STI, acute resp, reactive airway, autoimmune 1 Flashcards Preview

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Flashcards in STI, acute resp, reactive airway, autoimmune 1 Deck (152)
1

majority of young, sexually active patients who have genital ulcers have

genital herpes, syphilis, or chancroid

2

*hallmark sign: chancre*

primary syphilis(painless, highly infective)

3

syphilis testing x3

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

4

*primary syphilis*

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

5

when to wean (labs)

- 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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shunting (what & fix)

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

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V/Q mismatch (what & fix)

Blood going by poorly ventilated alveoliResponds to ↑FiO2

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rapid shallow breathing index (calculation)

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

9

weaning daily screening criteria x4

- PaO2/FiO2 gt 200- PEEP gt/eq 5- cough with suction- RSBI lt 105 B/min/L

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time to intubate criteria x5

- 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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t tube trial result indicating ok to wean

30-90 minutes on trial

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ideal parameters for weaning: RR

lt 25

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ideal parameters for weaning: MV

5-10

14

MV =

RR x TV

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ideal parameters for weaning: PaO2

60-80

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ideal parameters for weaning: SaO2

gt 90%

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ideal parameters for weaning: pH

gt 7.35

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ideal parameters for weaning: PaCO2

whatever is acceptable for patient

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ideal parameters for weaning: PEEP

lt/eq 5

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ideal parameters for weaning: max negative inspiratory pressure

gt -20(patient can cough)

21

PAO2 calculation

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

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PaO2 / PAO2 ratio norm

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

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

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

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PaO2/FiO2what, norm, shunts x2

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

29

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)

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methotrexate beneficial effects when

2-6 weeks

35

antiphospholipid antibody syndrome

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

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VTEs & antibodies

antiphospholipid antibody syndrome

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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

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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

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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%)

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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

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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

74

decreased temporal pule or enlarged temporal artery

GCA!

75

gold standard for GCA treatment

temporal biopsy at time fo treatment initiation

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GCA treatment

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

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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