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monster management > STI, acute resp, reactive airway, autoimmune 1 > Flashcards

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

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2
Q

hallmark sign: chancre

A

primary syphilis(painless, highly infective)

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3
Q

syphilis testing x3

A

culture not possible: dark field examserologic ab testing: VDRL, RBRFTA-ABS (confirmatory if reactive non-treponemal test)

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4
Q

primary syphilis

A
  • chancre hallmark-

spontaneously resolves 3-6 weeks- incubation period 10-90 days (avg 3 weeks)

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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
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6
Q

shunting (what & fix)

A

Blood bypassing ventilated alveoli -or- going by non-ventilated alveoliNeeds PEEP

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7
Q

V/Q mismatch (what & fix)

A

Blood going by poorly ventilated alveoliResponds to ↑FiO2

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8
Q

rapid shallow breathing index (calculation)

A

frequency (RR) / TVlower ratio = slower, comfortable breathingCALCULATE IN LITERS

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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
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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
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11
Q

t tube trial result indicating ok to wean

A

30-90 minutes on trial

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12
Q

ideal parameters for weaning: RR

A

lt 25

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13
Q

ideal parameters for weaning: MV

A

5-10

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14
Q

MV =

A

RR x TV

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15
Q

ideal parameters for weaning: PaO2

A

60-80

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16
Q

ideal parameters for weaning: SaO2

A

gt 90%

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17
Q

ideal parameters for weaning: pH

A

gt 7.35

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18
Q

ideal parameters for weaning: PaCO2

A

whatever is acceptable for patient

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19
Q

ideal parameters for weaning: PEEP

A

lt/eq 5

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20
Q

ideal parameters for weaning: max negative inspiratory pressure

A

gt -20(patient can cough)

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21
Q

PAO2 calculation

A

[FiO2 x (760-47)] - (pCO2/0.8)

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22
Q

PaO2 / PAO2 ratio norm

A

arterial/alveolar ratio ie % O2 diffusing across alveoli into bloodnormal: gt 0.75

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23
Q

P(A-a)O2 gradient: equationnorm v shunting

A

P(A-a)O2normal: lt 15-20shunt: gt 20

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24
Q

PaO2/FiO2what, norm, shunts x2

A

simplified PaO2/PAO2normal: gt 286shunts: lt 200 = gt 20% shunt- ALI: lt 300- ARDS: lt 200

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25
Q

theophylline + nota bene

A

bronchodilator that increases respiratory muscle functionNARROW THERAPEUTIC WINDOW: 10-20ug/mL

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26
Q

BPAP settings x2

A

IPAP: PS- 10 usually, up to 30EPAP: PEEP- 5 usually

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27
Q

CPAP settings x3

A

FiO2, PS, PEEP

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28
Q

rheumatoid arthritis hallmark test

A

anti-CCP antibodies

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29
Q

rheumatoid arthritis

A

chronic SYSTEMIC inflammatory disease with synovial manifestations in multiple jointswithout treatment can cause deformity and shorten life expectancy

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30
Q

RA: s/s specific to joints

A

symmetric swelling of jointsstiffness > 30 min (mainly AM)PIP in fingers, MCP & MTP, wrists, knees, ankles

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31
Q

RA: joint deformities

A

ulnar deviation (fingers)boutonniere deformity“swan neck” deformityvalgus deformity (knee)volar subluxation (MTP joints)

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32
Q

RA: mild to moderate tx

A

hydroxychloroquinesulfasalazine (prevent joint erosion, give alone or with hdq)

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33
Q

RA: moderate to severe tx

A

methotrexate (PO, IM, SC)- beneficial effects 2-6 wks- usual dose 7.5-15mg q wk- monitor LFT q12 wk (hepatitis)

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34
Q

methotrexate beneficial effects when

A

2-6 weeks

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35
Q

antiphospholipid antibody syndrome

A

→ VTEs & antibodiesrecurrent non-inflammatory venous/arterial occlusions and thrombocytopenia with antiphospholipid antibodies

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36
Q

VTEs & antibodies

A

antiphospholipid antibody syndrome

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37
Q

Catastrophic anti-phospholipid syndrome

A

lt 1% of antiphospholipid antibody syndrome patientsdiffuse thromboses, thrombotic microangiopathy, MODSmimics sepsis, systemic vasculitis, DIC, TTPevolves within 24 hours + DEATH IMMINENT

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38
Q

antiphospholipid antibody syndrome: labs x4

A
  • IgG, IgM, IgA anti-cardiolipin autoantibodies (ACA) – IgG more pathologic- ELISA: B2GP1 positive- IgM & IgG anti-B2GP1 antibodies- lupus anticoagulant (prolongs coag test)
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39
Q

antiphospholipid antibody syndrome: diagnosis

A

positive serology 2+ occasions 12 weeks apart

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40
Q

anti-cardiolipin autoantibodies nota bene

A

serological test for antiphospholipid antibody syndromeIgG more pathologic than IgM, IgA

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41
Q

antiphospholipid antibody syndrome tx x2

A

lifelong anticoagulation: Warfarin to maintain INR 2-3teratogenic therefore SQ heparin + ASA if pregnant

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42
Q

antiphospholipid antibody syndrome tx for pregnancy

A

SQ heparin + ASAwarfarin teratogenic

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43
Q

raynaud phenomenon

A

paroxysmal digital ischemia caused by stress (weather, materials, emotions) affecting fingers, toes, ears- 2 phases- 2 types: primary v secondary

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44
Q

raynaud phenomenon: phases

A

phase 1: excess vasoconstriction = well demarcated pallor/cyanosisphase 2: vasodilation leading to hyperemia + rubor (recovery phase)

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45
Q

primary raynaud

A

UNILATERAL involvement15-30 mostly women2-6% occurence

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46
Q

secondary raynaud

A

commonly assoc with rheumatic disease (scleroderma, lupus, RA)potential for gangrene/ulcerative digitsSYMMETRIC involvement

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47
Q

vincristine or bleomycin significance

A

history of these chemos can lead to raynaud phenomenon

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48
Q

raynaud s/s x3

A

early: only 2 digitsprogression: all fingers down to distal palm, thumbs rarelytermination: warmth to affected areas (recovery phase)

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49
Q

mainstay of raynaud phenomenon treatment

A

calcium channel blockers- NIFEDIPINE- amlodipine

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50
Q

scleroderma

A

diffuse, systemic sclerosis of skin/internal organs - VERY PAINFULpts typically die from secondary complication

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51
Q

pts with scleroderma typically die from

A

secondary complication

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52
Q

1 cause of death in scleroderma patients

A

pulmonary fibrosis

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53
Q

survival rate for scleroderma

A

9 yearsmortality 40% if internal organ involvement within first 3 yearsmortality 72% if no interal organ involvement within first 3 years

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54
Q

scleroderma s/s

A

childhood; skin + subcu tissues; morpheapredominantly UNILATERAL distributino

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55
Q

morphea

A

sclerotic plaques on skin (trunk/limbs - local/general) developed in scleroderma

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56
Q

types of scleroderma disease x2

A

limited disease (80%) aka CREST syndromesystemic disease (20%)

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57
Q

typical first manifestation of scleroderma

A

RAYNAUD!

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58
Q

scleroderma: limited disease

A

aka CREST syndrome 80% skin: face, neck, distal extremitiesmore susceptible to digital ischemia, pulmonary hypertension

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59
Q

CREST syndrome

A

aka limited sclerodermacalcinosis cutis, reynaud phenom, esophageal motility disorder, sclerodactyly, teleangectasia

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60
Q

scleroderma diagnosis

A

by exclusion, no labs

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61
Q

anti-SCL 70

A

positive in scleroderma pts:- systemic 1/3- CREST 20%may portend poor prognosis with high likelihood of serious internal organ involvement

62
Q

anticentromere antibodies

A

specific for limited scleroderma

63
Q

steroid therapy is not effective for

A

scleroderma

64
Q

scleroderma treatment

A

symptomatic vs supportive- organ based- assess inflammation, vascular problems - immunosuppressive therapy started early- CCB for RaynaudSTEROIDS NOT EFFECTIVE

65
Q

sjogren syndrome

A

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
Q

2nd most common rheumatologic disorder after SLE

A

sjogren syndrome

67
Q

hallmark for diagnosis for sjogren

A

salivary gland biopsy

68
Q

pharm tx for sjogren

A

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
Q

polymyalgia rheumatica vs giant cell arteritis

A

PM: does NOT cause blindness, responds to LOW dose steroidsGCA: causes BLINDNESS, responds to HIGH dose steroidscan co-occur

70
Q

polymyalgia rheumatica

A

bilateral proximal aching and morning stiffness, ESR gt 40severe hampering of ADLs rapid improvement with glucocorticoid

71
Q

giant cell arteritis

A

PAIN! systemic affecting medium and large sized vessels

72
Q

accounts for 15% of all fever of unknown origin

A

giant cell arteritis

73
Q

GCA diagnosis

A

very bad unilateral HAscalp tenderness, abrupt visual changes, jaw claudication (usually side of arteritis), decreased temporal pulse

74
Q

decreased temporal pule or enlarged temporal artery

75
Q

gold standard for GCA treatment

A

temporal biopsy at time fo treatment initiation

76
Q

GCA treatment

A

URGENT to prevent blindnesshigh dose steroidsprednisone 40-60, methylprednisolone 1g/daily/3 days if visual lossASA sufficient to prevent clots

77
Q

polymyalgia rheumatica treatment

A

prednisone 10-20symptoms improve within 72 hours

78
Q

best opioids for asthma + surgery

A

fentanyl or hydromorphone

79
Q

avoid these opioids with asthma

A

MORPHINE! rapid large dosing = histamine release = bronchospasmmeperidine! high levels of histamine release + build up of metabolites after 72 hours

80
Q

beta blockers for surgery in asthmatics

A

esmolol + metoprolol - selective beta 1: bronchospasm unlikelylabetalol - beta/alpha activity: least likely to cause bronchospasm

81
Q

give for refractory bronchospasm (asthma)

A

epinephrine

82
Q

chronic bronchitis

A

chronic productive cough > 3 months for at least 2 successive yrs

83
Q

emphysema

A

enlargement of air spaces distal to the terminal bronchioleswall destruction = no fibrosis

84
Q

type of emphysema associated with alpha-1 antitrypsin deficiency

85
Q

bronchiectasis

A

chronic cough with viscid sputumLARGE airway collapse = obstructive airflow

86
Q

mainstay of bronchiectasis treatment

A

hydration!!!

87
Q

bronchiectasis treatment

A

supportive, no cureHYDRATION!! pulmonary toilet like whoa

88
Q

bronchiolitis obliterans

A

affects SMALL airways (lt 2mm diameter) in bronchiolar epitheliuminsidious coughexcessive granulation process and intraluminal fibrotic process

89
Q

bronchiolitis obliterans & PFTs

A

can show both obstructive and restrictive patterns!!constrictive type = obstructiveproliferative type = restrictive

90
Q

cryptogenic organizing pneumonia

A

diffuse interstitial lung disease in bronchioles, alveolar ducts and wallsinsidious cough that won’t stop + inspiratory crackles

91
Q

cryptogenic organizing pneumonia treatment

A

mild to stable: spontaneously resolves + macrolidespersistent/worsening: glucocorticoid or cytotoxic therapy

92
Q

alpha-1 antitrypsin

A

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
Q

AAT: normal

A

AAT protein not present in plasma

94
Q

AAT: deficient:

A

plasma AAT levels lt 35%

95
Q

AAT: null

A

most severe lung disease

96
Q

AAT: dysfunctional

A

normal quantity of non-functional protein

97
Q

AAT: treatment

A

IV pooled human alpha‐1 anti‐proteaseSupportiveLung volume reduction surgeryLung/Liver transplant

98
Q

anion gap calculation

A

Na - (Cl + HCO3)

99
Q

anion gap gt 15 causes

A

organy problems(cardiogenic) shock, cardiac arrestrenal failuretissue hypoxialactic acidosisdiabetic ketoacidosis*malnutrition….starvationsalicylate overdose

100
Q

anion gap lt 15 causes

A

loss of liquiddiarrheadrainage of pancreatic juiceshyperalimentation (tpn)ureterosigmoidostomy

101
Q

respiratory acidosis compensation

A

kidneys excrete H+ & reabsorb HCO3-↑ reabsorption Na+ & accompanying loss of chloride↑ excretion of NH4+ (ammonium)regenerate HCO3- from excessive CO2

102
Q

respiratory alkalosis compensation

A

CELLULAR LEVELintracellular H+ exchanged for extracellular K+ to ↑ H+Cl- exchanged for HCO3- kidneys excrete HCO3- (hours to days)

103
Q

steps to determine acidotic or alkalotic

A

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
Q

most common cause of intrinsic AKI

A

nephrotoxic drugs

105
Q

ACE/ARB in prerenal AKI

A

impair renal perfusion with dilation of efferent arterioles

106
Q

NSAIDS in prerenal AKI

A

inhibit prostaglandins = inhibit vasodilation of afferent arterioles → ischemia

107
Q

port wine urine

A

rhabdomyolysis (intrinsic AKI)

108
Q

nephritic syndrome

A

hematuria, proteinuria lt 3g/day, ↑ creatinine, RBC castsdifferentials: postinfectious glomerulonephritis, Berger, Goodpasture, cryogloblin-associated, Hep C, lupus, idiopathic membranoproliferative glomerulonephritis

109
Q

nephrotic syndrome

A

proteinuria gt 3g/day, hypoalbuminuria, no cells or castsdifferentials: membranous or diabetic or HIV-associated nephropathy, focal/segmental glomerulosclerosis (obesity, heroin, HIV), amyloidosis

110
Q

nephritic v nephrotic: onset

A

nephritic: abruptnephrotic: insidious

111
Q

nephritic v nephrotic: edema, BP, JVD

A

nephritic: BP and JVD elevated, a little edemanephrotic: BP and JVD normal, hella edema

112
Q

nephritic v nephrotic: proteinuria, hematuria, RBC casts, serum albumin

A

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
Q

FENa

A

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
Q

BUN/Cr ratio in AKI

A

gt 20:1 = prerenal azotemia d/t hypovolemialt 20:1 = acute tubular necrosis (kidney can’t concentrate urine)

115
Q

FENa equation

A

urine Na x plasma Crdivided byplasma Na x urine Crtimes 100

116
Q

syphilis: latent x2

A

early latent: within 1 year of initial infectionlate latent: gt 1 year after infection or time of infection unknown

117
Q

tertiary syphilis

A

1/3 untreated latent stagecan occur any timeCNS problems, gummatous disease, CV disease

118
Q

syphilis treatment

A

benzathine pencillins or doxy

119
Q

primary/secondary syphilis management

A

follow up 6 & 12 mo clinically/serologically

120
Q

latent syphilis management

A

repeat series if:- missed doses gt 14 days- 4x increase in RPR titerfollow up 6, 12, 24 mo

121
Q

HSV-1

A

cutaneous disease of upper body with fewer outbreaks

122
Q

HSV-2

A

usually affects genitals/lower body with 4-6 outbreaks per year

123
Q

HSV etiology

A

contact with abraded skin/mucosal tissue initiates epidermis infection → travels to dorsal root ganglion: replicates & becomes latent

124
Q

HSV: primary infection s/s

A

PAPULES TO VESICLES

clear fluid in vesicles, superficial PAINFUL ulcerations, eroding pustules

125
Q

HSV: initial non-primary infection s/s

A

atypical symptoms: non-specific discharge, fissure, erythema, back pain, cystitis

126
Q

HSV: recurrent infection s/s

A

reactivation of latent virusmost frequent with HSV2fewer lesionsasymptomatic or prodrome

127
Q

HSV diagnostic testing

A

PCR preferred to viral with cultureIgM is not useful!

128
Q

most commonly reported bacterial infection (STI)

A

chlamydiahighest prev in under 25

129
Q

leading preventable cause of infertility

130
Q

chlamydia s/s

A

many asymptomatic & undiagnosed

  • cervicitis
  • urethritis
  • discharge
  • dysuria
131
Q

chlamydia pathogenesis

A

reproduces inside host cells, 36-48 hours to incubate

132
Q

chlamydia diagnostic testing gold standard

A

nucleic acid amplification test (NAAT)

133
Q

CT/GC testing for ladies

A

self-collected vaginal swabsmore sensitive that UA

134
Q

chlamydia treatment

A

azithromycin (1 dose) or doxy (7 days)

  • retest 3-4 mo to r/o reinfection
  • can be cured but repeat infection is common!
135
Q

gonorrhea pathogenesis

A

gram neg diplococcus
preferentially infects columnar cells

incubation: 3-5 days

136
Q

gonorrhea risk factors

A

multiple/new partners, AA 18x, adolescent women, urban, drug use

137
Q

gonorrhea popular infection sites

A

anorectal, pharyngeal

138
Q

preferred screening test for gonorrhea

A

NAAT for both genital and non-genital sites

139
Q

cause majority of cervical cancers

A

HPV 16 & 18

140
Q

all squamous cell cervical cancers result from

A

persistent HPV infection

141
Q

anogenital warts

A

betcha it’s HPV … 6 & 11 most associated

142
Q

HPV transmission

A

skin-to-skin - microabrasions during sexual activity

143
Q

HPV s/s

A

most asymptomaticthe typicalsANOGENITAL WARTS!

144
Q

HPV postive vs negativehead & neck cancers

A

positive: better prognosis, men, high SES, sex + weed– incidence increasingnegative: older, men, low SES, EtOH + tobacco, diet, hygiene – incidence decreasing

145
Q

HSV tx

146
Q

gonorrhea s/s

A

vaginal discharge
abd pain
dysuria
or may be asx!

147
Q

gonorrhea tx

A

cefixime (Suprax)
ceftriaxone
+ azithromycin or doxycycline

148
Q

gonorrhea + chlamydia

A

always test for C when test for G!

149
Q

pelvic inflammatory disease

A

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
Q

PID s/s

A

abd pain/tenderness
cervical motion tenderness (chandelier sign)
adnexal tenderness

may have: fever, wet prep w WBC 10+

151
Q

chandelier sign

A

cervical motion tenderness - sign of PID

152
Q

PID tx

A

levaquin, flagyl

monster management (29 decks)

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