regenerate AChE

Atropine -> muscarinic antagonist

47
Q

List some anticholinergics (7 on this slide)

A 
Antihistamines
TCA
Muscle relaxants
Antipsychotics 
Antispasmodics 
Mushrooms 
Plants
48
Q

Tx for anticholinergic poisoning?

A
  1. lower temp
  2. give bezos: seizures, reduce agitations
  3. physostigmine
    - help make dx
    - crosses CNS
    - physostigmine phyxes atropine overdose
49
Q

How to tx beta blocker toxicity

A

Glucagon -> inc adenyl cyclase activity independent of beta-adrenergic receptor binding -> improved muscle contraction -> inc cardiac output

Also can add other drugs if necessary
-beta agonists
-calcium
insulin

50
Q

Some signs of alcohol w/drawal? what can it mimic? Tx?

A
  • tremor
  • delirium tremens
  • tachy
  • malaise
  • nausea

Mimics sympathetic drug overdose; NMDA receptors become dominant over GABA -> autonomic stimulation

Tx -> BENZOS or barbiturates

51
Q

immunoglobulins for which infectious agent are present in almost all lupus patients?

A

EBV

52
Q

Chronic mucocutaneous involvement with lupus

  • most common type (systemic localized?)
  • followed by
A
  1. DISCOID RASH -> Raised patches, adherent keratotic scaling, follicular plugging; older lesions may cause scarring
    - mostly stays localized but can become systemic in 2-10%
  2. Lupus panniculitis -> less common in chronic
    - systemic in 50% of cases
    - painful!
    - scarring and atrophy
    - inflammation of fat lobular septa -> hyalinization of adipose cells
53
Q

Which rash of lupus indicates systemic disease

A

Malar rash (Acute) -> fixed erythema, flat or raise, with sparing of nasolabial folds

54
Q

Appearance of subacute cutaneous lupus rash

  • is there scarring?
  • photosensitive?
A
  • annular
  • NO SCARRING
  • very photosensitive
55
Q

Diffuse alopecia in lupus patient suggests localized or systemic disease?

A

SYSTEMIC

56
Q

Type of arthropathy seen with SLE?

A

Jaccoud’s -> correctable

57
Q

Which SLE Abs are suggestive of renal disease and poor prognosis?

A

Anti-dsDNA -> active lupus nephritis

58
Q

6 classes of lupus nephritis

A

I - minimal mesangial LN
II - mesangial proliferative LN
III - focal LN
IV - Diffuse LN (subendothelial and intramembranous deposits)
V - membranous LN (subepithelial deposits)
VI - advanced sclerosis LN

59
Q

“Full house” IgG deposition of immunofluorescence -> think?

A

LUPUS

60
Q

General guidelines for txing lupus nephritis

for class 4 disease?

A

General

  • Continue hydroxychloroquine
  • ACE if proteinuria
  • BP control

Class 4 - worst prognosis
-Induction -> mycophenolate (cellcept) or cyclophosphamide
-Maintenance -> mycophenolate or azathioprine (Imuran)
Refractory -> rituxan or tacrolimus

61
Q

Signs/sxs of shrinking lung syndrome? cause?

A

Seen with lupus

Diaphragm muscle weakness -> elevated hemidiaphragm

  • unexplained dyspnea
  • RESTRICTIVE pattern of PFT
62
Q

Acute lupus pneumonitis signs and sxs

A
  • diffuse alveolar hemorrhage
  • hemoptysis
  • falling Hct
  • infiltrates
  • dyspnea

rare but 50% mortality

63
Q

which complement levels can be low in SLE? Why?

A

C4 and C3

CH50 (first aid)

Due to immune complex formation

64
Q

SLICC classification criterion for SLE

A

A) 4 criteria (see card 65 or lecture table) including at least ONE clinical and ONE immunological criterion

B) bx proven nephritis compatible w/ SLE and w/ ANA or anti-dsDNA Abs

65
Q

Clinical and immunological criteria for lupus

for reference only

A

CLINICAL

  • acute cutaneous lupus
  • chronic cutaneous lupus
  • oral ulcers
  • non-scarring alopecia
  • synovitis (2+ joints)
  • serositis
  • renal
  • neurologic
  • hemolytic anemia
  • leukopenia
  • lymphopenia
  • thrombocytopenia

IMMUNOLOGIC

  • ANA above lab ref range
  • Anti-dsDNA
  • Anti-Sm
  • Antiphospholipid Ab
  • Low complement
  • direct coombs test in absence of hemolytic anemia
66
Q

1st line IM agent in mild SLE?

  • what inferes w/ efficacy
  • toxicity
A

HYDROXYCHLOROQUINE aka Plaquenil (antimalarial)

smoking interferes w/ efficacy

Side effects

  • RETINAL TOXICITY -> srs bzns but rare (bull’s eye maculopathy)
  • GI intolerance
  • blue-grey discolouration
  • cardiotoxicity and myopathy (rare)
  • hypoglycemic effect
67
Q

Drug induced lupus associated w/ which Abs?

A

Anti-histone Abs

68
Q

list 4 drugs that can induce lupus? How does sx presentation differ from SLE?

A

She mentioned the following (see table for rest):

  • hydralazine
  • procainamide
  • INH
  • TNF-inhibitors

Renal, derm and neuro involvement is RARE

69
Q

Hip/joint pain in SLE patient may be due to which serious complication?

A

Avascular necrosis

70
Q

Best time to plan pregnancy in SLE patients?

A

When SLE is quiescent for at least 6 MONTHS

-measure complement levels

71
Q

Guidelines for anticoag if lupus patient has positive antiphospholipid Abs based on:

  • prior thrombosis
  • prior pregnancy loss
  • no prior pregnancy loss
A
  • prior thrombosis -> Heparin + ASA
  • prior pregnancy loss -> heparin + ASA
  • no prior pregnancy loss -> ASA 81mg alone or nothing
72
Q

Neonatal lupus

  • abs
  • permanent or self limited
  • scarring
  • tx
  • most dreaded complication
A

Anti-Ro (SSA) and Anti-La (SSB) Abs

Self limited and NON-scarring

Usually self resolving in 6 months

CONGENITAL HEART BLOCK

  • rare but very srs (1-3%)
  • give Dex if 1st or 2nd degree
  • 60% -> pacemakers
  • 20% mortality
  • risk jumps to 15% if previous sibling affected by CHB or rash

Can also get

  • thrombocytopenia
  • anemia
  • hepatic failure, hyperbilirubinemia or elevated liver enzymes
73
Q

Which drugs MUST be continued during pregnancy in a SLE patient

Which SLE drugs are Class X?

A

Plaquenil (HCQ)

Class X

  • MTX
  • Arava
  • thalidomide
74
Q

How many days does it take for effects of warfarin to kick in? Why?

A

4 days

  • half life of factor X = 48 hours
  • need to drop 2 half lives before anticoagulation effects are seen
75
Q

First 3 steps in clotting

A

platelet shape change, adhesion and aggregation

76
Q

What is the final common mediator that is blocked with the following drugs

  • clopidogrel
  • dabigatran
  • aspirin
  • abciximab
A

Dec expression of Gp IIb-IIIa - fibrinogen receptor which cause AGGREGATION of platelets

Note: all these drugs have different MoA but have the same end result = dec aggregation of platelets

77
Q

Which drug should be avoided when using clopidogrel? Why?

A

Proton pump inhibitors (e.g. omeprazole and esomeprazole)

PPIs INHIBIT the CP450 enzymes needed to ACTIVATE clopidogrel

78
Q

List 3 DIRECT inhibitors of Gp IIb/IIIa

A

Abciximab (MAb)

Eptifibatide (cyclic peptide)

Tirofaban (non-peptide)

79
Q

When should thrombolytics NOT be used for stroke tx?

A

INTRACRANIAL HEMORRHAGE - DO NOT USE!!!

80
Q

Why does tenecteplase have improved efficacy and bioavailability as compared to tPA

A

Tenecteplase - TNK-tPA
-3 point mutations to improve efficacy and bioavailability

Threonine (T) and Asparagine (N) mutation -> inc half life by 20 min

Lys (K) -> inc activity

81
Q

Which thrombolytic does NOT have intrinsic enzyme activity?

A

Streptokinase -> binds plasminogen, exposes active site, and promotes conversion of additional plasminogen to plasmin

82
Q

Dibigatran

  • MoA
  • benefit over warfarin
A

DIRECT thrombin (IIa) inhibitor

DOES NOT requires routine plasma concentration monitoring

oral alternative to warfarin

83
Q

UFH heparin vs LMWH -> compare:

  • MoA
  • which one is better/safer choice and why
  • name one LMWH drug mentioned in lecture and target
A

LMWH -> unable to to bind to thrombin (IIa) and ATIII simultaneously BUT can catalyze inhibition of Xa by ATIII

Advantage of LMWH over UFH

  • less binding to plasma and EC proteins
  • higher Bioavailability
  • more predictable response
  • less patient to patient variation
  • LESS NEED FOR MONITORING
  • lower incidence of THROMBOCYTOPENIA

Use LMWH for

  • prophylaxis and tx of DVT/PE
  • management of acute coronary syndrome
  • pregnant patients (no need to monitor)

enoXaparin -> selective Xa inhibitor (LMWH)

84
Q

Match the following skin prestations with size of affected vessel and the type of vasculitis

  1. Palpable purpura
  2. Skin ulcers
  3. Gangrene
A
  1. Palpable purpura
    - Vessel -> postcapillary venule (small)
    - Vasculitis -> any EXCEPT large vessel (e.g. giant cell)
    - goes to areas of dependence (gravity dependent)
  2. Skin ulcers
    - Vessel -> arteriole/small artery (small and medium arteries)
    - Vasculitis -> polyarteritis, granulomatosis w/ polyangiitis (Wegener’s)
  3. Gangrene
    - Vessel -> small and medium arteries
    - Vasculitis -> same as #2
85
Q

Match the following renal diseases with size of affected vessel and the type of vasculitis

  1. Glomerulonephritis
  2. Ischemic renal failure
A
  1. Glomerulonephritis
    Vessel -> capillary
    -Vasculitis -> any of the small vessel vasculitides
  2. Ischemic renal failure
    - Vessel -> small/medium arteries
    - Vasculitis -> usually polyarteritis nodosa or Takayasu’s
86
Q

Extreme diastolic HTN suggests a problem where?

A

Small/medium sized arteries and blood flow to kidneys

87
Q

C-ANCA Abs are against

A

proteinase 3 -> cytoplasmic granule in neutrophils

High Sp for Granulomatosis w/ polyangiitis (Wegener)

88
Q

P-ANCA stains

A

Perinuclear granules in neutrophils

target -> Myeloperoxidase

Seen in:

  • microscopic polyangiitis
  • Churg Strauss -> eosinophilic granulomatosis w/ angiitis
89
Q

Gold standard for making dx of vasculitis

A

Tissue bx

90
Q

What role do corticosteroids have txing vasculitis?

A

Reduce the fibrinoid necrosis and inflammation but crap for improving long term outcomes

91
Q

Improvement in long term outcomes in vasculitis agents is accomplished through?

A

Immunosuppressives (e.g. cyclophosphamide)

92
Q

Henoch Schonlein Purpura

  • age group
  • triad
  • deposition of
  • tx
  • prognosis
A

Children and young adults (younger than 20)

Triad:

  • abdominal (pain)
  • joint (Arthralgia)
  • skin (palpable purpura)

Can be w/ or w/out kidney involvement (IgA nephropathy)

IgA and complement tissue deposition

Tx

  • if abdomen and kidney involvement -> corticosteroids
  • cytoxan (cyclophosphamide) -> significant kidney involvement

Prognosis

  • 40% recurrence rate of IgA nephritis
  • 0.5% progress to end stage renal disease
93
Q

Difficult to tx asthma for several years is seen in which vasculitis?

A

Churg strauss

94
Q

Criteria for churg strauss dx

Treatment

A

NEED 4/6:

  • asthma
  • eosinophila > 10%
  • mono/polyneuropathy -> peripheral nerves
  • pulmonary infiltrates
  • paranasal sinus involvement (nondestructive)
  • eosinophils on organ tissue bx

Treatment

  • steroids
  • use IMS agents if myocarditis
95
Q

Criteria for granulomatosis w/ polyangiitis

A

2 or more:

  • nasal/oral ulcers or purulent/blood discharge
  • CXR -> nodules, infiltrates, cavities
  • Hematuria/RBC casts
  • granulomatous inflammation on bx either w/in or near a vessel wall

Tx

  • INTENSE IMMUNOSUPPRESSION
  • steroids + cytoxan -> huge impact on long term outcome
96
Q

Polyarteritis Nodosa

  • seen with which other disease?
  • never hits the?
  • Males vs females?
  • kidney involvement
  • other organ involvement
  • Tx
A 
Hep B (up to 50%)
RA

Lungs

M:F = 2:1

Severe diastolic HTN b/c reduces blood flow to kidneys
-NO CASTS

Organ involvement

  • joints
  • neurological -> peripheral nerves (e.g. foot drop)
  • Cardiac
  • GI -> mesenteric ischemia following a meal

Tx
-steroid + cytoxan -> 80% 5 year survival

97
Q

Giant cell arteritis

  • age group
  • sxs
  • vessels involved
  • cause of stroke
  • lab value used to screen
  • bx will show
  • Tx
A

Age -> 50+ (median 70)

Sxs

  • headache
  • scalp tenderness or nodules (not common)
  • visual sxs (e.g. double vision) -> risk of blindness 15%
  • jaw, tongue and extremity claudication
  • weight loss, fever, failure to thrive

Vessels

  • superficial temporal and ophthalmic arteries
  • branches of aortic arch (10-15% of time)

TIA/stroke -> 2ndary to thrombi from CAROTID ARTERY
-put them on ASA along w/ steroids

Lab -> elevated SED rate
-can be normal

Bx

  • segmental inflammation
  • multinucleated giant cells (not required) and LYMPHOCYTES

Tx

  • prednisone (at least 2 year) -> side effects = osteoporosis, diabetes, cataract etc.
  • prednisone for 1 month will prevent blindness
  • DON’T WAIT FOR BX to start tx if suspicion is high!!!
98
Q

Which constituents of E. coli are important in prompting the inflammasome? What is an inflammasome?

A
  1. PG cell wall

Inflammasome

  • Complex of genes that are intracellular receptors
  • Very important in driving pro-inflammatory cytokines
  • IL-1 beta
  • Chemoattractant
  • T-cell -> TH17 switch for host defense and pathologic inflammation
  1. Flagella
99
Q

Type 2 vs Type 3 secretion systems

A

T2SS
-enzymes and toxins exported to PERIPLASMIC space and then to external environment

T3SS

  • exports proteins through inner and outer bacterial membranes -> injects them into host cells
  • type thrEE “EEnjects”
  • Examples: E. coli and yersinia pestis
100
Q

Uropathogenic E. coli produce (blank) that allows binding to (blank) receptor on bladder epithelium

A

Type 1 (P) fimbriae binds to glycoprotein receptor

101
Q

Dysentery vs. diarrhea

A
  1. The typical symptom of diarrhea is watery stool. It is a dysentery if the stool is in the form of mucous, includes blood and the patient suffers from cramping and fever.
  2. Diarrhea usually affects the smaller bowel while dysentery affects the colon.
  3. The effects of diarrhea are not that serious, apart from a risk of dehydration. Dysentery can cause a lot of complications, if left untreated.
    http: //www.differencebetween.net/science/health/difference-between-dysentery-and-diarrhea/
102
Q

Tx for E. coli meningitis in neonate? What should NOT be used?

A

Ceftriaxone (3rd gen cephalosporin) or Ampicillin

DON’T use TMP-SMX -> kernicterus: bilirubin deposits in the basal ganglia (due to the sulfonamide)

103
Q

Leading cause of neonatal meningitis? followed by?

A

Group B streptococcus > E. coli

104
Q

What mech does E. coli use to cause neonatal meningitis

-discuss the strains

A

K1 capsule -> transport across BBB and serum resistance

Toxins

  • hemolysin
  • cytotoxic necrotizing factor (impairs host cytoskeleton)
  • cytolethal distending toxin -> DNase activity
105
Q

ETEC

  • acquired through
  • sxs
  • path
A

T - toxigenic/traveller’s

Acquired through
-ingestion of contaminated water/food

Sxs

  • diarrhea + nausea and cramps
  • vomiting, severe cramps, fever -> NOT TYPICAL

Path
-pili attach to gut epithelium -> production of heat stable and heat labile enterotoxins -> release of fluids

Extra info

  • HS -> guanylate cyclase
  • HL -> adenylate cyclase
106
Q

EPEC

  • population
  • acquired through
  • sxs
  • path
A

Population
-P -> peds/pathogenic

Acquired through
-person-person transmission

Sxs

  • diarrhea + nausea and cramps
  • low grade fever and vomiting

Path

  • attach to mucosa and cause effacement (flattening of vili)
  • T3SS
107
Q

EHEC

  • serotype
  • transmission
  • path
  • sxs
  • age group
  • which antibiotic
A

H - hemorrhage/hemolytic/hamburger

Serotype -> O:157:H7

Transmission
-undercooked meats (esp. ground beef)

Path
-shiga toxin (verotoxin)

Sxs

  • blood diarrhea
  • hemorrhagic colitis
  • HUS

Age
-extremes of age (young and old)

Tx

  • DON’T give antibiotics -> increased release of more toxins
  • supportive care -> dialysis
108
Q

EAEC

  • path
  • sxs
A

A - aggregative

Path
-use fimbriae (aggregative adherence fimbriae) to form biofilm -> mucosal damage w/ loss of microvilli

Sxs
-Mucoid diarrhea

109
Q

EIEC

  • path
  • sxs
A

I - invasive

Path

  • invasion plasmid: invades epithelial cells -> multiply in cytoplasm
  • thwarts phagosome formation

Sxs

  • diarrhea -> dysentery
  • severe cramps, fever, tenesmus
  • small volume mucous containing stools
110
Q

D-dimer sensitivity and specificity

A

Good Sn but crappy Sp (high FP rate)

-lots of things aside from PE can elevate D-dimer

111
Q

When should D-dimer be used for evaluating PE

A

Low (not too low or too high) clinical suspicion

112
Q

When should thrombolysis be used for PE?

A

If hemodynamically UNSTABLE and no CIs

Maybe if hypotensive but showing signs of right heart strain

  • on echo
  • or elevated troponin
113
Q

In which situations should V/Q be used over CTPA?

A
  • renal disease

- allergy to contrast

114
Q

When should CTPA be used over V/Q

A
  • patient is unstable
  • pregnancy -> less radiation to fetus w/ CTPA
  • after hours
  • crappy CXR

Multisystems (3 decks)

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