STI, acute resp, reactive airway, autoimmune 1 Flashcards
1
Q
majority of young, sexually active patients who have genital ulcers have
A
genital herpes, syphilis, or chancroid
2
Q
hallmark sign: chancre
A
primary syphilis(painless, highly infective)
3
Q
syphilis testing x3
A
culture not possible: dark field examserologic ab testing: VDRL, RBRFTA-ABS (confirmatory if reactive non-treponemal test)
4
Q
primary syphilis
A
- chancre hallmark-
spontaneously resolves 3-6 weeks- incubation period 10-90 days (avg 3 weeks)
5
Q
when to wean (labs)
A
- Mg: 1.8-2.4 mg/dL- Phosphate: 2.5-4.5 mg/dL - Albumin: 3.5-4.7 g/dL- K: 3.5-5.5 mEq/L- Total protein: 6.0-8.0 g/dL- Calcium: 8.5-10.5 mg/dL- Hgb: 14-18 men, 12-16 women
6
Q
shunting (what & fix)
A
Blood bypassing ventilated alveoli -or- going by non-ventilated alveoliNeeds PEEP
7
Q
V/Q mismatch (what & fix)
A
Blood going by poorly ventilated alveoliResponds to ↑FiO2
8
Q
rapid shallow breathing index (calculation)
A
frequency (RR) / TVlower ratio = slower, comfortable breathingCALCULATE IN LITERS
9
Q
weaning daily screening criteria x4
A
- PaO2/FiO2 gt 200- PEEP gt/eq 5- cough with suction- RSBI lt 105 B/min/L
10
Q
time to intubate criteria x5
A
- RR gt 35- TV lt 4-5- VC lt 10- max inspiratory P -10 to -5- lack ability to take deep breath
11
Q
t tube trial result indicating ok to wean
A
30-90 minutes on trial
12
Q
ideal parameters for weaning: RR
A
lt 25
13
Q
ideal parameters for weaning: MV
A
5-10
14
Q
MV =
A
RR x TV
15
Q
ideal parameters for weaning: PaO2
A
60-80
16
Q
ideal parameters for weaning: SaO2
A
gt 90%
17
Q
ideal parameters for weaning: pH
A
gt 7.35
18
Q
ideal parameters for weaning: PaCO2
A
whatever is acceptable for patient
19
Q
ideal parameters for weaning: PEEP
A
lt/eq 5
20
Q
ideal parameters for weaning: max negative inspiratory pressure
A
gt -20(patient can cough)
21
Q
PAO2 calculation
A
[FiO2 x (760-47)] - (pCO2/0.8)
22
Q
PaO2 / PAO2 ratio norm
A
arterial/alveolar ratio ie % O2 diffusing across alveoli into bloodnormal: gt 0.75
23
Q
P(A-a)O2 gradient: equationnorm v shunting
A
P(A-a)O2normal: lt 15-20shunt: gt 20
24
Q
PaO2/FiO2what, norm, shunts x2
A
simplified PaO2/PAO2normal: gt 286shunts: lt 200 = gt 20% shunt- ALI: lt 300- ARDS: lt 200
25
theophylline + nota bene
bronchodilator that increases respiratory muscle functionNARROW THERAPEUTIC WINDOW: 10-20ug/mL
26
BPAP settings x2
IPAP: PS- 10 usually, up to 30EPAP: PEEP- 5 usually
27
CPAP settings x3
FiO2, PS, PEEP
28
rheumatoid arthritis hallmark test
anti-CCP antibodies
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rheumatoid arthritis
chronic SYSTEMIC inflammatory disease with synovial manifestations in multiple jointswithout treatment can cause deformity and shorten life expectancy
30
RA: s/s specific to joints
symmetric swelling of jointsstiffness > 30 min (mainly AM)PIP in fingers, MCP & MTP, wrists, knees, ankles
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RA: joint deformities
ulnar deviation (fingers)boutonniere deformity“swan neck” deformityvalgus deformity (knee)volar subluxation (MTP joints)
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RA: mild to moderate tx
hydroxychloroquinesulfasalazine (prevent joint erosion, give alone or with hdq)
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RA: moderate to severe tx
methotrexate (PO, IM, SC)- beneficial effects 2-6 wks- usual dose 7.5-15mg q wk- monitor LFT q12 wk (hepatitis)
34
methotrexate beneficial effects when
2-6 weeks
35
antiphospholipid antibody syndrome
→ VTEs & antibodiesrecurrent non-inflammatory venous/arterial occlusions and thrombocytopenia with antiphospholipid antibodies
36
VTEs & antibodies
antiphospholipid antibody syndrome
37
Catastrophic anti-phospholipid syndrome
lt 1% of antiphospholipid antibody syndrome patientsdiffuse thromboses, thrombotic microangiopathy, MODSmimics sepsis, systemic vasculitis, DIC, TTPevolves within 24 hours + DEATH IMMINENT
38
antiphospholipid antibody syndrome: labs x4
- IgG, IgM, IgA anti-cardiolipin autoantibodies (ACA) -- IgG more pathologic- ELISA: B2GP1 positive- IgM & IgG anti-B2GP1 antibodies- lupus anticoagulant (prolongs coag test)
39
antiphospholipid antibody syndrome: diagnosis
positive serology 2+ occasions 12 weeks apart
40
anti-cardiolipin autoantibodies nota bene
serological test for antiphospholipid antibody syndromeIgG more pathologic than IgM, IgA
41
antiphospholipid antibody syndrome tx x2
lifelong anticoagulation: Warfarin to maintain INR 2-3teratogenic therefore SQ heparin + ASA if pregnant
42
antiphospholipid antibody syndrome tx for pregnancy
SQ heparin + ASAwarfarin teratogenic
43
raynaud phenomenon
paroxysmal digital ischemia caused by stress (weather, materials, emotions) affecting fingers, toes, ears- 2 phases- 2 types: primary v secondary
44
raynaud phenomenon: phases
phase 1: excess vasoconstriction = well demarcated pallor/cyanosisphase 2: vasodilation leading to hyperemia + rubor (recovery phase)
45
primary raynaud
UNILATERAL involvement15-30 mostly women2-6% occurence
46
secondary raynaud
commonly assoc with rheumatic disease (scleroderma, lupus, RA)potential for gangrene/ulcerative digitsSYMMETRIC involvement
47
vincristine or bleomycin significance
history of these chemos can lead to raynaud phenomenon
48
raynaud s/s x3
early: only 2 digitsprogression: all fingers down to distal palm, thumbs rarelytermination: warmth to affected areas (recovery phase)
49
mainstay of raynaud phenomenon treatment
calcium channel blockers- NIFEDIPINE- amlodipine
50
scleroderma
diffuse, systemic sclerosis of skin/internal organs - VERY PAINFULpts typically die from secondary complication
51
pts with scleroderma typically die from
secondary complication
52
#1 cause of death in scleroderma patients
pulmonary fibrosis
53
survival rate for scleroderma
9 yearsmortality 40% if internal organ involvement within first 3 yearsmortality 72% if no interal organ involvement within first 3 years
54
scleroderma s/s
childhood; skin + subcu tissues; morpheapredominantly UNILATERAL distributino
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morphea
sclerotic plaques on skin (trunk/limbs - local/general) developed in scleroderma
56
types of scleroderma disease x2
limited disease (80%) aka CREST syndromesystemic disease (20%)
57
typical first manifestation of scleroderma
RAYNAUD!
58
scleroderma: limited disease
aka CREST syndrome 80% skin: face, neck, distal extremitiesmore susceptible to digital ischemia, pulmonary hypertension
59
CREST syndrome
aka limited sclerodermacalcinosis cutis, reynaud phenom, esophageal motility disorder, sclerodactyly, teleangectasia
60
scleroderma diagnosis
by exclusion, no labs
61
anti-SCL 70
positive in scleroderma pts:- systemic 1/3- CREST 20%may portend poor prognosis with high likelihood of serious internal organ involvement
62
anticentromere antibodies
specific for limited scleroderma
63
steroid therapy is not effective for
scleroderma
64
scleroderma treatment
symptomatic vs supportive- organ based- assess inflammation, vascular problems - immunosuppressive therapy started early- CCB for RaynaudSTEROIDS NOT EFFECTIVE
65
sjogren syndrome
systemic autoimmune disorder with clinical presentation dominated dry eyes/mouth due to immune-mediated dysfunction of lacrimal & salivary glands (exocrine gland disease)most frequently associated with RA
66
2nd most common rheumatologic disorder after SLE
sjogren syndrome
67
hallmark for diagnosis for sjogren
salivary gland biopsy
68
pharm tx for sjogren
methotrexate 7.5-15 mg/wkhydroxychloroquine up to 8 mg/kg/dTNF inhibitors (poor literature)or B cell therapy for refractory- rituximab for extraglandular dysfunction
69
polymyalgia rheumatica vs giant cell arteritis
PM: does NOT cause blindness, responds to LOW dose steroidsGCA: causes BLINDNESS, responds to HIGH dose steroidscan co-occur
70
polymyalgia rheumatica
bilateral proximal aching and morning stiffness, ESR gt 40severe hampering of ADLs rapid improvement with glucocorticoid
71
giant cell arteritis
PAIN! systemic affecting medium and large sized vessels
72
accounts for 15% of all fever of unknown origin
giant cell arteritis
73
GCA diagnosis
very bad unilateral HAscalp tenderness, abrupt visual changes, jaw claudication (usually side of arteritis), decreased temporal pulse
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decreased temporal pule or enlarged temporal artery
GCA!
75
gold standard for GCA treatment
temporal biopsy at time fo treatment initiation
76
GCA treatment
URGENT to prevent blindnesshigh dose steroidsprednisone 40-60, methylprednisolone 1g/daily/3 days if visual lossASA sufficient to prevent clots
77
polymyalgia rheumatica treatment
prednisone 10-20symptoms improve within 72 hours
78
best opioids for asthma + surgery
fentanyl or hydromorphone
79
avoid these opioids with asthma
MORPHINE! rapid large dosing = histamine release = bronchospasmmeperidine! high levels of histamine release + build up of metabolites after 72 hours
80
beta blockers for surgery in asthmatics
esmolol + metoprolol - selective beta 1: bronchospasm unlikelylabetalol - beta/alpha activity: least likely to cause bronchospasm
81
give for refractory bronchospasm (asthma)
epinephrine
82
chronic bronchitis
chronic productive cough > 3 months for at least 2 successive yrs
83
emphysema
enlargement of air spaces distal to the terminal bronchioleswall destruction = no fibrosis
84
type of emphysema associated with alpha-1 antitrypsin deficiency
panacinar
85
bronchiectasis
chronic cough with viscid sputumLARGE airway collapse = obstructive airflow
86
mainstay of bronchiectasis treatment
hydration!!!
87
bronchiectasis treatment
supportive, no cureHYDRATION!! pulmonary toilet like whoa
88
bronchiolitis obliterans
affects SMALL airways (lt 2mm diameter) in bronchiolar epitheliuminsidious coughexcessive granulation process and intraluminal fibrotic process
89
bronchiolitis obliterans & PFTs
can show both obstructive and restrictive patterns!!constrictive type = obstructiveproliferative type = restrictive
90
cryptogenic organizing pneumonia
diffuse interstitial lung disease in bronchioles, alveolar ducts and wallsinsidious cough that won't stop + inspiratory crackles
91
cryptogenic organizing pneumonia treatment
mild to stable: spontaneously resolves + macrolidespersistent/worsening: glucocorticoid or cytotoxic therapy
92
alpha-1 antitrypsin
long arm of chromosome 4 = autosomal codominant gene = lung disease- can also impact skin, liverphenotypes normal: AAT protein not present in plasmadeficient: plasma AAT levels lt 35%null: most severe lung diseasedysfunctional: normal quantity of non-functional protein
93
AAT: normal
AAT protein not present in plasma
94
AAT: deficient:
plasma AAT levels lt 35%
95
AAT: null
most severe lung disease
96
AAT: dysfunctional
normal quantity of non-functional protein
97
AAT: treatment
IV pooled human alpha‐1 anti‐proteaseSupportiveLung volume reduction surgeryLung/Liver transplant
98
anion gap calculation
Na - (Cl + HCO3)
99
anion gap gt 15 causes
organy problems(cardiogenic) shock, cardiac arrest*renal failuretissue hypoxialactic acidosis*diabetic ketoacidosis*malnutrition....starvationsalicylate overdose
100
anion gap lt 15 causes
loss of liquiddiarrheadrainage of pancreatic juiceshyperalimentation (tpn)ureterosigmoidostomy
101
respiratory acidosis compensation
kidneys excrete H+ & reabsorb HCO3-↑ reabsorption Na+ & accompanying loss of chloride↑ excretion of NH4+ (ammonium)regenerate HCO3- from excessive CO2
102
respiratory alkalosis compensation
CELLULAR LEVELintracellular H+ exchanged for extracellular K+ to ↑ H+Cl- exchanged for HCO3- kidneys excrete HCO3- (hours to days)
103
steps to determine acidotic or alkalotic
norms: pH 7.40PaCO2 40HCO3 241. subtract patient values from “norm”2. divide “norm” into difference found in step 2 (create a %)convert result → percentage -- larger percentage = main problem-- smaller percentage = degree of compensation or may represent a “combined or mixed problem”
104
most common cause of intrinsic AKI
nephrotoxic drugs
105
ACE/ARB in prerenal AKI
impair renal perfusion with dilation of efferent arterioles
106
NSAIDS in prerenal AKI
inhibit prostaglandins = inhibit vasodilation of afferent arterioles → ischemia
107
port wine urine
rhabdomyolysis (intrinsic AKI)
108
nephritic syndrome
hematuria, proteinuria lt 3g/day, ↑ creatinine, RBC castsdifferentials: postinfectious glomerulonephritis, Berger, Goodpasture, cryogloblin-associated, Hep C, lupus, idiopathic membranoproliferative glomerulonephritis
109
nephrotic syndrome
proteinuria gt 3g/day, hypoalbuminuria, no cells or castsdifferentials: membranous or diabetic or HIV-associated nephropathy, focal/segmental glomerulosclerosis (obesity, heroin, HIV), amyloidosis
110
nephritic v nephrotic: onset
nephritic: abruptnephrotic: insidious
111
nephritic v nephrotic: edema, BP, JVD
nephritic: BP and JVD elevated, a little edemanephrotic: BP and JVD normal, hella edema
112
nephritic v nephrotic: proteinuria, hematuria, RBC casts, serum albumin
nephritic:- proteinuria lt 3 g/day- hematuria yasss- RBC casts present- serum albumin normalnephrotic:- proteinuria gt 3g/day- hematuria meh- RBC casts absent- serum albumin low
113
FENa
fractional excretion of sodium - % Na filtered by glomeruli excreted in urine CAN INDICATE PRERENAL AZOTEMIAlt 1% prerenalgt 1% acute tubular necrosis (tubular integrity compromised resulting in more Na lost)
114
BUN/Cr ratio in AKI
gt 20:1 = prerenal azotemia d/t hypovolemialt 20:1 = acute tubular necrosis (kidney can't concentrate urine)
115
FENa equation
urine Na x plasma Crdivided byplasma Na x urine Crtimes 100
116
syphilis: latent x2
early latent: within 1 year of initial infectionlate latent: gt 1 year after infection or time of infection unknown
117
tertiary syphilis
1/3 untreated latent stagecan occur any timeCNS problems, gummatous disease, CV disease
118
*syphilis treatment*
benzathine pencillins or doxy
119
primary/secondary syphilis management
follow up 6 & 12 mo clinically/serologically
120
latent syphilis management
repeat series if:- missed doses gt 14 days- 4x increase in RPR titerfollow up 6, 12, 24 mo
121
HSV-1
cutaneous disease of upper body with fewer outbreaks
122
HSV-2
usually affects genitals/lower body with 4-6 outbreaks per year
123
HSV etiology
contact with abraded skin/mucosal tissue initiates epidermis infection → travels to dorsal root ganglion: replicates & becomes latent
124
*HSV: primary infection s/s*
PAPULES TO VESICLES
| clear fluid in vesicles, superficial PAINFUL ulcerations, eroding pustules
125
HSV: initial non-primary infection s/s
atypical symptoms: non-specific discharge, fissure, erythema, back pain, cystitis
126
HSV: recurrent infection s/s
reactivation of latent virusmost frequent with HSV2fewer lesionsasymptomatic or prodrome
127
HSV diagnostic testing
PCR preferred to viral with cultureIgM is not useful!
128
most commonly reported bacterial infection (STI)
chlamydiahighest prev in under 25
129
leading preventable cause of infertility
chlamydia
130
*chlamydia s/s*
many asymptomatic & undiagnosed
- cervicitis
- urethritis
- discharge
- dysuria
131
chlamydia pathogenesis
reproduces inside host cells, 36-48 hours to incubate
132
chlamydia diagnostic testing gold standard
nucleic acid amplification test (NAAT)
133
CT/GC testing for ladies
self-collected vaginal swabsmore sensitive that UA
134
*chlamydia treatment*
*azithromycin (1 dose) or doxy (7 days)*
- retest 3-4 mo to r/o reinfection
- can be cured but repeat infection is common!
135
gonorrhea pathogenesis
gram neg diplococcus
preferentially infects columnar cells
incubation: 3-5 days
136
gonorrhea risk factors
multiple/new partners, AA 18x, adolescent women, urban, drug use
137
gonorrhea popular infection sites
anorectal, pharyngeal
138
preferred screening test for gonorrhea
NAAT for both genital and non-genital sites
139
cause majority of cervical cancers
HPV 16 & 18
140
all squamous cell cervical cancers result from
persistent HPV infection
141
anogenital warts
betcha it's HPV ... 6 & 11 most associated
142
HPV transmission
skin-to-skin - microabrasions during sexual activity
143
HPV s/s
most asymptomaticthe typicalsANOGENITAL WARTS!
144
HPV postive vs negativehead & neck cancers
positive: better prognosis, men, high SES, sex + weed-- incidence increasingnegative: older, men, low SES, EtOH + tobacco, diet, hygiene -- incidence decreasing
145
*HSV tx*
acyclovir
146
*gonorrhea s/s*
vaginal discharge
abd pain
dysuria
or may be asx!
147
*gonorrhea tx*
cefixime (Suprax)
ceftriaxone
+ azithromycin or doxycycline
148
*gonorrhea + chlamydia*
always test for C when test for G!
149
*pelvic inflammatory disease*
inflammatory process caused by infection involving any organ(s) of upper genital tract (uterus, fallopian tubes, ovaries, entire peritoneal cavity = most severe form)
d/t gonorrhea, trachomatis, other STDs - migrate from vagina & cause it
150
*PID s/s*
abd pain/tenderness
cervical motion tenderness (chandelier sign)
adnexal tenderness
may have: fever, wet prep w WBC 10+
151
*chandelier sign*
cervical motion tenderness - sign of PID
152
*PID tx*
levaquin, flagyl
