January 2020 Flashcards
1
Q
Positive predictive value: definition
A
Percentage of people that actually have the disease out of all positive test results (ie probability that a patient actually has the disease given a positive test result).
PPV = TP / (TP + FP)
TP = true positive FP = false positive
2
Q
Sensitivity
A
Sensitivity is the likelihood a patient with the disease will test positive.
Sensitivity = TP/(TP + FN)
TP = true positive FN = false negative
3
Q
Specificity
A
Specificity is the likelihood a patient without a disease will test negative.
Specificity = TN/ (TN+FP)
TN = true negative FP = false positive
4
Q
Young patient presenting w/ vague, nonspecific mono-like symptoms (fever, lymphadenopathy, wt loss, sore throat, myalgias, diarrhea, headache) should be evaluated for what, with what?
A
- Check for HIV w/ detailed sexual hx and IV drug use
- test w/ fourth-generation HIV test and HIV viral load.
5
Q
Treatment options for latent TB infection
A
- isoniazid + rifapentine weekly x3 months under direct observation (not for HIV pts)
- Isoniazid monotherapy x6-9 months
- Rifampin x4 months
add pyridoxine to prevent neuropathies in pts taking isoniazid w/ following conditions: diabetes, uremia, alcoholism, malnutrition, HIV, pregnancy, or epilepsy
6
Q
What is latent TB infection (LTBI)?
A
Patients w/ >/= 10mm induration of tuberculin skin test who don’t have CXR abnormalities and no symptoms (eg no wt loss, night sweats, chronic cough)
7
Q
Is latent TB infection (LTBI) infectious?
A
No. LTBI is no infectious.
8
Q
Should latent TB infection (LTBI) be treated?
A
Lifetime risk of advancement 5-10%, so typically only offer treatment to:
- pts at higher risk of developing active TB (eg immunosuppressed)
- pts who live or work in high-risk congregate settings (eg prisons or health care personnel)
9
Q
What happens if a healthcare worker has latent TB infection?
A
They may continue to work without restrictions (even if refuse treatment) and don’t need precautions (eg N95 mask)
10
Q
Can pts exposed to TB several years prior have false-negative initial tuberculin skin testing?
A
YES.
Recommendation is repeat testing in 1-3 weeks if initial test neg.
11
Q
When are pts treated for active TB considered non infectious?
A
After 3 consecutive acid-fast bacilli sputum smears negative
*Samples taken 8-24-hour intervals w/ 1 or more early-morning samples
12
Q
Signs + symptoms of lupus nephritis
A
LEE
Proteinuria
Renal dysfunction
Urinalysis with active sedimentation (eg hematuria, red blood cell casts)
13
Q
How is lupus nephritis classified?
A
6 classes and NEED a renal biopsy prior to treatment to determine class
14
Q
What guides treatment for lupus nephritis?
A
Disease classification, which is determined on pathology by renal biopsy
15
Q
Class 1 Lupus nephritis subtype: histology and clinical features
A
histo: Minimal mesangial
Clin: usually asymptomatic
16
Q
Class 2 lupus nephritic subtype: histology and clinical features
A
Histo: mesangial proliferative
Clin:
- microscopic hematuria, proteinuria
- favorable prognosis
17
Q
Class III lupus nephritis subtype: histology and clinical features
A
Histo: focal
Clin:
- hematuria, proteinuria (possible nephrotic syndrome)
- possible HTN, decr GFR
- variable prognosis
18
Q
Class IV lupus nephritis subtype: histology and clinical features
A
Histo: diffuse
Clin:
- most common
- similar to focal lupus nephritis (hematuria, proteinuria, possible nephrotic syndrome, possible HTN, decr GFR)
- POOR prognosis
19
Q
Class V lupus nephritis: histology and clinical features
A
Histo: membranous
Clin:
- nephrotic syndrome
- ?poor prognosis?
20
Q
Class VI lupus nephritis: histology and clinical features
A
Histo: advanced sclerosing
Clin:
- progressive CKD w/ bland urinary sediment
- immunosuppressive therapy not recommended
21
Q
How should classes I & II lupus nephritis be treated?
A
Typically mild, don’t need treatment unless disease progresses
22
Q
How should classes III & IV lupus nephritis be treated?
A
Immunosuppression w/ glucocorticoids and either cyclophosphamide or mycophenolate mofetil
23
Q
How to treat class V lupus nephritis?
A
May require immunosuppression if there are proliferative lesions or nephrotic syndrome
24
Q
How to treat class VI lupus nephritis?
A
No immunosuppression bc this is advanced sclerosing disease. Renal transplant…?
25
What to monitor in SLE patients w/ renal involvement?
Anti-double stranded DNA and complement levels
26
What do complement levels look like in SLE pt with renal involvement?
Decreased during active disease bc immune complement deposition w/in glomerulus induces complement fixation —> decreased levels
27
What are anti-smith antibodies highly specific for?
SLE
28
What are anti-smith antibodies useful for?
Identifying pts at risk of developing renal involvement of SLE, however, NOT good for monitoring renal disease progression (remain elevated/don’t change w/ active disease)
29
Relative risk reduction: formula
RRR = risk in unexposed - risk in exposed) / (risk in unexposed)
30
Relative risk reduction: alternative formula
RRR = 1 - RR
RR = relative risk
31
Relative risk: formula
RR = risk of disease in exposed group / risk of disease in unexposed group
32
How to use relative risk to compare risk for disease at different levels of an intervention or risk factor?
RR <1.0 -> decr risk in group in numerator
RR = 1.0 -> no diff in risk bt groups
RR >1.0 -> incr risk in group in numerator
RR = risk disease in exposed grp/ risk disease in unexposed grp
33
Definition of neonatal polycythemia
Hematocrit >65% in term infant
34
Causes of neonatal polycythemia
- increased erythropoiesis from intrauterine hypoxia (maternal diabetes, smoking, HTN, IUGR)
- erythrocyte transfusion (delayed cord clamping, twin-twin transfusion)
- genetic / metabolic disease (hypo or hyperthyroid, genetic trisomy 13, 18, 21)
35
Clinical presentation of neonatal polycythemia
- asymptomatic (most common)
- ruddy skin
- hypoglycemia, hyperbilirubinemia
- respiratory distress, cyanosis, apnea
- irritability, jitteriness
- abd dissension
36
Treatment for neonatal polycythemia
IVF
Glucose
Partial exchange transfusion
37
Are neonatal hematocrit levels from capillary sample (heel prick) reliable?
No.
If heel sticks shows polycythemia, must repeat with venous sample.
38
What does hyperviscosity cause in neonates?
Complications:
Hypoperfusion
Tissue hypoxia
```
Clinically:
Lethargy
Irritability
Drowsiness
Abd distension
Poor feeding
Hypotonia
Metabolic derangements — hypoglycemia, hyperbilirubinemia
```
39
Initial treatment of neonatal polycythemia
Hydration
| Correction of hypoglycemia
40
Alternate management of neonatal polycythemia
Partial exchange transfusion
— > withdraw blood from infant and infuse w normal saline
41
Glucose-6-phosphate deficiency epidemiology
X-linked
| Asian, African, or Middle Eastern descent
42
Manifestations of G6PD
Neonatal unconjugated hyperbilirubinemia — jaundice & anemia day of life 2-3
Acute hemolytic episode — secondary to oxidative stress (eg fava beans, sulfa drugs); jaundice, pallor, dark urine, abdominal/back pain
43
Laboratory findings of G6PD
Hemolytic anemia
Bite cells with Heinz bodies on peripheral smear
Low glucose-6-phosphate deficiency assay (may be normal during attack)
44
What helps differentiate between G6PD and hemolytic anemia of the neonate?
Timing of jaundice onset.
Hemolytic anemia (typically infant w A or B blood type born to type O mother) presents in first 24 hrs of life; G6PD generally presents day 2-3 of life
45
How does breast milk jaundice present?
Indirect hyperbilirubinemia over first few weeks of life
46
Why does breast milk jaundice happen?
Increased enterohepatic circulation
47
Physiologic jaundice
Happens in almost every newborn because of:
- increased RBC count w/ a shorter RBC life span
- decreased hepatic bilirubin clearance
- increased enterohepatic circulation
*NOT associated w/ anemia.
48
Acute mitral regurgitation: etiology
Ruptured mitral chordae tendineae from:
- mitral valve prolapse
- infective endocarditis
- rheumatic heart disease
- trauma
Papillary muscle rupture due to MI or trauma
49
Acute mitral regurgitation: clinical features
- rapid onset of pulmonary edema
- biventricular heart failure
- hypotension, cardiogenic shock
50
Acute mitral regurgitation: physical exam
- Diaphoresis, cool extremities
- Jugular venous distension, pulmonary crackles
- Hyperdynamic cardiac impulse
- Apical decrescendo systolic murmur (often absent)
51
Acute mitral regurgitation: management
- Bedside echocardiogram
| - Emergent surgical intervention
52
Who is at risk for mitral chordae tendineae rupture?
Patients with mitral valve prolapse, esp when it’s related to an underlying connective tissue disorder (Ehlers-Danlos syndrome, Marfan syndrome).
53
What happens to cardiac pressures in acute mitral regurgitation?
Patients w acute, severe MR have early equalization of left atrial and left ventricular pressures, and up to 50% (esp w/ ischemic MR) may have no audible murmur (silent MR).
54
Skin features of Ehlers-Danlos
- Transparent and hyperextensible
- Easy bruising, poor healing
- Velvety with atrophy and scaring
55
Skin features of Marfan Syndrome
No features other than striae
56
Musculoskeletal features of Ehlers-Danlos syndrome
- Joint hypermobility
- Pectus excavated
- Scoliosis
- High, arched palate
57
Cardiac features of Ehlers-Danlos Syndrome
Mitral valve prolapse ( can lead to acute mitral regurgitation)
58
Associated with Ehlers-Danlos
Abdominal and inguinal hernias
| Uterine prolapse
59
Genetics of Ehlers-Danlos syndrome
COL5A1 and COL5A2 mutation
Autosomal dominant
60
Musculoskeletal features of Marfan Syndrome
Joint hypermobility
Pectus excavatum or carinatum
Scoliosis
Tall w/ long extremities
61
Cardiac features of Marfan Syndrome
Progressive aortic root dilation
| Mitral valve prolapse
62
Other associations with Marfan Syndrome
Lens and retinal detachment
| Spontaneous pneumothorax
63
Genetics of Marfan Syndrome
FBN1 mutation
Autosomal dominant
64
Empiric treatment of CAP: Outpatient
Macrolide or doxycycline (healthy)
| Fluoroquinolone or beta lactam + macrolide (comorbidities)
65
Empiric treatment of CAP: Inpatient (non-ICU)
Fluoroquinolone
| Beta lactam + macrolide (IV)
66
Empiric treatment of CAP: ICU
Beta-lactam + macrolide (IV)
| Beta-lactam + fluoroquinolone (IV)
67
What two scales determine appropriate clinical setting for treatment of CAP?
CURB-65 and pneumonia severity index
68
What does metformin do additionally that is helpful?
Decreases triglycerides, increases HDL and improves nonalcoholic steatohepatitis (NASH)
69
How can analgesic-induced nephropathy present?
- florid nephrotic range proteinuria
| - acute interstitial nephritis
70
What do NSAIDs do to kidneys?
Reversible decline in GFR due to inhibition of vasodilatory prostaglandin production
71
What would kidney biopsy of NSAID-induced acute interstitial nephritis look like?
Minimal changes and a typical interstitial inflammatory pattern
72
Absolute risk reduction
ARR obtained by subtracting risk of relapses in a treatment group from that of the placebo group
73
Number needed to treat
NNT = 1/ARR
ARR = absolute risk reduction
74
Two steps for screening for gestational diabetes melitus
1) glucose challenge test (GCT)
| 2) if GCT failed, do 3-hour glucose tolerance test (GTT)
75
Are HgA1C levels sensitive for screening pregnant women?
No, bc physiologic increase in RBC mass and cell turnover lowers HgA1C
76
Target blood glucose levels during pregnancy
Fasting = 95mg/dL (5.3 mmol/L)
1-hr postprandial = 140 mg/dL (7.8 mmol/L)
2-hour postprandial = 120 mg/dL (6.7 mmol/L)
77
Treatment for gestational diabetes
1st line: exercise and dietary modification
2nd line: insulin, metformin, maybe glyburide (although glyburide associated w higher risk of neonatal hypoglycemia than insulin)
78
How can analgesic-induced nephropathy present?
- florid nephrotic range proteinuria
| - acute interstitial nephritis
79
What do NSAIDs do to kidneys?
Reversible decline in GFR due to inhibition of vasodilatory prostaglandin production
80
What would kidney biopsy of NSAID-induced acute interstitial nephritis look like?
Minimal changes and a typical interstitial inflammatory pattern
81
Absolute risk reduction
ARR obtained by subtracting risk of relapses in a treatment group from that of the placebo group
82
Number needed to treat
NNT = 1/ARR
ARR = absolute risk reduction
83
Two steps for screening for gestational diabetes melitus
1) glucose challenge test (GCT)
| 2) if GCT failed, do 3-hour glucose tolerance test (GTT)
84
Are HgA1C levels sensitive for screening pregnant women?
No, bc physiologic increase in RBC mass and cell turnover lowers HgA1C
85
Target blood glucose levels during pregnancy
Fasting = 95mg/dL (5.3 mmol/L)
1-hr postprandial = 140 mg/dL (7.8 mmol/L)
2-hour postprandial = 120 mg/dL (6.7 mmol/L)
86
Treatment for gestational diabetes
1st line: exercise and dietary modification
2nd line: insulin, metformin, maybe glyburide (although glyburide associated w higher risk of neonatal hypoglycemia than insulin)
87
Can patients refuse to receive medical information?
Yes. Included in the ethical principle of autonomy is the right to receive or refuse to receive medical information.
*excludes genetic testing for newborn babies or children for treatable conditions
88
What are the effects of radiation-induced cardiotoxicity?
1. Myocardial ischemia and/or infarction
2. Restrictive cardiomyopathy with diastolic dysfunction
3. Constrictive pericarditis
4. Valvular abnormalities (mitral or aortic stenosis/regurgitation)
5. Conduction defects (sick sinus syndrome or variable degrees of heart block)
89
What are side effects of the anthracycline class of drugs?
Causes a dose-dependent decline in the ejection fraction, leading to dilated cardiomyopathy.
90
When does breastfeeding failure jaundice begin?
First week of life
91
What is the pathophysiology of breastfeeding failure jaundice?
Lactation failure resulting in:
- decreased bilirubin elimination
- increased enterohepatic circulation
92
What are the clinical features of breastfeeding failure jaundice?
- suboptimal breastfeeding
| - signs of dehydration
93
What is the timing of breast milk jaundice?
Starts at age 3-5 days; peaks at 2 weeks
94
What is the pathophysiology of breast milk jaundice?
High levels of beta-glucuronidase in breast milk deconjugate intestinal bilirubin & increase enterohepatic circulation
95
What are clinical features of breast milk jaundice?
- adequate breastfeeding
| - normal elimination
96
What should babies with breast milk jaundice do for nutrition?
Continue breastfeeding exclusively, assuming the neonate is gaining weight and has a normal exam, and the mother’s breast milk supply is adequate.
97
What should be performed for neonate with conjugated hyperbilirubinemia?
If direct bilirubin is elevated (>20% of total bilirubin), ultrasound of biliary tree should be performed to evaluate for biliary atresia.
98
When should breast milk jaundice resolve?
Spontaneous resolution by age 3 months.
99
What separates the upper and lower GI tract?
Ligament of Treitz
100
What signs are suggestive of upper GI bleed?
Hemodynamics compromise, orthostasis, BUN to Cr ratio >20:1
101
Bright red blood per rectum is nearly always due to _______ GI bleed.
lower
102
What signs are more common in upper GI bleed?
Hematemesis and melena
103
In a patient with hematochezia who is hemodynamically stable, perform a ________ first.
Colonoscopy
104
In a patient with hematochezia who is hemodynamically unstable or suspected upper GI bleed...
1) Resuscitate
2) +/- Surgery/IR consult
3) EGD
105
If source is not found in a hemodynamically unstable patient after EGD....
Perform angiography
106
If source of GI bleed after EGD and colonoscopy not found, what do you do?
obscure GI bleed evaluation
| Eg capsule endoscopy, repeat EGD/colonoscopy
107
What is a secondary / obscure CT scan that could be (but rarely is) used to detect GI bleed?
Arterial-phase contrast-enhanced CT with negative oral contrast
108
What medication is used to treat bleeding esophageal varices?
Octreotide
109
Hazard ratio: definition
Likelihood of an event occurring in a treatment group relative to the control group
HR <1.0 indicates an event is less likely to occur in a treatment group than the control group
110
Diverticular bleeding: etiology
Arterial erosion due to conflicting mucosal outcropping
111
Diverticula bleeding: Clinical presentation
Painless hematochezia in patients age >40
Bleeding often self-limited but can recur
112
Diverticular bleeding: diagnosis
Colonoscopy or tagged red blood cell scan
113
Diverticular bleeding: treatment
- Intravenous volume replacement
- endoscopic therapy or angiographic embolization
- colonic resection for persistent bleeding
114
What causes colonic diverticulosis?
Outpouching of the colon wall at points of weakness where the vasa recta penetrate the circular muscle layer of the colon.
115
Infectious mononucleosis: etiology
Epstein-Barr virus most common
116
Infectious mononucleosis: clinical features
```
Fever
Tonsillitis/pharyngitis +/- exudates
Posterior or diffuse cervical lymphadenopathy
Significant fatigue
+/- hepatosplenomegaly
+/- rash after amoxicillin
```
117
Infectious mononucleosis: diagnostic findings
Positive heterophile antibody (Monospot) test (25% false-negative rate during 1st week of illness)
Atypical lymphocytosis
Transient hepatitis
118
Infectious mononucleosis: management
Avoid sports for >/= 3 weeks (contact sports >/= 4 weeks) due to risk of splenic rupture
119
What is the primary means of treatment for infectious mononucleosis?
Supportive care - eg rest, adequate hydration, nutrition, avoidance of strenuous activity.
No sports for >/= 3 weeks, no contact sports >/= 4 weeks.
Can give acetaminophen or NSAIDS for symptomatic relief (do not shorten duration of illness)
120
When are corticosteroids warranted in the treatment of infectious mononucleosis?
Rare cases when airway obstruction appears imminent
Warning signs:
SOB while recumbent
Tachypnea
Inability to swallow
Also, possibly in immunocompromised patients
121
What happens to a patient’s chronic cough after they quit smoking?
Initial temporarily increase in cough during first few weeks after cessation; ultimately chronic cough improves.
122
Who experiences more benefit in pulmonary function after smoking cessation?
Younger quitters (vs older quitters)
123
What does smoking do to bones?
Accelerates osteoporosis
Cessation can reverse loss of bone density and decrease the excess risk of fracture but benefits may not be apparent in first 10 yrs after quitting
124
Is nicotine withdrawal worse, the same, or better in old vs young?
Same
Peak in first few days, improve over course of the next few weeks
125
What does smoking cessation do for mortality?
Cessation at age 60 or older has been shown to lower the risk of all-cause mortality and cardiovascular events
Benefit seen within 5 years of quitting
Gain even greater for those who quit at a younger age
126
Benefits of smoking cessation
Reduction in mortality
Reduced risk of cardiac events
Reduced risk of osteoporosis
Less decline in lung function over time in comparison to current smokers
127
What are symptoms of vertebrobasilar insufficiency?
Vertigo
Dizziness
Diplopia
Numbness
128
Risk factors for vertebrobasilar insufficiency
```
DM
HTN
Hypercholesterolemia
Arrhythmia
CAD
Circulatory problems
Hx of smoking cigarettes
```
129
Symptoms of labyrinthitis
```
Vertigo
Tinnitus
Nausea
Loss of balance
Often follows a viral illness
Can also be cause by bacterial inf, allergies, benign tumors, and certain meds
```
130
What is benign proximal vertigo (BPV)?
Abnormal feeling of motion triggered by certain provocative positions
Most often attributed to calcium debris w/in posterior semicircular canal
Nystagmus commonly seen
131
What are panic attacks?
Discreet periods of intense fear or discomfort
```
Sx include:
Palpitations
Seating
Trembling
SOB
Choking sensation
CP
Nausea
Dizziness
Paresthesias
A fear of dying or losing control
```
132
Cataplexy: define
Sudden, temporary loss of muscle tone that can result in collapse.
Often caused by intense emotions, including laughter.
133
What are keloids?
Benign fibrous growths that develop in scar tissue secondary to an overproduction of extracellular matrix and dermal fibroblasts.
134
Preferred treatment of most keloids?
Intralesional glucocorticoids preferred treatment — Up to 70% patients respond
Silicone sheeting can reduce symptoms (pain or itching) associated w/ keloids or reduce formation, but data poor and not understood
135
How to treat pregnant women w/ TB?
3-drug therapy:
Isoniazid (INH) + Rifampin (RIF) + Ethambutol for 2 months followed by INH and RIF for an additional 7 months
All 3 meds do cross placenta but not assoc w/ fetal toxicity
Don’t give pyrazinamide bc uncertain teratogenicity, not very effective
**also need to give pregnant women pyridoxine (vitamin B6) supplementation to prevent INH-induced neurotoxicity.**
