Quiz 1 Flashcards
(114 cards)
1
Q
Diffuse scleroderma has a early and significant incidence of? (list 2 organ systems involved)
A
Renal and interstitial lung disease
2
Q
Ab assoc w/ diffuse scleroderma
-what is the Ab against?
A
Anti-Scl 70 -> anti-DNA Topoisomerase I
3
Q
Skin involvement w/ lmtd scleroderma
A
Hands, face, feet and forearms (Acral distribution)
4
Q
Pulm HTN and renal disease incidence in lmtd scleroderma
A
Late incidence PHTN -> 10-15%
Renal disease RARELY occurs
5
Q
Ab seen w/ lmtd scleroderma
At which stage of the cell cycle does it attack?
A
Anticentromere Ab (ACA)
metaphase
6
Q
Define CREST
A
Calcinosis -> dystrophic calcification of subcutaneous tissue
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly -> tight skin
Telangiectasia -> punctate blood vessel dilations
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
8
Q
PHTN etiology in systemic vs lmtd scleroderma
A
Systemic -> 2ndary to ILD
Lmtd -> vaso-occlusive
9
Q
Imaging of intestines in scleroderma patients with GI involvement
A
Stacked coin pattern w/ pseudodiverticula (doesn’t go through the muscle)
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
11
Q
MCTD contains clinical features of which disorders?
A
SLE, Scleroderma, polymyositis
Occasionally Sjogren’s and RA
12
Q
High titer of which Ab in MCTD?
A
Anti-U1RNP Abs = HALLMARK
antibodies against a U1 ribonucleoprotein complex
13
Q
Early clinical manifestations of MCTD
A
generalized malaise
arthralgias
low-grade fever
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
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
16
Q
Confirmatory dx for Sjogren’s
A
Labial salivary gland bx
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
18
Q
Abs seen w/ Sjogren’s
A
Anti-Ro and/or SS-B (anti-La)
Also RF
19
Q
Define Sjogren’s. Which type of HSR?
A
Autoimmune destruction of exocrine glands
-lacrimal and salivary are top 2
TYPE IV HSR
20
Q
Define fibromyalgia
- criteria for dx
- proposed cause
- factors involved in the etiology
A
- Chronic widespread pain and tenderness (>/= 3 months)
- Due to abnormal responsiveness or function of CNS
- Familial, environmental and genetic factors involved
21
Q
Hallmark clinical features of fibromyalgia (list 8)
A
- chronic widespread pain
- sleep disturbance
- fatigue
- tenderness
- stiffness
- mood disturbances (anxiety, depression)
- Cognitive difficulties (dec concentration, forgetfulness, disorganization)
- Fxal impairment
22
Q
Central pain disorders respond which type of pharmacologic tx?
A
neuroactive compounds
DESCENDING PATHWAY TARGETS
- serotonin
- NE
ASCENDING PATHWAY
- glutamate
- substance P
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
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
25
Duloxetine (cymbalta) and milnacipran (savella) MoA
- ascending or descending pathway?
- MC side effect reported?
SNRIs -> inhibit serotonin and NE reuptake
- DESCENDING pathway
- Nausea and headache
26
Non-pharm tx approaches for management of FM (list 4)
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
27
Match the appropriate drug choice for FM with the following presentations:
- pain, fatigue, depressed mood
- pain, sleep disturbance, anxiety
- pain, fatigue, depressed mood -> use SNRI (duloxetine, milnacipran)
- pain, sleep disturbance, anxiety -> pregabalin (alpha-2-delta ligand)
28
5 components of metabolic syndrome
- high fasting glucose
- high TG
- low HDL
- high BP
- high waist circumference
29
Impaired fasting glucose / impaired glucose tolerance
IFG -> 100-125
IGT -> 140-199
30
Diabetes criteria based on fasting plasma glucose and OGTT
FPG >/= 126
OGTT (2 hr post glucose load) >/= 200
31
General HbA1c target range
Post and pre prandial glucose?
HbA1c < 7.0% (individualize to the patient)
Pre-prend< 130 mg/dL
Post-prandial PG <180 mg/dL
32
Biguanides (metformin)
- MoA
- side effects
MECH
- Activates AMP-kinase
- dec hepatic glucose production
SE
- Gastrointestinal
- Lactic acidosis -> rare but 50% mortality
- B-12 deficiency
- Contraindications -> renal failure
33
Sulfonylureas/meglitinides
- MoA
- side effects
MECH
-Closes KATP channels -> Insulin secretion
SE
- Hypoglycemia
- Weight gain
- Low durability
Meglitinides are NON-sulfonylurea secretagogues
34
Thiazolidinediones (pioglitazone)
- MoA
- side effects
MECH
Binds to PPAR-gamma nuclear transcription regulator -> inc insulin sensitivity in peripheral tissues
SE
- weight gain
- edema
- hepatotoxicity
- heart failure
- bone fractures
35
DPP-4 inhibitors
- linagliptin
- saxagliptin
- sitagliptin
inhibits breakdown of incretins (GLP-1 and GIP) -> DEC glucagon release and INC insulin release
SE
- only modest dec in A1c
- maybe pancreatitis
- urticaria
36
Alpha-glucosidase inhibitors
* Inhibits α- glucosidase
* Slows carbohydrate absorption -> dec postprandial hyperglycemia
Basically medically induced lactose intolerance
SE
-GI -> osmotic diarrhea, gas
37
Insulin independent glucose uptake
BRICK L
- Brain
- RBCs
- Intestine
- Cornea
- Kidney
- Liver
38
human health hazard =
(Inherent toxicity) x (exposure)
Exposure = (dose) x (time)
39
How do people get poisoned?
1) 1-5 years
2) 5 - 18
3) Adult
1-5 -> accidental
5-18 -> accidental but increasingly intentional
Adults
- intentional -> OD, suicide
- accidental -> occupational exposure or incorrect dosing (elderly)
40
Opioid Toxidrome
| -antidote?
Classic triad -> opioid OD until proven otherwise
- coma
- resp depression
- miosis
Also
- hypoTN
- bradycardia
Antidote -> Naloxone
41
Cholinergic toxidrome (use mnemonic)
antidote
```
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)
42
Sympathomimetic toxidrome
- think?
- some drugs
- treatment?
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
43
Anticholinergic toxidromes
Think opposite of DUMBBeLSS
```
Hot as a hare
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter
```
44
How can you distinguish b/w parasympatholytic and sympathomimetic syndromes?
DIAPHORESIS -> only with sympathomimetic syndrome!
45
Life threats to muscarinic and nicotinic systems
Muscarinic -> bradycardia, bronchorrhea, seizures
Nicotoinic -> resp failure
46
Tx for organophosphate poisoning vs. carbamates
Organophosphates require OXIME in addition to ATROPINE
Oximes (e.g. pralidoxime) -> regenerate AChE
Atropine -> muscarinic antagonist
47
List some anticholinergics (7 on this slide)
```
Antihistamines
TCA
Muscle relaxants
Antipsychotics
Antispasmodics
Mushrooms
Plants
```
48
Tx for anticholinergic poisoning?
1. lower temp
2. give bezos: seizures, reduce agitations
3. physostigmine
- help make dx
- crosses CNS
- physostigmine phyxes atropine overdose
49
How to tx beta blocker toxicity
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
Some signs of alcohol w/drawal? what can it mimic? Tx?
- tremor
- delirium tremens
- tachy
- malaise
- nausea
Mimics sympathetic drug overdose; NMDA receptors become dominant over GABA -> autonomic stimulation
Tx -> BENZOS or barbiturates
51
immunoglobulins for which infectious agent are present in almost all lupus patients?
EBV
52
Chronic mucocutaneous involvement with lupus
- most common type (systemic localized?)
- followed by
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
Which rash of lupus indicates systemic disease
Malar rash (Acute) -> fixed erythema, flat or raise, with sparing of nasolabial folds
54
Appearance of subacute cutaneous lupus rash
- is there scarring?
- photosensitive?
- annular
- NO SCARRING
- very photosensitive
55
Diffuse alopecia in lupus patient suggests localized or systemic disease?
SYSTEMIC
56
Type of arthropathy seen with SLE?
Jaccoud's -> correctable
57
Which SLE Abs are suggestive of renal disease and poor prognosis?
Anti-dsDNA -> active lupus nephritis
58
6 classes of lupus nephritis
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
"Full house" IgG deposition of immunofluorescence -> think?
LUPUS
60
General guidelines for txing lupus nephritis
for class 4 disease?
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
Signs/sxs of shrinking lung syndrome? cause?
Seen with lupus
Diaphragm muscle weakness -> elevated hemidiaphragm
- unexplained dyspnea
- RESTRICTIVE pattern of PFT
62
Acute lupus pneumonitis signs and sxs
- diffuse alveolar hemorrhage
- hemoptysis
- falling Hct
- infiltrates
- dyspnea
rare but 50% mortality
63
which complement levels can be low in SLE? Why?
C4 and C3
CH50 (first aid)
Due to immune complex formation
64
SLICC classification criterion for SLE
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
Clinical and immunological criteria for lupus
| for reference only
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
1st line IM agent in mild SLE?
- what inferes w/ efficacy
- toxicity
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
Drug induced lupus associated w/ which Abs?
Anti-histone Abs
68
list 4 drugs that can induce lupus? How does sx presentation differ from SLE?
She mentioned the following (see table for rest):
- hydralazine
- procainamide
- INH
- TNF-inhibitors
Renal, derm and neuro involvement is RARE
69
Hip/joint pain in SLE patient may be due to which serious complication?
Avascular necrosis
70
Best time to plan pregnancy in SLE patients?
When SLE is quiescent for at least 6 MONTHS
| -measure complement levels
71
Guidelines for anticoag if lupus patient has positive antiphospholipid Abs based on:
- prior thrombosis
- prior pregnancy loss
- no prior pregnancy loss
- prior thrombosis -> Heparin + ASA
- prior pregnancy loss -> heparin + ASA
- no prior pregnancy loss -> ASA 81mg alone or nothing
72
Neonatal lupus
- abs
- permanent or self limited
- scarring
- tx
- most dreaded complication
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
Which drugs MUST be continued during pregnancy in a SLE patient
Which SLE drugs are Class X?
Plaquenil (HCQ)
Class X
- MTX
- Arava
- thalidomide
74
How many days does it take for effects of warfarin to kick in? Why?
4 days
- half life of factor X = 48 hours
- need to drop 2 half lives before anticoagulation effects are seen
75
First 3 steps in clotting
platelet shape change, adhesion and aggregation
76
What is the final common mediator that is blocked with the following drugs
- clopidogrel
- dabigatran
- aspirin
- abciximab
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
Which drug should be avoided when using clopidogrel? Why?
Proton pump inhibitors (e.g. omeprazole and esomeprazole)
PPIs INHIBIT the CP450 enzymes needed to ACTIVATE clopidogrel
78
List 3 DIRECT inhibitors of Gp IIb/IIIa
Abciximab (MAb)
Eptifibatide (cyclic peptide)
Tirofaban (non-peptide)
79
When should thrombolytics NOT be used for stroke tx?
INTRACRANIAL HEMORRHAGE - DO NOT USE!!!
80
Why does tenecteplase have improved efficacy and bioavailability as compared to tPA
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
Which thrombolytic does NOT have intrinsic enzyme activity?
Streptokinase -> binds plasminogen, exposes active site, and promotes conversion of additional plasminogen to plasmin
82
Dibigatran
- MoA
- benefit over warfarin
DIRECT thrombin (IIa) inhibitor
DOES NOT requires routine plasma concentration monitoring
oral alternative to warfarin
83
UFH heparin vs LMWH -> compare:
- MoA
- which one is better/safer choice and why
- name one LMWH drug mentioned in lecture and target
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
Match the following skin prestations with size of affected vessel and the type of vasculitis
1. Palpable purpura
2. Skin ulcers
3. Gangrene
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
Match the following renal diseases with size of affected vessel and the type of vasculitis
1. Glomerulonephritis
2. Ischemic renal failure
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
Extreme diastolic HTN suggests a problem where?
Small/medium sized arteries and blood flow to kidneys
87
C-ANCA Abs are against
proteinase 3 -> cytoplasmic granule in neutrophils
High Sp for Granulomatosis w/ polyangiitis (Wegener)
88
P-ANCA stains
Perinuclear granules in neutrophils
target -> Myeloperoxidase
Seen in:
- microscopic polyangiitis
- Churg Strauss -> eosinophilic granulomatosis w/ angiitis
89
Gold standard for making dx of vasculitis
Tissue bx
90
What role do corticosteroids have txing vasculitis?
Reduce the fibrinoid necrosis and inflammation but crap for improving long term outcomes
91
Improvement in long term outcomes in vasculitis agents is accomplished through?
Immunosuppressives (e.g. cyclophosphamide)
92
Henoch Schonlein Purpura
- age group
- triad
- deposition of
- tx
- prognosis
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
Difficult to tx asthma for several years is seen in which vasculitis?
Churg strauss
94
Criteria for churg strauss dx
Treatment
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
Criteria for granulomatosis w/ polyangiitis
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
Polyarteritis Nodosa
- seen with which other disease?
- never hits the?
- Males vs females?
- kidney involvement
- other organ involvement
- Tx
```
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
Giant cell arteritis
- age group
- sxs
- vessels involved
- cause of stroke
- lab value used to screen
- bx will show
- Tx
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
Which constituents of E. coli are important in prompting the inflammasome? What is an inflammasome?
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
2. Flagella
99
Type 2 vs Type 3 secretion systems
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
Uropathogenic E. coli produce (blank) that allows binding to (blank) receptor on bladder epithelium
Type 1 (P) fimbriae binds to glycoprotein receptor
101
Dysentery vs. diarrhea
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
Tx for E. coli meningitis in neonate? What should NOT be used?
Ceftriaxone (3rd gen cephalosporin) or Ampicillin
DON'T use TMP-SMX -> kernicterus: bilirubin deposits in the basal ganglia (due to the sulfonamide)
103
Leading cause of neonatal meningitis? followed by?
Group B streptococcus > E. coli
104
What mech does E. coli use to cause neonatal meningitis
| -discuss the strains
K1 capsule -> transport across BBB and serum resistance
Toxins
- hemolysin
- cytotoxic necrotizing factor (impairs host cytoskeleton)
- cytolethal distending toxin -> DNase activity
105
ETEC
- acquired through
- sxs
- path
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
EPEC
- population
- acquired through
- sxs
- path
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
EHEC
- serotype
- transmission
- path
- sxs
- age group
- which antibiotic
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
EAEC
- path
- sxs
A - aggregative
Path
-use fimbriae (aggregative adherence fimbriae) to form biofilm -> mucosal damage w/ loss of microvilli
Sxs
-Mucoid diarrhea
109
EIEC
- path
- sxs
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
D-dimer sensitivity and specificity
Good Sn but crappy Sp (high FP rate)
| -lots of things aside from PE can elevate D-dimer
111
When should D-dimer be used for evaluating PE
Low (not too low or too high) clinical suspicion
112
When should thrombolysis be used for PE?
If hemodynamically UNSTABLE and no CIs
Maybe if hypotensive but showing signs of right heart strain
- on echo
- or elevated troponin
113
In which situations should V/Q be used over CTPA?
- renal disease
| - allergy to contrast
114
When should CTPA be used over V/Q
- patient is unstable
- pregnancy -> less radiation to fetus w/ CTPA
- after hours
- crappy CXR
