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CPR Remediation > Clin Med > Flashcards

Clin Med Flashcards

1
Q

fever is a rise in body temperature in response to ____

A

endogenous cytokines

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2
Q

fever is controlled by the ____ area of the hypothalamus

A

preoptic (thermoregulatory)

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3
Q

what cytokines act on the thermoregulatory portion of the hypothalamus?

A

endogenous pyrogens (IL-1, TNF, IFNa)

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4
Q

range for fever

A

99.4-100.4F (37.4-38C)

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5
Q

normal range of body temperature

A

96.8-100.0F (36.0-37.8C)

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6
Q

universal core body temperature for fever

A

100.9F (38.3C)

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7
Q

what mediates fever production?

A

PGE2, Na, Ca2+, cAMP, monoamines

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8
Q

temperatures of hyperthermia

A

105.8F (41C)

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9
Q

what is the mechanism of hyperthermia?

A

loss of homeostatic mechanism that makes the body unable to dissipate heat

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10
Q

what is the underlying cx of CAD? (90% cases of MI and HF)

A

atherosclerosis –> supply and demand imbalance

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11
Q

describe supply angina

A

decreased O2 delivery to tissue causes ischemia (ex: coronary stenosis, vasoconstriction)

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12
Q

describe demand angina

A

increased myocardial O2 requirement and workload leads to ischemia (ex: stress, exercise, fever, thyrotoxicosis, LVH, anemia)

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13
Q

symptoms of stable angina

A 
chest discomfort (pain, squeezing, pressure, tightness)
brought on by exertion, emotion, stress
substernal pain
lasts 5-10-15 min
relieved by rest or nitro 
predictable, not changing frequency, duration, or intensity 
50% normal ECG
others have ST depression or elevation
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14
Q

cause of unstable angina

A

atherosclerotic plaque rupture or erosion –> platelet aggregation and thrombus with partial occlusion of artery

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15
Q

symptoms of unstable angina

A 
new or worsening chest pain
tempo change
occurs more often
increasing severity
lasts longer than 15-20 min
brought on by less effort, require more meds for relief
may occur at rest
normal cardiac enzymes (troponin I, CKMB)
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16
Q

if cardiac enzymes are elevated and ECG shows ST depression/T wave inversion, what does this result in?

A

Non-STEMI (NSTEMI)

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17
Q

clinical presentation of STEMI

A

substernal CP
radiation to jaw and left arm
crushing sensation
nausea and diaphoresis

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18
Q

lab findings of STEMI

A

initial cardiac enzymes may be normal if early presentation
cardiac enzymes may become positive as early has 4-6hrs
troponin may stay elevated for 5-7 days after STEMI

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19
Q

ST elevations in II, III, aVF =

A

inferior wall STEMI

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20
Q

new LBBB in pt with symptoms of AMI =

A

STEMI

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21
Q

indications for percutaneous coronary intervention (PCI)

A 
patients with ACS and high risk features: 
recurrent angina/ischemia at rest
elevated troponin or ST segment depression
recurrent ischemia with evidence of HF
high risk stress test result
EF <40%
hemodynamic instability
sustained VTach
PCI w/in 6 min
prior CABG
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22
Q

indications for stress testing to risk stratify

A

ACS patients without high risk features or otherwise low risk pts

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23
Q

mainstays of tx for ACS

A

antiplatelet and anticoagulation therapies

coronary intervention

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24
Q

why is it essential to distinguish ACS in patients with and without ST elevation?

A

determines the need for reperfusion therapy

fibrinolytic/thrombolytic therapy in NSTE-ACS is harmful
only helpful in STE-ACS

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25
Q

how to manage STEMIs

A

ASA + P2Y12 inhibitors (clopidogrel, ticragelor) + reperfusion therapy

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26
Q

reperfusion therapy choices for acute STEMI

A

choice 1: immediate coronary angiography and primary PCI (door to balloon time <90 min)
choice 2: if primary PCI unavailable, give thrombolytics and transfer pt to facility capable of primary PCI (door to balloon time <120 min)
choice 3: if total time from first contact to balloon time is >120 min, give thrombolytics and transfer to capable facility

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27
Q

if a STEMI pt comes in and PCI is not available and pt cannot have thrombolytics, what must be done?

A

proceed with medical tx (nitro, P2Y12 inhibitors, etc.) and transfer anyway

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28
Q

other treatment measures for STEMI

A 
CCU monitoring
low flow O2 therapy if SaO2 is reduced
analgesia = sublingual nitro or IV opiate analgesia
beta blockers
nitrates
ACEi/ARBs
aldosterone antagonists
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29
Q

most common cause of death in the first 24 hrs of MI =

A

ventricular arrhythmia

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30
Q

most common complication in inferior MI or with meds =

A

sinus bradycardia

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31
Q

complete AV block is more common in what type of MI?

A

inferior MI

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32
Q

prognosis of a complete AV block is worse with what kind of MI? why?

A

anterior MI since it is usually a sign of extensive infarction and usually requires permanent pacing

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33
Q

when can post infarction ischemia be seen?

A

after thrombolytic therapy for STEMI or after medical treatment of NSTEMI

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34
Q

if any arrhythmia is unstable, what must be done?

A

pt must be cardioverted

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35
Q

how must every hemodynamically significant arrhythmia be treated (VT or VF)?

A

prompt defibrillation

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36
Q

how are hemodynamically stable ventricular arrhythmias treated?

A

anti-arrhythmic therapy (amiodarone)

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37
Q

how to RV infarcts after MIs present?

A

hypotension
normal LV function
elevated JVP
clear lungs

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38
Q

how to treat RV infarct?

A

IV fluids (never give vasodilators)

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39
Q

list of mechanical complications / defects post-MI

A 
papillary muscle rupture
VSD
myocardial rupture
LV aneurysm
pericarditis
mural thrombus
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40
Q

how do papillary muscle ruptures present?

A

usually 3-7 days after
usually of mitral valve
usually seen in pts with given thrombolytics or those who had late presentations
new systolic murmur
clinical deterioration with pulmonary edema

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41
Q

how to VSD present?

A

parasternal murmur

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42
Q

how do myocardial ruptures present?

A

usually 2-7 days post MI
usually associated with immediate death
located in anterior wall

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43
Q

how does pericarditis present?

A

audible friction rubs with positional chest discomfort

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44
Q

with what does a mural thrombus generally present?

A

with large anterior infarctions

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45
Q

how does myocardial dysfunction present?

A

hypotension not responsive to fluid resuscitation

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46
Q

what does acute LV failure present with?

A

pulmonary edema

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47
Q

main difference between cardiogenic shock and myocardial dysfunction presentations =

A

pts with myocardial infarction may have normal BP

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48
Q

how does cardiogenic shock present?

A

systolic BP <90
signs of diminished perfusion (cold, clammy extremities, confusion)
does NOT respond to fluid resuscitation

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49
Q

how to tx cardiogenic shock?

A 
echo to assess LV function
inotropic support (dopamine, dobutamine, NE)
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50
Q

clinical findings, cause, and most common info of croup

A

most common cx of infectious airway obstruction in kids ages 6-36 months
most often viral, less often allergic
px as stridor

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51
Q

cx of epiglottis

A

H. flu type B

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52
Q

cx of bronchiolitis

A

RSV, influenza, parainfluenza, adenovirus, etc.

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53
Q

clinical findings and cx of pneumonia

A

most common in kids = Streptococcus pneumoniae

bacterial = lobar, localized, higher fever, ill-appearing

viral and atypical = diffuse, peribronchial

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54
Q

triggers of asthma

A

infection, exercise, environmental irritants, stress, GERD

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55
Q

clinical findings of anaphylaxis

A

food or meds –> retropharyngeal/laryngeal edema

sx often sudden and associated with facial edema and urticaria

bronchospasm in lower airways is common

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56
Q

clinical findings of foreign body aspiration in trachea

A

sudden, dramatic coughing
stridor
drooling
choking in upper airway

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57
Q

3 most important agents used in tx of anaphylaxis

A

epinephrine, oxygen, steroids

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58
Q

cyanotic congenital heart defects

A 
5Ts with 1-5 
trunks arteriosus (1 vessel)
transposition of great vessels (2 vessels switched)
tricuspid atresia (3)
tetralogy of fallout (4 defects)
total anomalous pulmonary vascular return (5 letters TAPVR)
hypoplastic left heart 
Epstein's anomaly
pulmonary atresia
single ventricle
double outlet R ventricle
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59
Q

non-cyanotic congenital heart defects

A

atrial septal defect
ventricular septal defect
patent ductus arteriosus
coarctation of aorta

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60
Q

clinical findings of asthma

A

inflammation, edema, bronchospasm, mucus

can result in sudden worsening due to alveolar disease and/or atelectasis

wheeze, prolonged expiratory phase

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61
Q

clinical findings of foreign body aspiration in lower foreign bodies

A

coughing
choking when FB first ingested
delayed dx = recurrent pneumonia, chronic cough

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62
Q

clinical findings of foreign body aspiration in esophagus

A

drooling

swallowing problems

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63
Q

physiological cx of asthma

A

inflammation, edema, bronchospasm, mucus

can result in sudden worsening due to alveolar disease and/or atelectasis

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64
Q

clinical findings of foreign body aspiration in esophagus

A

drooling

swallowing problems

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65
Q

how do you collect urine in a child who can void on command?

A

clean catch urine

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66
Q

if a child cannot void on command, how do you collect urine?

A

catheterization or suprapubic aspiration

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67
Q

if a child is acutely ill, febrile, and empiric abx are going to be given, how od you collect urine?

A

via catheterization or SPA prior to medication being given

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68
Q

are bag urine samples appropriate for culture?

A

no

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69
Q

essentials of dx of asthma

A

episodic or chronic sx of airflow obstruction
reversibility of airflow obstruction (via spontaneously or following bronchodilator therapy)
sx frequently worse at night or early morning
prolonged expirations and diffuse wheezes
limitation of airflow on PFT or positive bronchiole-provocation challenge (methacholine)

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70
Q

clinical sx of asthma

A

cough, wheezing, chest tightness, prolonged expiration, shortness of breath

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71
Q

triggers of asthma

A

exposure to allergens

72
Q

systolic murmurs

A

mitral regurgitation
tricuspid regurgitation
aortic stenosis
pulmonic stenosis

VSD
ASD

73
Q

diastolic murmurs

A

aortic regurgitation
pulmonic regurgitation
mitral stenosis
tricuspid stenosis

atrial myxoma

74
Q

ausculatory and physical findings and common cx of mitral regurgitation

A

decreased S1
wide-splitting S2
S3
holosystolic murmur ar apex

common cx = mitral valve prolapse

exaggerated by valsalva
reduced by squatting

75
Q

ausculatory and physical findings and common cx of aortic stenosis

A

decreased S2
S4
crescendo-decrescendo systolic murmur at right 2nd ICS
radiates to carotids/sternal notch & apex

common cx = degeneration of bicuspid valve

px with dyspnea, angina, syncope

76
Q

ausculatory and physical findings of tricuspid regurgitation

A

systolic at left sternal border, 4th ICS

increased by inspiration
decreased by standing

px with pulmonary HTN, lung dz, RV infarct, MI

77
Q

ausculatory and physical findings of aortic regurgitation

acute cx
chronic cx

A

decrescendo at left sternal border, 3rd ICS

acute cx = infective endocarditis, aortic dissection, chest trauma
chronic cx = calcific degeneration, congenital bicuspid valve, dilated aortic root, rheumatic fever

px with Marfans syndrome and Turner syndrome

78
Q

ausculatory and physical findings and cause of mitral stenosis

A

mumbling murmur
palpable S1 and S2 + opening snap

cx by rheumatic fever

79
Q

ausculatory and physical findings and cause of tricsupid stenosis

A

rumbling murmur at LSB

cx by rheumatic fever

increased with inspiration

almost always associated with Mitral Stenosis

80
Q

common diagnostic tests for lightheadedness, dizziness, and syncope

A 
H &amp; P, first (orthostatic vital signs) 
tilt table test
ECG
CBC (anemia, glucose)
BUN/Cr (dehydration)
81
Q

what do you perform in a patient with high risk PE or intermediated risk of PE with elevated D-dimer?

A

CT pulmonary angiography or
V/Q scan in pts who can’t have iodine contrast dye or
MR pulmonary angiography or
pulmonary angiography

82
Q

what helps determine pretest probability of PE?

A

Wells criteria

83
Q

in patients with low or intermediate risk of PE per Wells Criteria, what effectively rules PE out?

A

normal D-dimer (<500 ng/mL)

84
Q

sx that patients present with on ROS that correlate with edema or underlying cause

A 
leg swelling - unilateral vs bilateral and extent
dyspnea
orthopnea
paroxysmal nocturnal dyspnea
chest pain, indigestion
wt changes
skin, hair, nail changes
GI changes suggesting malabsorption or thyroid disorder
frothy urine (proteinuria)
85
Q

what is lipidema?

A

fat cells grow and proliferate –> fluid retention around cells
can be localized or generalized as seen with morbid obesity

86
Q

what presents with morbid obesity and/or lymphedema?

A

organ dysfunction like CHF, nephrotic syndrome, severe liver disease

87
Q

what is lymphedema?

A

impaired fluid return in the lymphatic system due to hereditary or secondary causes (crush injuries and tropical infections)

most commonly secondary to axillary LN dissection during mastectomy

88
Q

what is pitting edema associated with?

A

underlying organ dysfunction (heart, kidney, liver)

89
Q

extrinsic factors contributing to edema?

A

sodium intake
sedentary lifestyle
increased calorie intake (wt gain, dec venous return)
NSAID at high doses, prolonged use
others meds
excess alcohol intake (cirrhosis and liver failure –> ascites)

90
Q

diagnostic testing to evaluate edema

A 
complete H&amp;P
bloodwork (CMP, TSH, CBC)
CXR-PA and lat (fluid in lungs/cardiac enlargement)
EKG
echo (movement)
BNP (CHF suspected)
91
Q

if diagnostics of edema are inconclusive, what do you do?

A

revisit H&P
consider additional labs (anti-nuclear ABs, Hep B and C serology, serum and urine protein electrophoresis)
renal U/S
possible renal biopsy

92
Q

where is edema first noticed? why?

A

LE due to gravity or periphery due to decreased venous return for a variety of reasons

93
Q

signs of CHF that differentiate it from edema

A 
exertion dyspnea 
orthopnea
paroxysmal dyspnea
S3 on cardiac exam
bilateral crackles on lung exam
94
Q

what is edema?

A

abnormally large amounts of fluid in intercellular spaces

95
Q

what is anasarca?

A

massive generalized edema

96
Q

what causes localized edema?

A

venous obstruction or lymphatic obstruction

97
Q

what causes generalized edema?

A

systemic causes like CHF and renal disease – though first apparent in LE due to gravity

98
Q

what is transient abnormal enlargement or increased volume of a body part or area?

A

swelling

seen with increased engorgement in tissues due to increased blood volume in dilated vessels

99
Q

what is transient eminence or elevation as seen with local inflammatory rxn to bites or immunization injections?

A

swelling

100
Q

what is non-pitting edema associated with?

A

no appreciable indentation
due to underlying metabolic dz (thyroid/myxedema or lymphatic system dz)
can be associated with warm weather

101
Q

how do you diagnosis diabetes insipidus?

A

24 hr urine volume collection (confirms polyuria)
urine osmalilty <300 mOsm/kg
water deprivation test

102
Q

how to treat central DI?

A

vasopressin

103
Q

how to treat nephrogenic DI?

A

decreased solute intake
thiazide diuretics
NSAIDs
vasopressin

104
Q

how to treat hypernatremia?

A

replace free water deficit

105
Q

how to diagnose orthostatic hypotension syncope

A

orthostatic vital signs – always first
lab testing (CBC, BUN/Cr, glucose)
ECG
tilt table testing

106
Q

symptoms of orthostatic hypotension syncope

A

manifest with sudden postural changes
generalized weakness
dizziness
visual blurring

107
Q

3 types of reflex syncope (neurally mediated)

A

carotid sinus HS and syndrome
situational syncope
vasovagal syncope (fainting)

108
Q

what triggers vasovagal syncope?

A

prolonged sitting or standing
emotional stress or fear
pain or anxious stimuli
heat

109
Q

what triggers situational syncope?

A

micturition, defecating, coughing, sneezing, swallowing, laughing

110
Q

what triggers carotid sinus HS and syndrome?

A

stimulation of carotid artery baroreceptor from mechanical forces like turning head, shaving, tight shirt collars, etc.

111
Q

what characterizes hypertrophic cardiomyopathy (HCM)?

A

left ventricular hypertrophy without a clear secondary cause

112
Q

symptoms of hypertrophic cardiomyopathy?

A 
dyspnea on exertion
fatigue
chest pain
presyncope and syncope (during or after exertion)
palpitations
113
Q

findings of hypertrophic cardiomyopathy

A

S4

systolic murmur

114
Q

dx of hypertrophic cardiomyopathy

A

FH or genetic testing

echo

115
Q

tx of hypertrophic cardiomyopathy

A

avoid strenuous activity
tx sx with B-blockers, CCBs, diuretics, implantable cardioverter-defibrillators
severe cases = surgery

116
Q

normal ABG values for pH, HCO3-, and PCO2

A

pH 7.35-7.44
HCO3- = 24 mEq/L
PCO2 = 40 mmHg

117
Q

ddx of respiratory alkalosis

A

anything that increases respiratory rate or tidal volume (incr CO2 out, decr PCO2/H+ in)

pulmonary embolus

118
Q

ddx of respiratory acidosis

A

anything that decreases respiratory rate/tidal volume (decr CO2 out, incr PCO2/H+ in)
anything increases dead space
anything that worsens airway obstruction

pulmonary embolus
inadequate ventilator settings

119
Q

acidosis associated with ___kalemia

A

hyperkalemia

120
Q

alkalosis is associated with ___kalemia

A

hypokalemia

121
Q

signs and sx of chronic kidney disease

A 
edema
HTN
decreased urine output
foamy urine (proteinuria)
uremia
pericardial friction rub
*asterixis
*uremic frost
122
Q

most common causes of CKD

A

diabetes

HTN

123
Q

clinical findings of CKD

A

proteinuria
urine sediment abnormalities
decr GFR (<60 m/min)
>3 months

124
Q

diagnostic testing for CKD

A

eGFR
albumin:Cr in urine
urinalysis with microscopy
renal U/S (atrophic kidneys, cortical thinning, incr echogenicity, incr resistiv e indices)

125
Q

treatment for CKD

A

renal replacement therapy
transplant
dialysis

126
Q

indications for dialysis

A 
AEIOU
acidosis (severe)
electrolyte imbalance (hyperkalemia)
ingestion
overload
uremia
127
Q

signs and sx of acute kidney injury

A

same as CKD
+ hematuria
+ SOB

128
Q

clinical findings of AKI

A

hematuria

dyspnea

129
Q

3 different cx of AKI

A 
prerenal (hypovolemia, decr CO, hypotension, vasodilation)
post renal (urinary obstruction, renal pelvis papillary necrosis)
intrinsic (GN, tubular necrosis, interstitial nephritis)
130
Q

dx testing for AKI

A

MUST get a urinalysis with microscopy
urine albumin:Cr
renal U/S

131
Q

tx of AKI

A

tx underlying dz

132
Q

clinical findings of nephrotic syndrome

A 
proteinuria
hyperlipidemia
lipiduria
HTN
generalized edema
133
Q

dx testing for nephrotic syndrome

A

renal biopsy

bland urinary sample/sediment

134
Q

tx of nephrotic syndrome

A

tx underlying dz

135
Q

clinical findings of nephritic syndrome

A 
hematuria
RBC casts/dysmorphic casts
active urinary sediment 
HTN
periorbital edema
136
Q

dx testing for nephritic syndrome

A 
renal biopsy
low complement (C3, C4) levels in serum
137
Q

urinalysis with microscopy: epithelial cells, granular casts, waxy casts

dx?

A

acute tubular necrosis

138
Q

urinalysis with microscopy: WBC, eosinophils

dx?

A

pyelonephritis

acute interstitial nephritis

139
Q

urinalysis with microscopy: dysmorphic RBC or casts

dx?

A

vasculitis

GN

140
Q

urinalysis with microscopy: hematuria, dysmorphic RBC or casts

dx?

A

nephritic

141
Q

urinalysis with microscopy: heavy proteinuria, lipiduria

dx?

A

nephrotic

142
Q

urinalysis with microscopy: hyaline casts

dx?

A

prerenal azotemia

143
Q

urinalysis with microscopy: WBC, RBC, bacteria

dx?

A

UTI

144
Q

what does hyponatremia primarily result from?

A

increases in total body water (TBW) and less from changes in total body sodium

145
Q

what do increases in TBW result from?

A

excessive intake of water

decreased renal excretion of water (inability to suppress ADH release)

146
Q

levels of mild, moderate, and severe hyponatremia

A

hyponatremia = serum sodium <135 mEq/L

mild 130-134 mEq/L
moderate 120-129 mEq/L
severe <120 mEq/L (symptomatic)

147
Q

what is the systemic diagnostic approach to hyponatremia?

A
  • ALL LABS DRAWN SIMULTANEOUSLY*
    1. measure serum osmolality (hypo, iso, hyper)
    2. if hypoosmotic hyponatremia, assess volume status of patient
    3. if hypo osmotic hyponatremia, measure random urine sodium level and urine osmolality
148
Q

essential diagnostic criteria of SIADH

A

DX OF EXCLUSION: must rule out cortisol deficiency, hypothyroidism, and other cx

decr ECF effective osmolality
inappropriate urine concentration
elevated urine [Na] under normal salt and water intake
absence of adrenal, thyroid, pituitary, or renal insufficiency or diuretic use

149
Q

most common malignancy associated with ectopic ADH production

A

small cell lung cancer

150
Q

treatment of symptomatic hyponatremic patients

A

100 ml IV bolus of hypertonic saline (3%) over 10 min, repeat if still symptomatic, up to 3 total infusions (300 ml)

hypertonic saline 3% continuous infusion

151
Q

clinical manifestations of hyperkalemia

A

depends on severity of the hyperkalemia

cardiac arrhythmia (vfib, bradycardia from AV block, systole)
skeletal muscle weakness (diaphragm weakness)
metabolic acidosis
152
Q

what are the 2 main reasons for hyperkalemia?

A
  1. transcellular shift (increased K+ release from cells) = metabolic acidosis
  2. decreased renal K+ excretion
153
Q

what causes central sleep apnea?

A

failure of respiratory center in brain stem which results in repetitive cessation or decr in airflow and ventilator effort during sleep

154
Q

what causes obstructive sleep apnea?

A

upper airway occlusion resulting in decreased airflow during sleep

155
Q

risk factors of OSA

A 
older age >60
male sex
obesity
large neck circumference
tonsilar/adenoid hypertrophy
nasal obstruction
156
Q

severity of OSA types

A 
mild = apnea-hypopnea-index 5-14 events/hr
moderate = AHI >15-29 events/hr
severe = AHA >30 events/hr
157
Q

diagnosis of OSA

A

polysomnography (sleep study)

dx = AHI >15 events/hr or AHI >5 events/hr in presence of sx or CV comorbidities

158
Q

treatment of OSA

A

weight loss

CPAP

159
Q

risk factors for heart failure

A 
age
female sex
obesity
HTN
DM
CAD
valvular heart disease
AFib
160
Q

ddx of dyspnea

A 
pneumonia
COPD
asthma
pneumothorax
PE
cardiac disease
161
Q

ddx of acute cough

A 
post-viral cough (most common)
viral URI
pneumonia
pulmonary edema
PE
162
Q

ddx of persistent cough (top causes)

A

postnasal drip
asthma
GERD
pulmonary infection

163
Q

essentials of dx for granulomatosis with polyangiitis

A

triad of upper respiratory tract disease + lower respiratory disease + glomerulonephritis

164
Q

lab testing for granulomatosis with polyangiitis

A

c-ANCA (abs to proteinase-3)
chest CT

+ confirmatory dx of tissue biospy

165
Q

histologic findings on biopsy of granulomatosis with polyangiitis

A 
vasculitis 
granulomatous inflammation
geographic necrosis
acute and chronic inflammation
segmental necrotizing GN with multiple crescents
166
Q

what is idiopathic vasculitis of small and medium-sized arteries seen in pts with sx of asthma?

A

Churg-Strauss

167
Q

essential clinical findings and histology for Churg-Strauss

A

marked peripheral eosinophils
fibrinoid necrotizing epithelioid
(asthma)

168
Q

what disease demonstrates noncaseating granulomas on biopsy specimen?

A

sarcoidosis

169
Q

signs and sx of sarcoidosis

A

malaise, fever, insidious dyspnea
restrictive cardiomyopathy
cardiac dysrhythmias
conduction disturbances

170
Q

what is clinically characterized by progressive parenchymal scarring and loss of pulmonary function?

A

idiopathic pulmonary fibrosis

171
Q

signs and sx of IPF patients

A

most present with gradual onset (>6 most) of exertion dyspnea and nonproductive cough
progressive dyspnea = most prominent symptom

172
Q

work up and what is seen for IPF

A

CXR (abnormal with bilateral reticular opacities and some peripheral honeycombing)

PFT (restrictive pattern)

173
Q

gold standard for dx of IPF

A

lung biopsy = heterogenous distribution of parenchymal fibrosis against background of mild inflammation (UIP)

biopsy critical to distinguish IPF from dz with better prognosis and different tx options

174
Q

what is the most common sx associated with heart failure

A

dyspnea

175
Q

KNOW THE MRC DYSPNEA SCALE

A
  1. SOB only on strenuous exercise
  2. SOB when hurrying on level or walking up slight hill
  3. walks slower than most on level, stops after mile or so, or stops 15 min walking at own pace
  4. stops for breath after walking about 100 yards or after few minutes on level ground
  5. too breathless to leave house or breathless while undressing
176
Q

KNOW THE GOLD CRITERIA for chronic obstructive pulmonary disease

A 
I = mild = FEV1/FVC <70%, FEV1 >80% predicted
II = moderate = FEV1/FVC <70%, 50% < FEV1 < 80% predicted
III = severe = FEV1/FVC <70%, 30% < FEV1 < 50% predicted
IV = very severe = FEV1/FVC <70%, 30% < FEV1 predicted / FEV1 <50% predicted + chronic respiratory failure
177
Q

what does the 6 minute walk test measure/do?

A

exercising capacity

functional assessment of the body (esp. heart ventricles)

CPR Remediation (2 decks)

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