Clin Med Flashcards
fever is a rise in body temperature in response to ____
endogenous cytokines
fever is controlled by the ____ area of the hypothalamus
preoptic (thermoregulatory)
what cytokines act on the thermoregulatory portion of the hypothalamus?
endogenous pyrogens (IL-1, TNF, IFNa)
range for fever
99.4-100.4F (37.4-38C)
normal range of body temperature
96.8-100.0F (36.0-37.8C)
universal core body temperature for fever
100.9F (38.3C)
what mediates fever production?
PGE2, Na, Ca2+, cAMP, monoamines
temperatures of hyperthermia
105.8F (41C)
what is the mechanism of hyperthermia?
loss of homeostatic mechanism that makes the body unable to dissipate heat
what is the underlying cx of CAD? (90% cases of MI and HF)
atherosclerosis –> supply and demand imbalance
describe supply angina
decreased O2 delivery to tissue causes ischemia (ex: coronary stenosis, vasoconstriction)
describe demand angina
increased myocardial O2 requirement and workload leads to ischemia (ex: stress, exercise, fever, thyrotoxicosis, LVH, anemia)
symptoms of stable angina
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
cause of unstable angina
atherosclerotic plaque rupture or erosion –> platelet aggregation and thrombus with partial occlusion of artery
symptoms of unstable angina
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)
if cardiac enzymes are elevated and ECG shows ST depression/T wave inversion, what does this result in?
Non-STEMI (NSTEMI)
clinical presentation of STEMI
substernal CP
radiation to jaw and left arm
crushing sensation
nausea and diaphoresis
lab findings of STEMI
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
ST elevations in II, III, aVF =
inferior wall STEMI
new LBBB in pt with symptoms of AMI =
STEMI
indications for percutaneous coronary intervention (PCI)
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
indications for stress testing to risk stratify
ACS patients without high risk features or otherwise low risk pts
mainstays of tx for ACS
antiplatelet and anticoagulation therapies
coronary intervention
why is it essential to distinguish ACS in patients with and without ST elevation?
determines the need for reperfusion therapy
fibrinolytic/thrombolytic therapy in NSTE-ACS is harmful
only helpful in STE-ACS
how to manage STEMIs
ASA + P2Y12 inhibitors (clopidogrel, ticragelor) + reperfusion therapy
reperfusion therapy choices for acute STEMI
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
if a STEMI pt comes in and PCI is not available and pt cannot have thrombolytics, what must be done?
proceed with medical tx (nitro, P2Y12 inhibitors, etc.) and transfer anyway
other treatment measures for STEMI
CCU monitoring low flow O2 therapy if SaO2 is reduced analgesia = sublingual nitro or IV opiate analgesia beta blockers nitrates ACEi/ARBs aldosterone antagonists
most common cause of death in the first 24 hrs of MI =
ventricular arrhythmia
most common complication in inferior MI or with meds =
sinus bradycardia
complete AV block is more common in what type of MI?
inferior MI
prognosis of a complete AV block is worse with what kind of MI? why?
anterior MI since it is usually a sign of extensive infarction and usually requires permanent pacing
when can post infarction ischemia be seen?
after thrombolytic therapy for STEMI or after medical treatment of NSTEMI
if any arrhythmia is unstable, what must be done?
pt must be cardioverted
how must every hemodynamically significant arrhythmia be treated (VT or VF)?
prompt defibrillation
how are hemodynamically stable ventricular arrhythmias treated?
anti-arrhythmic therapy (amiodarone)
how to RV infarcts after MIs present?
hypotension
normal LV function
elevated JVP
clear lungs
how to treat RV infarct?
IV fluids (never give vasodilators)
list of mechanical complications / defects post-MI
papillary muscle rupture VSD myocardial rupture LV aneurysm pericarditis mural thrombus
how do papillary muscle ruptures present?
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
how to VSD present?
parasternal murmur
how do myocardial ruptures present?
usually 2-7 days post MI
usually associated with immediate death
located in anterior wall
how does pericarditis present?
audible friction rubs with positional chest discomfort
with what does a mural thrombus generally present?
with large anterior infarctions
how does myocardial dysfunction present?
hypotension not responsive to fluid resuscitation
what does acute LV failure present with?
pulmonary edema
main difference between cardiogenic shock and myocardial dysfunction presentations =
pts with myocardial infarction may have normal BP
how does cardiogenic shock present?
systolic BP <90
signs of diminished perfusion (cold, clammy extremities, confusion)
does NOT respond to fluid resuscitation
how to tx cardiogenic shock?
echo to assess LV function inotropic support (dopamine, dobutamine, NE)
clinical findings, cause, and most common info of croup
most common cx of infectious airway obstruction in kids ages 6-36 months
most often viral, less often allergic
px as stridor
cx of epiglottis
H. flu type B
cx of bronchiolitis
RSV, influenza, parainfluenza, adenovirus, etc.
clinical findings and cx of pneumonia
most common in kids = Streptococcus pneumoniae
bacterial = lobar, localized, higher fever, ill-appearing
viral and atypical = diffuse, peribronchial
triggers of asthma
infection, exercise, environmental irritants, stress, GERD
clinical findings of anaphylaxis
food or meds –> retropharyngeal/laryngeal edema
sx often sudden and associated with facial edema and urticaria
bronchospasm in lower airways is common
clinical findings of foreign body aspiration in trachea
sudden, dramatic coughing
stridor
drooling
choking in upper airway
3 most important agents used in tx of anaphylaxis
epinephrine, oxygen, steroids
cyanotic congenital heart defects
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
non-cyanotic congenital heart defects
atrial septal defect
ventricular septal defect
patent ductus arteriosus
coarctation of aorta
clinical findings of asthma
inflammation, edema, bronchospasm, mucus
can result in sudden worsening due to alveolar disease and/or atelectasis
wheeze, prolonged expiratory phase
clinical findings of foreign body aspiration in lower foreign bodies
coughing
choking when FB first ingested
delayed dx = recurrent pneumonia, chronic cough
clinical findings of foreign body aspiration in esophagus
drooling
swallowing problems
physiological cx of asthma
inflammation, edema, bronchospasm, mucus
can result in sudden worsening due to alveolar disease and/or atelectasis
clinical findings of foreign body aspiration in esophagus
drooling
swallowing problems
how do you collect urine in a child who can void on command?
clean catch urine
if a child cannot void on command, how do you collect urine?
catheterization or suprapubic aspiration
if a child is acutely ill, febrile, and empiric abx are going to be given, how od you collect urine?
via catheterization or SPA prior to medication being given
are bag urine samples appropriate for culture?
no
essentials of dx of asthma
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)
clinical sx of asthma
cough, wheezing, chest tightness, prolonged expiration, shortness of breath
triggers of asthma
exposure to allergens
systolic murmurs
mitral regurgitation
tricuspid regurgitation
aortic stenosis
pulmonic stenosis
VSD
ASD
diastolic murmurs
aortic regurgitation
pulmonic regurgitation
mitral stenosis
tricuspid stenosis
atrial myxoma
ausculatory and physical findings and common cx of mitral regurgitation
decreased S1
wide-splitting S2
S3
holosystolic murmur ar apex
common cx = mitral valve prolapse
exaggerated by valsalva
reduced by squatting
ausculatory and physical findings and common cx of aortic stenosis
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
ausculatory and physical findings of tricuspid regurgitation
systolic at left sternal border, 4th ICS
increased by inspiration
decreased by standing
px with pulmonary HTN, lung dz, RV infarct, MI
ausculatory and physical findings of aortic regurgitation
acute cx
chronic cx
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
ausculatory and physical findings and cause of mitral stenosis
mumbling murmur
palpable S1 and S2 + opening snap
cx by rheumatic fever
ausculatory and physical findings and cause of tricsupid stenosis
rumbling murmur at LSB
cx by rheumatic fever
increased with inspiration
almost always associated with Mitral Stenosis
common diagnostic tests for lightheadedness, dizziness, and syncope
H & P, first (orthostatic vital signs) tilt table test ECG CBC (anemia, glucose) BUN/Cr (dehydration)
what do you perform in a patient with high risk PE or intermediated risk of PE with elevated D-dimer?
CT pulmonary angiography or
V/Q scan in pts who can’t have iodine contrast dye or
MR pulmonary angiography or
pulmonary angiography
what helps determine pretest probability of PE?
Wells criteria
in patients with low or intermediate risk of PE per Wells Criteria, what effectively rules PE out?
normal D-dimer (<500 ng/mL)
sx that patients present with on ROS that correlate with edema or underlying cause
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)
what is lipidema?
fat cells grow and proliferate –> fluid retention around cells
can be localized or generalized as seen with morbid obesity
what presents with morbid obesity and/or lymphedema?
organ dysfunction like CHF, nephrotic syndrome, severe liver disease
what is lymphedema?
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
what is pitting edema associated with?
underlying organ dysfunction (heart, kidney, liver)
extrinsic factors contributing to edema?
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)
diagnostic testing to evaluate edema
complete H&P bloodwork (CMP, TSH, CBC) CXR-PA and lat (fluid in lungs/cardiac enlargement) EKG echo (movement) BNP (CHF suspected)
if diagnostics of edema are inconclusive, what do you do?
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
where is edema first noticed? why?
LE due to gravity or periphery due to decreased venous return for a variety of reasons
signs of CHF that differentiate it from edema
exertion dyspnea orthopnea paroxysmal dyspnea S3 on cardiac exam bilateral crackles on lung exam
what is edema?
abnormally large amounts of fluid in intercellular spaces
what is anasarca?
massive generalized edema
what causes localized edema?
venous obstruction or lymphatic obstruction
what causes generalized edema?
systemic causes like CHF and renal disease – though first apparent in LE due to gravity
what is transient abnormal enlargement or increased volume of a body part or area?
swelling
seen with increased engorgement in tissues due to increased blood volume in dilated vessels
what is transient eminence or elevation as seen with local inflammatory rxn to bites or immunization injections?
swelling
what is non-pitting edema associated with?
no appreciable indentation
due to underlying metabolic dz (thyroid/myxedema or lymphatic system dz)
can be associated with warm weather
how do you diagnosis diabetes insipidus?
24 hr urine volume collection (confirms polyuria)
urine osmalilty <300 mOsm/kg
water deprivation test
how to treat central DI?
vasopressin
how to treat nephrogenic DI?
decreased solute intake
thiazide diuretics
NSAIDs
vasopressin
how to treat hypernatremia?
replace free water deficit
how to diagnose orthostatic hypotension syncope
orthostatic vital signs – always first
lab testing (CBC, BUN/Cr, glucose)
ECG
tilt table testing
symptoms of orthostatic hypotension syncope
manifest with sudden postural changes
generalized weakness
dizziness
visual blurring
3 types of reflex syncope (neurally mediated)
carotid sinus HS and syndrome
situational syncope
vasovagal syncope (fainting)
what triggers vasovagal syncope?
prolonged sitting or standing
emotional stress or fear
pain or anxious stimuli
heat
what triggers situational syncope?
micturition, defecating, coughing, sneezing, swallowing, laughing
what triggers carotid sinus HS and syndrome?
stimulation of carotid artery baroreceptor from mechanical forces like turning head, shaving, tight shirt collars, etc.
what characterizes hypertrophic cardiomyopathy (HCM)?
left ventricular hypertrophy without a clear secondary cause
symptoms of hypertrophic cardiomyopathy?
dyspnea on exertion fatigue chest pain presyncope and syncope (during or after exertion) palpitations
findings of hypertrophic cardiomyopathy
S4
systolic murmur
dx of hypertrophic cardiomyopathy
FH or genetic testing
echo
tx of hypertrophic cardiomyopathy
avoid strenuous activity
tx sx with B-blockers, CCBs, diuretics, implantable cardioverter-defibrillators
severe cases = surgery
normal ABG values for pH, HCO3-, and PCO2
pH 7.35-7.44
HCO3- = 24 mEq/L
PCO2 = 40 mmHg
ddx of respiratory alkalosis
anything that increases respiratory rate or tidal volume (incr CO2 out, decr PCO2/H+ in)
pulmonary embolus
ddx of respiratory acidosis
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
acidosis associated with ___kalemia
hyperkalemia
alkalosis is associated with ___kalemia
hypokalemia
signs and sx of chronic kidney disease
edema HTN decreased urine output foamy urine (proteinuria) uremia pericardial friction rub *asterixis *uremic frost
most common causes of CKD
diabetes
HTN
clinical findings of CKD
proteinuria
urine sediment abnormalities
decr GFR (<60 m/min)
>3 months
diagnostic testing for CKD
eGFR
albumin:Cr in urine
urinalysis with microscopy
renal U/S (atrophic kidneys, cortical thinning, incr echogenicity, incr resistiv e indices)
treatment for CKD
renal replacement therapy
transplant
dialysis
indications for dialysis
AEIOU acidosis (severe) electrolyte imbalance (hyperkalemia) ingestion overload uremia
signs and sx of acute kidney injury
same as CKD
+ hematuria
+ SOB
clinical findings of AKI
hematuria
dyspnea
3 different cx of AKI
prerenal (hypovolemia, decr CO, hypotension, vasodilation) post renal (urinary obstruction, renal pelvis papillary necrosis) intrinsic (GN, tubular necrosis, interstitial nephritis)
dx testing for AKI
MUST get a urinalysis with microscopy
urine albumin:Cr
renal U/S
tx of AKI
tx underlying dz
clinical findings of nephrotic syndrome
proteinuria hyperlipidemia lipiduria HTN generalized edema
dx testing for nephrotic syndrome
renal biopsy
bland urinary sample/sediment
tx of nephrotic syndrome
tx underlying dz
clinical findings of nephritic syndrome
hematuria RBC casts/dysmorphic casts active urinary sediment HTN periorbital edema
dx testing for nephritic syndrome
renal biopsy low complement (C3, C4) levels in serum
urinalysis with microscopy: epithelial cells, granular casts, waxy casts
dx?
acute tubular necrosis
urinalysis with microscopy: WBC, eosinophils
dx?
pyelonephritis
acute interstitial nephritis
urinalysis with microscopy: dysmorphic RBC or casts
dx?
vasculitis
GN
urinalysis with microscopy: hematuria, dysmorphic RBC or casts
dx?
nephritic
urinalysis with microscopy: heavy proteinuria, lipiduria
dx?
nephrotic
urinalysis with microscopy: hyaline casts
dx?
prerenal azotemia
urinalysis with microscopy: WBC, RBC, bacteria
dx?
UTI
what does hyponatremia primarily result from?
increases in total body water (TBW) and less from changes in total body sodium
what do increases in TBW result from?
excessive intake of water
decreased renal excretion of water (inability to suppress ADH release)
levels of mild, moderate, and severe hyponatremia
hyponatremia = serum sodium <135 mEq/L
mild 130-134 mEq/L
moderate 120-129 mEq/L
severe <120 mEq/L (symptomatic)
what is the systemic diagnostic approach to hyponatremia?
- 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
essential diagnostic criteria of SIADH
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
most common malignancy associated with ectopic ADH production
small cell lung cancer
treatment of symptomatic hyponatremic patients
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
clinical manifestations of hyperkalemia
depends on severity of the hyperkalemia
cardiac arrhythmia (vfib, bradycardia from AV block, systole) skeletal muscle weakness (diaphragm weakness) metabolic acidosis
what are the 2 main reasons for hyperkalemia?
- transcellular shift (increased K+ release from cells) = metabolic acidosis
- decreased renal K+ excretion
what causes central sleep apnea?
failure of respiratory center in brain stem which results in repetitive cessation or decr in airflow and ventilator effort during sleep
what causes obstructive sleep apnea?
upper airway occlusion resulting in decreased airflow during sleep
risk factors of OSA
older age >60 male sex obesity large neck circumference tonsilar/adenoid hypertrophy nasal obstruction
severity of OSA types
mild = apnea-hypopnea-index 5-14 events/hr moderate = AHI >15-29 events/hr severe = AHA >30 events/hr
diagnosis of OSA
polysomnography (sleep study)
dx = AHI >15 events/hr or AHI >5 events/hr in presence of sx or CV comorbidities
treatment of OSA
weight loss
CPAP
risk factors for heart failure
age female sex obesity HTN DM CAD valvular heart disease AFib
ddx of dyspnea
pneumonia COPD asthma pneumothorax PE cardiac disease
ddx of acute cough
post-viral cough (most common) viral URI pneumonia pulmonary edema PE
ddx of persistent cough (top causes)
postnasal drip
asthma
GERD
pulmonary infection
essentials of dx for granulomatosis with polyangiitis
triad of upper respiratory tract disease + lower respiratory disease + glomerulonephritis
lab testing for granulomatosis with polyangiitis
c-ANCA (abs to proteinase-3)
chest CT
+ confirmatory dx of tissue biospy
histologic findings on biopsy of granulomatosis with polyangiitis
vasculitis granulomatous inflammation geographic necrosis acute and chronic inflammation segmental necrotizing GN with multiple crescents
what is idiopathic vasculitis of small and medium-sized arteries seen in pts with sx of asthma?
Churg-Strauss
essential clinical findings and histology for Churg-Strauss
marked peripheral eosinophils
fibrinoid necrotizing epithelioid
(asthma)
what disease demonstrates noncaseating granulomas on biopsy specimen?
sarcoidosis
signs and sx of sarcoidosis
malaise, fever, insidious dyspnea
restrictive cardiomyopathy
cardiac dysrhythmias
conduction disturbances
what is clinically characterized by progressive parenchymal scarring and loss of pulmonary function?
idiopathic pulmonary fibrosis
signs and sx of IPF patients
most present with gradual onset (>6 most) of exertion dyspnea and nonproductive cough
progressive dyspnea = most prominent symptom
work up and what is seen for IPF
CXR (abnormal with bilateral reticular opacities and some peripheral honeycombing)
PFT (restrictive pattern)
gold standard for dx of IPF
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
what is the most common sx associated with heart failure
dyspnea
KNOW THE MRC DYSPNEA SCALE
- SOB only on strenuous exercise
- SOB when hurrying on level or walking up slight hill
- walks slower than most on level, stops after mile or so, or stops 15 min walking at own pace
- stops for breath after walking about 100 yards or after few minutes on level ground
- too breathless to leave house or breathless while undressing
KNOW THE GOLD CRITERIA for chronic obstructive pulmonary disease
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
what does the 6 minute walk test measure/do?
exercising capacity
functional assessment of the body (esp. heart ventricles)
