Renal/Pulm/Acid-Base Flashcards
cor pulmonale
RH from pulm HTN (which is due to underlying lung disease)
- pulm HTN - mean pulm art P > 25 mm Hg at rest (30 mm Hg during exercise)
etiologies -COPD, ILD, pulmonary vascular disease (thromboembolic, venous HTN), OSA, chest wall disorders (?), idiopathic, hypoxemia
sxs - DOE, fatigue, lethargy, exertional syncope (due to low CO), exertional angina (due to increased myocardial demand)
- sxs are usu gradual onset
- but can present suddenly if there is a sudden increase in pulm artery pressures (PE)
exam - signs of RH overload (…tricuspid regurg murmur)
imaging
- CXR - enlarged pulm arteries
- EKG - partial or complete RBB, right axis deviation, RVH, RA enlargement
- echo - pulm HTN, dilated RV, tricuspid regurg
- RH cath - gold std for dx, shows RH disease (no LH disease), though dx is clinical
- PFTs - normal volumes and FEV1/FVC, decreased DLCO
tx - optimize preload, afterload, and contractility
- supp O2, diuretics, IV inotropes
- treat underlying etiology
glomerulonephritis
PSGN - low serum C3
rapidly progressive glomerulonephritis
- crescent formation
idiopathic crescentic glomerulonephritis
- cell-mediated injury
lupus nephritis
acid-base disorders
nl pH = 7.35-7.45
met acidosis
compensation by blowing off CO2 (Winters Formula): PaCO2 = 1.5*bicarb + 8 +/- 2
met alkalosis
increase in PaCO2 by 0.7 mm Hg for every 1 meq/L rise in bicarb
acute respiratory acidosis
increase in bicarb by 1 meq/L for every 10 mm Hg rise in PaCO2
- things that impair ventilation - stridor
acute respiratory alkalosis
decrease in bicarb by 2 meq/L for every 10 mm Hg decrease in PaCO2
- things that cause tachypnea - asthma exacerbation
compensatory mechanisms dont normalize or overcorrect pH
non-cardiogenic pulm edema
negative pressure pulm edema - occurs with upper airway obstruction
- negative intrathoracic pressure occurs with inspiration against obstruction
- more common in young men or after head and neck surgery
acute cystitis and pyelonephritis in non-pregnant women
UTIs are more common in women because of shorter urethral length
uncomplicated cystitis
- nitrofuranotin for 5d
- bactrim for 3d
- fosfomycin single dose
- urine culture only if initial treatment fails
complicated cystitis (factors that increase the risk of abx resistance) - associated with DM, pregnancy, renal failure, urinary tract obstruction, cath, urinary procedure, immunosuppression, hospital-acquired
- FQs 5-14d
- amp/gent (extended spectrum) for more severe cases
- urine culture prior to starting therapy
- DONT use FQs in pregnancy
pyelo
- outpatient - Fqs
- inpatient - IV FQ or AG+amp
- urine culture prior to starting therapy
urine dipstick - high false pos and neg rates
- if pt has sxs of UTI but negative dipstick - STILL get urine culture
- leuk esterase - WBC marker
- nitrites - marker for Enterobacteriaceae
when would you give Na bicarb
salicylate tox, TCADs, metabolic acidosis (renal failure), hyperkalemia
anaphylaxis
anaphylactic reaction may be delayed
CV - distributive shock, tachy
respiratory - upper airway edema (stridor), bronchospasm (wheezing)
cutaneous - urticaria, pruritis, flushing
GI upset
tx - FIRST IM epi (vasoconstriction –> reduced edema)
- secure airway, volume resuscitate
- anti-histamines, glucocorticoids (take several hours to take action)
- note - give epi before intubation because it can reduce upper airway edema and prevent the need for intubation
notes - latex allergy (short term foley catheters contain latex, can be mimic for fat embolism)
aspergillosis
occurs in a cavity - TB, sarcoid, bronchial cysts, neoplasm
invasive aspergillosis
- occurs in immunocompromised - neutropenia, glucocorticoids, HIV
- triad: fever, CP, hemoptysis
- pulmonary nodules with halo sign
- pos cultures
- tx - voriconazole +/- caspofungin
chronic pulmonary aspergillosis
- occurs in lung disease/damage - cavitary Tb
- > 3 mos of weight loss, cough, hemoptysis, fatigue
- cavitary lesions +/- fungus ball
- pos aspergillus IgG serology
- tx - resect (if possible), voriconazole, embolization for severe hemoptysis
simple aspergilloma - typically quiescent
airway obstruction
fixed upper airway obstruction limits inspiration and expiration
- flattening of flow volume loop
- causes - laryngeal edema (food allergy)
asthma - bronchoconstriction
- decreased airflow during expiration
- scooped out expiration curve
restrictive pattern (includes PE) - loop shifted to the right (smaller lung volumes at same flow rates)
interstitial cystitis
painful bladder syndrome
- more common in women, associated with psychiatric disorders (anxiety) and pain syndromes (fibromyalgia)
sxs - bladder pain with filling and relief voiding
- increased frequency, urgency
- dyspareunia
- pain can be exacerbated by exercise, alcohol
ddx - UTI, STI, cancer, cystocele (bladder prolapse)
dx - bladder pain with no cause 6 wks
- normal UA
tx - not curative, focus on quality of life
- behavioral modification and trigger avoidance
- amitriptyline
- analgesics for exacerbation
Goodpastures
anti-GBM abx, linear IgG deposition on IF
rapidly progressive GN or alveolar hemorrhage
mixed cryoglobulinemia
palpable purpura, proteinuria, hematuria
- non-specific sxs - arthralgias, HSM, hypocomplementemia
- membranoproliferative
circulating cryoglobulins
most pts will have underlying HCV infection - test for HCV antibodies
rhinitis
nonallergic (vasomotor rhinitis) = common cold
- nasal congestion, rhinorrhea, sneezing, PND (will present as dry cough)
- later onset - 20s
- no allergic trigger, perennial sxs
- erythematous nasal mucosa
allergic
- watery rhinorrhea, sneezing, eye symptoms
- early onset, allergen trigger, other allergic disorders
- pale/bluish nasal mucosa
- will have elevated serum IgE
treatment for BOTH: intranasal glucocorticoids and antihistamines
pulm auscultation findings
normal peripheral lung fields - vesicular breath sounds
consolidation (PNA)
- increased breath sounds
- increased tactile fremitus, dull to percussion
- egophony - E–>A
- sounds travel faster in solids/liquids than in air - fremitus and breath sounds will be increased if there is solid/liquid INSIDE the lung
- visible costophrenic angles
pleural effusion - decreased tactile fremitus, dull to percussion
- outside the lung, solids/liquids/air can insulate sounds - decreased breath sounds and tactile fremitus
- blunted costophrenic angles
atelectasis (mucus plugging)
- decreased breath sounds, decreased tactile fremitus
- because lung is collapsed (and not filled with solid/liquid)
tactile fremitus is decreased in most lung pathology - except with consolidation where it is increased
hyperresonance - sign of air
lupus
gradual symptom onset, malar or discoid rash
- joint, renal, serosal
- neuro involvement - strokes, seizures, headaches (due to vasculitis)
labs
- anemia, leukopenia, TCP
- pos ANA (FIRST get an ANA), anti-ds-DNA, anti-Smith
- increased immune complexes (of anti-dS-DNA and antibody) deposit in mesangium and subendothelial space –> trigger intense inflammatory reaction and activation of complement –> low C3 (and C4)
- if immune complexes deposit in subepithelial space –> nephrotic syndrome without hypocomplementemia
urinary incontinence in women
get UA and postvoid residual to rule out overflow incontinence
- normal PVR < 150 mL in women, < 50 mL in men
stress - lifestyle modifications, pelvic floor exercises, pessary (if surgery is contraindicated), pelvic floor surgery
urge
- RFs - age > 40 , female, pelvic surgery
- tx - lifestyle modifications (reduce consumption of caffeine, alcohol, soda), bladder training, anti-muscarinic drugs (oxybutynin)
mixed - depends on predominant sxs
overflow - involuntary dribbling, incomplete empyting
- correct underlying cause, cholinergic agonists (bethanechol), intermittent self cath
diuretics
can cause AKI - due to hypovolemia, low CO, and renal hypoperfusion
–> prerenal azotemia
thiazides and loops - renal tubular chloride loss
- metabolic alkalosis (contraction alkalosis)
other than thiazides - most diuretics increase urinary cal excretion
hypovolemic hyponatremia and RAAS
solute and water loss
1) decreased renal perfusion –> activation RAAS –> ang2 –> thirst, ADH
- angiotension also causes arteriolar constriction (efferent > afferent, protects GFR), among other functions
2) hypotension –> baroreceptors (carotid arteries) –> nonosmotic stimulation of ADH
3) hypovolemia –> L atrial stretch receptor stimulation –> nonosmotic stimulation of ADH
end results: increased renin, aldosterone, and ADH
note - because of ongoing ADH secretion –> can get hypotonic hypovolemic hyponatremia (due to excess of total body water)
renal transplant
early dysfunction - oliguria, HTN, increased BUN/Cr
- causes are ureteral obstruction, acute rejection, cyclosporine tox, vascular obstruction, ATN
acute rejection - heavy lymphocyte infiltration and swelling of vascular intima
- give IV steroids
exercise-induced bronchoconstriction
can occur in pts with or without asthma
high volumes of dry, cold air –> mast cell degranulation
tx - beta-agonist and mast cell stabilizers
- first line - albuterol 10-20 min prior to exercise, intermittent use
- alternative - anti-leukotriene agent (montelukast) 15-20 min prior to exercise
- combo in high performance athletes
electrolyte wasting
salt wasting:
diuretic use, cerebral salt wasting, adrenal insufficiency
renal K wasting:
diuretic use, hyperaldosteronism, RTA
of note - self-induced vomiting, diuretic abuse, and laxative abuse can all lead to electrolyte abnormalities
- but urine electrolytes will clue you in to what is occuring
urinary incontinence in elderly
anatomy - urge, overflow, obstruction, pelvic floor/sphincter weakness, fistula
neuro - MS, dementia, SC injury, disc herniation
reversible causes (DIAPERS)
- delirium
- infection - UTI
- atrophic urethritis/vaginitis
- pharmaceuticals - a-blockers, diuretics, CCBs, opiates, anticholinergics
- psych - depression
- excess out - DM, CHF
- restricted mobility - post-surg
- stool impaction
nephrotic syndrome
- 6 causes
altered permeability of glomerular membrane for proteins
proteinuria > 3.5g, hypoalbuminemia, edema
- HLD (and increased lipids in urine) - due to increased liver protein and lipid synthesis
- protein loss –> decreased oncotic pressure –> hypovolemia –> RAAS –> fluid retention and increased hydrostatic pressure ==> edema
- loss of AT3 (protein) –> hypercoagulable (affects veins more than arteries) - at risk for RVT and VTE events
- -> RVT - acute abd pain, fever, hematuria, and worsening renal function
Fe-resistant microcytic hypochromic anemia - due to transferrin loss
vitamin D deficiency due to increased excretion of cholecalciferol-binding protein
decreased thyroxine due to loss of thyroxine-binding globulin
TYPES:
FSGS - AA, hispanic, obesity, HIV, heroin use
membranous nephropathy - adenocarcinoma (breast, lung), NSAIDs, HBV, SLE
- RVT is most commonly see with membranous nephropathy
membranoproliferative glomerulonephritis - HBV and HCV, lipodystrophy, endocarditis
- dense intramembranous (GBM) deposits - stain pos for C3
- IgG antibodies directed against C3 convertase –> persistent complement activation –> low complement levels
- occurs in association with mixed cryoglobulinemia syndrome
minimal change disease - NSAIDs, (Hodgkin’s) lymphoma
- kids
- MCD will resolve after treatment of lymphoma
IgA nephropathy - URI, HSP
- can present with nephrotic syndrome - BUT more commonly presents with hematuria
- immune complex nephropathy
diabetic nephropathy - occurs 10-15 yrs after disease onset
- diabetes is the leading cause of ESRD in the US
- RFs - poor glycemic control, elevated BP, cigarette smoking, age, AA or mexican
- disease progression can be slowed by glycemic control, tx of HTN, and angiotensin axis blockade
1) first sign of injury = glomerular hyperfiltration and renal hypertrophy (–> intraglomerular HTN –> progressive glomerular damage…)
- -> ACEi reduce intraglomerular HTN
2) within 5-10 yrs - hyalinosis of afferent and efferent arterioles (microangiopathy), thickening of GBM and mesangial expansion, microalbuminuria (30-300g/day), HTN
3) nodular glomerulosclerosis (KW nodules, pathognomonic), nephrotic syndrome, decreased GFR - if proteinuria occurs <5 yrs after disease onset, pt has urine sed, or experiences >30% reduction in GFR within 2-3 mi of starting ACEi/ARB - albuminuria is NOT due to diabetic nephropathy
amyloidosis
- AL (light chain) amyloidosis - MM, Waldenstrom macroglobulinemia
- AA (inflammatory conditions, amyloid is abnormally folded proteins) - RA, IBD, chronic osteomyelitis, Tb (chronic infection)
- will appear as deposits that stain with Congo red and have apple-green birefringence (under polarized light)
- will deposit in GBM, blood vessel, renal interstitium - appear as thin fibrils on EM
alcohol withdrawal
agitation, tachy, HTN, mental status changes
urine dip
can only detect macroalbuminuria >300 mg/24hrs
nephrolithiasis
TYPES:
75-90% of stones are Ca oxalate
- radio-opaque, enveloped-shaped
- risk factors - small bowel disease (Crohns), surgical resection, chronic diarrhea –> malabsorption of fat –> Ca starts to bind fat instead of oxalate –> oxalate is absorbed more
Ca phos stones - in primary hyperparathyroidism, RTA
struvite stones/staghorn calculi - Proteus, urease-producing orgs
cystinura
- impaired amino acid transport (COLA)
- radio-opaque stones, hexagonal crystals
- pos urinary cyanide nitroprusside test - used as a screening test, detects homozyotes
uric acid - needle shaped crystals, low urine pH, radiolucent stones
- tx - hydration, alkalinization of urine (with K citrate), low purine diet, allopurinol
xanthine stones are also radiolucent
stones < 1 cm will pass spontaneously
can get vagal reaction reaction with ureteral colic –> can cause ileus
obstructive ureterolithiasis (or anything obstruction of hollow viscus) - colicky, poorly localized referred pain
- to dx stone - US or non-con spiral CT
- non-con CT due to risks associated with contrast administration - allergy, AKI, (clinically, concern for obscuration of stone by contrast dye)
tx
- NSAIDs > narcotics - narcotics can exacerbate N&V
- 2L or more water/day
- tamsulosin - a1 antagonist –> relaxes ureteral muscle, decreases intraureteral pressure –> facilitates stone passage
recurrent renal stones - 24hr urine to id underlying metabolic disorder
- increase fluids, reduce Na (because Ca is reabsorbed passively with active Na absorption., intake more Na –> more is excreted) , reduce protein, normal Ca intake, increase citrate, reduce oxalate
- drugs: thiazide, urine alkalinization, allopurinol
thiazide
hyponatremia, hypoK, hypoMg
hyperCa
decreased renal uric acid excretion - gout
impairs insulin release and glucose utilization in peripheral tissues = hyperglycemia
- worse with chlorthalidone (but is the preferred agent because of results of ALLHAT, showed decrease in CV mortality)
increase LDL and triglycerides
acute oliguria
oliguria < 500/24hrs (or less than 0.5 mL/kg/hr)
H&P –> bedside bladder scan to assess for urinary RT
- if bladder scan is inconclusive (obesity) –> cath
no urine RT –> serum and urine chem and imaging
- pre-renal - hypovolemia, sepsis, low CO –> give fluids
- renal - ATN, interstitial nephritis, glomerular disease
urine RT –> urethral catheter –> serum and urine biochem and imaging
- > 50 mL postvoid residual bladder volume is diagnostic for urinary RT/bladder outlet obstruction
- treat underlying cause (BPH, malignancy aka extrinsic compression) with uro consultation
- meds can cause this - amitriptyline, first gen H1 blockers (diphenhydramine, chlorpheniramine, hydroxyzine, have anticholinergic effects)
constipation and urinary sxs can be linked
analgesic nephropathy
most common from of drug-induced chronic renal failure
(3-5% of ESRD in USA) - seen in 50s females who use combined analgesics (ASA and naproxen)
chronic tubulointerstitial nephritis
- focal glomerulosclerosis, papillary necrosis
- polyuria and sterile pyuria are early manifestations
- microscopic hematuria and renal colic may occur following sloughing of renal papilla
- HTN, mild proteinuria, impaired urinary concentration
- CT can show small kidneys with bilateral renal papillary calcifications
pt with chronic analgesic abuse - more likely to develop premature aging, atherosclerotic vascular disease, urinary tract cancer
glomerular vs nonglomerular hematuria
hematuria in general
- neoplasms, infections, trauma, nephrolithiasis, glomerulonephritis, prostatic disease (BPH)
glomerular
- microscopic (but gross hematuria can be present)
- glomerulonephritis, Alport syndrome
- sxs - non-specific
- UA - blood AND protein, RBC casts, dysmorphic RBCs
nonglomerular
- gross
- causes - nephrolithiasis, cancer, PKD, infection, papillary necrosis
- px - dysuria, urinary obstruction
- UA - blood (NO protein)
hyperkalemia
most often due to decreased urinary K excretion
- most common causes - CKD, meds that impair RAAS
acute hyperkalemia - ascending muscle weakness and flaccid paralysis, peak T waves –> short QT –> wide QRS –> disappearance of P –> sine wave, v fib
- emergent treatment if serum K is rapidly rising, > 6.5, or pt has ECG changes
chronic hypokalemia is more insidious - no sxs until > 7.0
1) med review
2) work-up for hypoaldosteronism
EMERGENT TX:
1) cardiac membrane stabilization - calcium gluconate infusion
rapid acting tx - insulin with glucose, b2-agonists (albuterol), sodium bicarb
- dont use b2-agonists in pts with CAD - can cause tachy and precipitate angina
removing K (slow-acting) - diuretics (30 min), K-exylate (remove via GI tract), hemodialysis (prep time) - diuretics are contraindicated in dehydrated patients)
all else fails - cardioversion for v fib, transvenous pacemaker for symptomatic bradycardia, IV amiodarone for v. arrhythmias
MEDS:
nonselective b-blockers - inhibit b2-mediated intracellular K uptake
ACEi, ARBs … decreased aldosterone secretion
K sparing diuretics, trimethoprim (blocks ENaC) - inhibit ENaC or aldosterone receptor
cardiac glycosides (digoxin) - inhibit Na/K pump
NSAIDs - inhibit local PG synthesis –> decreased renin and aldosterone secretion
cyclosporine - blocks aldosterone activity
heparin - blocks aldosterone production
sux - causes extracellular leakage of K through AchR
HTN and kidneys
HTN is the second leading cause of ESRD in the US (behind diabetes)
benign nephrosclerosis –> glomerulosclerosis
1) arteriosclerotic lesions, glomerular capillary tufts
2) decrease in RBF and GFR
- nephrosclerosis - hypertrophy and intimal medial fibrosis of renal arterioles
- glomerulosclerosis - loss of glomerular capillary surface area with glomerular and peritubular fibrosis, microscopic hematuria, proteinuria, kidneys decrease in size
diabetic autonomic neuropathy
CV - tachy, impaired exercise tolerance, orthostasis
peripheral nerves - dry skin, pruritis, callus formation
- foot ulcers and poor wound healing
- charcot arthorpathy (neurogenic arthropathy) - increased fracture risk with resultant secondary ulceration
gastrointestinal
- gastroparesis
- esophageal dysmotility with dyspepsia
- intestinal involvement with diarrhea, constipation, or fecal incontinence
GU
- ED, decreased libido and dyspareunia in F
- neurogenic bladder = decreased ability to sense full bladder –> incomplete emptying, decreased urination
- eventually recurrent UTIs or overflow incontinence
hypokalemia
increased K entry into cells, renal K wasting, GI fluid loss
adrenergic agents - stimulate Na/K ATPase and release of insulin
hypoMg - cause of refractory hypoK
- intracellular Mg inhibits K secretion in the collecting tubules of the kidney
- causes: chronic alcoholism - malnutrition, associated with a number of electrolyte abnormalities, hypoMg is the most common
- -> acute alcohol withdrawal -increase SNS activity –> K shifts into cells –> hypokalemia
increased hematopoiesis, GCSF
- increased K uptake by cells
pulmonary embolism
sudden-onset pleuritic CP, dyspnea, tachycardia
- hemoptysis - due to pulm infarct
- pts will also develop small pleural effusions (exudative, grossly bloody)
RFs - … HIV, hemoconcentration (dehydrated)
wedge shaped infarct on CT
EKG - S1Q3T3 occurs in minority of pts
indicators of poor prognosis - afib and low O2 sat
approach:
1) stabilize with O2 and IVFs
2) evaluate for abs contraindications to anticoag –> if yes –> get CT angio and place IVC filter
- if no - get D-dimer if PE is unlikely (Wells) and CT angio if PE is likely
- early effective anti-coag reduces mortality risk of PE - so if pt likely has PE and presents with concerning hx –> start anti-coag while you are waiting for CT angio
Wells score - 4 is cutoff
- most important (3 pts each) - signs of DVT and PE is most likely dx
- other things - hx of PE/DVT, tach, recent surgery/immobilization (flights DONT count), hemoptysis, cancer
massive PE with cardiogenic shock
- syncope
- will see R heart strain - JVD, RBBB on EKG
- tx - fibrinolysis (surgery within the preceding 10 ds is a contraindication)
- survival is poor - death often occurs within an hr of sxs
- distinguishing this from an MI - CVD risk factors, EKG signs (ST elevation, T wave inversion, Q waves)
RTA
remaining nephrons maintain the kidney’s ability to excrete acid (by producing more NH3 buffer –> H+ NH3 excreted as NH4)
- metabolic acidosis is not seen until there is advanced kidney dysfunction (GFR < 20 mL/min)
RTA - metabolic acidosis that occurs with normal/preserved kidney function
- type 1 - hypOkalemia
- type 2 - hypOkalemia and low bicarb
- hyperkalemic RTA (type 4) - occurs in poorly controlled diabetics –> damage to JG apparatus –> hyporeninemic hypoaldosteronism –> acidosis, hyperkalemic
unilateral obstructive uropathy
flank pain, poor urine output
- can have intermittent episodes of high volume urination when obstruction is overcome by large volume of retained urine (post-obstructive diuresis)
excessive diuresis may lead to K wasting –> weakness
ADH and aldosterone
ADH secreted with high serum osm and hypovolemia
aldosterone escape - escape from sodium-retaining effects of excess aldosterone
- by volume and/or pressure natriuresis
acute bronchitis
most often due to preceding respiratory illness (viral)
px - cough for 5d-3wks
- can have purulent, blood-tinged sputum - sputum is due to epithelial sloughing (not bacterial infection)
- no systemic findings
- can have wheezing or rhonchi, crackles that are cleared with cough - secretions are easily mobilized
clinical dx
- get CXR if you are concerned about pna
- otherwise symptomatic tx with bronchodilators and NSAIDs
- abx NOT recommended
DLCO
low - anemia, PE, pulm HTN
high - pulm hemorrhage, polycythemia
nl - bronchitis, asthma, MSK disease
ILD
progressive fibrosis of interstitium, alveoli, and conducting airways
- restrictive disease
- DLCO is decreased (increased thickness of alveolar membrane)
px - progressive dyspnea over mo
causes
- asbestos (navy, shipyard, insulation), Be, silicon dioxide, HS pneumonitis
- amiodarone, bleomycin, nitrofurantoin
- infections - PNA, fungal, TB
- radiation
- RA, scleroderma, vasculitis, SLE
exam - fine crackles during mid-late inspiration, clubbing
CXR - reticular or nodular opacities
- HRCT - fibrosis, honeycombing, traction bronchiectasis
- PFTs - normal-inc FEV1/FVC, decreased DLCO (and increased Aa gradient), decreased TLC and RV (increased elastic recoil)
- resting ABG may be normal or show mild hypoxemia - hypoxemia becomes significant with exertion (V/Q mismatch)
NOTES:
silicosis increases the risk of developing Tb
hypersensitivity pneumonitis
aka bird fancier’s lung/farmers lung - occurs due to repeated inhalation of antigen –> alveolar inflammation
acute episode - cough, breathlessness, fever, malaise 4-6hrs after exposure
chronic exposure –> pulmonary fibrosis and restrictive lung disease
- noncaseating granulomas
tx - avoid antigen exposure (will produce remission in most pts)
- for acute/severe episodes - SYSTEMIC corticosteroids speed recovery
metabolic alkalosis
disorder that produces excess bicarb (generation phase) + process that prevents renal bicarb excretion (maintenance phase)
RESPONDS to saline administration = volume depletion
- vomiting, gastric suctioning, diuretics, laxative abuse, decreased oral fluid intake
- will have generally have low urine Cl (unless pt is currently using diuretics, current diuretic use will increase urine Cl) - because RAAS is activated –> increased renal Na and Cl reabsorption, increased urinary H+ and K+ secretion
- urine Cl < 20
does NOT respond to saline administration = mineralocorticoid excess
- hyperaldosteronism, Cushing disease, ectopic ACTH production, severe hypokalemia (<2 meQ/L)
- will have hypervolemia - because of excess mineralocorticoid –> Na and volume RT…
- Cl usu > 20 (aldosterone has nothing to do with Cl reabsorption)
- Bartter and Gitelman syndromes - hypo/euvolemic
- need to treat underlying cause
AKI
PRERENAL
due to decreased renal perfusion
- true volume depletion
- decreased arterial blood volume (HF, cirrhosis)
- displacement of intravascular fluid (sepsis, pancreatitis)
- renal artery stenosis
- afferent arteriole vasoconstriction - NSAIDs
decreased GFR
- increased Cr, decreased urine output, BUN/Cr > 20, FeNa 1%, bland urine sed
- can see metabolic acidosis - this would occur in uremia
- if hypoperfusion persists –> renal ischemia –> ATN
treat with IVFs - NS
AKI - AG metabolic acidosis, hyperkalemia
A1AT
panacinar (panlobular) emphysema
- lower lobe emphysema (vs emphysema due to smoking, which would be in the upper lung lobes)
liver - asx until endstage disease
- LFTs will be normal
tx - AAT supplementation
- bronchodilators and corticosteroids as needed
RCC
triad: flank pain, hematuria, mass
- scrotal varicoceles - left-sided (gonadal vein enters renal vein on the left side, mass obstruction)
- paraneoplastic syndromes - anemia (advanced tumors) OR erythrocytosis, thrombocytosis, fever, hyperCa, cachexia
hematuria - tumor invasion into the collecting system
dx - CT abd
anion gap
Na - bicarb - Cl
normal = 8 - 12 (sometimes Uworld says 6-12)
elevated AG - means presence of non-Cl containing acids
AG metabolic acidosis
M - methanol (risk is blindness), formaldehyde
U - uremia (ESRD, impaired excretion H+)
D - dka
P - paraldehyde
I - inh, iron
L - lactic acidosis (postictal, sepsis, hypoperfusion and shock, ESLD)
E - ethylene glycol (urinary ca oxalate crystals, envelope shaped crystals)
S - salicylate
osmolar gap = measured - calculated serum osmolality
- useful when ethanol, methanol, or ethylene glycol tox is suspected
**************************************** causes of non-AG metabolic acidosis - diarrhea - RTA - fistulas - pancreatic, ileocutaneous - acetazolamide - causes decreased reabsorption of bicarb, Na, Cl - ureteral diversion (ileal loop) - iatrogenic
can calculate urine AG to distinguish between renal and intestinal bicarb losses
give bicarb if pH < 7.1
- bicarb can cause myocardial depression and increased lactic acid production - so not recommended for high pHs
sarcoidosis
asx or can present with fatigue, weight loss, cough, dyspnea, or chest pain
CXR - bilateral hilar LAD
cough
subacute - chronic (8+ wks) cough
for:
- ACEis - stop ACEi
- upper airway cough syndrome (PND, worse at night) - first gen H1 blocker
- asthma (can present with white sputum) - PFTs (alternatively, can treat with 2-4 wks of inhaled glucocorticoids (?), response suggests asthma)
- GERD - empiric PPI
- -> if no improvement after 2-3 wks above - CXR
for: parenchymal disease, purulent sputum/immunocompromised, no specific etiology
- -> straight to CXR
pleural effusions
EXUDATIVE - occurs when fluid moves into pleural space due to increased permeability of membranes
= leakage of fluid
for an exudative effusion:
- pleural protein/serum protein ratio >0.5
- pleural/serum LDH > 0.6
- pleural LDH > 2/3 ULN for serum LDH
etiologies of exudative effusion - empyema, chylothorax, malignancy, Tb (acid fast bac)
- malignant effusion - will be subacute in onset; lung, breast, and lymphoma are the 3 most common causes
TRANSUDATIVE effusions - oncotic or hydrostatic pressure differentials
1) thoracentesis –> 2) bronch if pt has lung mass and pleural fluid cytology is non-diagnostic
- if cytology shows cancer - no need for bronch
hemoptysis
most common - bronchitis, lung cancer, bronchiectasis
- bronchitis - cough (white sputum) for 3+ mo in 2 successive yrs, prominent bronchovascular markings
- bronchiectasis - chronic cough, inadequate mucus clearance, associated with recurrent respiratory tract infections, daily copious mucopurulent sputum
mitral stenosis, acute pulm edema
tb, lung abscess, bac pna, aspergillosis
coaguloapthy
PE, AV malformation
Wegners, Goodpastures
trauma, cocaine use
hyponatremia
increased water intake or decreased water excretion
px - headache, N&V, AMS
–> cerebral edema and brain herniation
risk factors for iatrogenic causes - hypotonic fluid hydration, hypoxia, CNS disorders; children, premenopausal women, elderly
- pain and morphine - associated with SIADH
A) serum osm low (<275)
1) assess volume status
a) hypovolemic –> UNa
- UNa <40 - nonrenal loss (GI, dehydration)
- UNa > 40 - renal loss (diuretics, p adrenal insufficiency)
- can give isotonic fluids to these pts for volume resus (NS, LR)
b) euvolemic –> Uosm
- <100 - psychogenic polydipsia (takes a LOT of water, eventually capacity of kidneys to excrete water becomes overwhelmed and pt develops euvolemic hyponatremia), Beer potomania
- >100 (and UNa >40) - SIADH (rule out hypothyroidism, secondary adrenal insufficiency)
c) hypervolemia - CHF, hepatic failure, nephrotic syndrome
B) serum osm nl-high
- urine findings will be variable (so dont carE)
- nl - pseudohyponatremia (due to proteins, lipids)
- high (>295) - hyperglycemia, mannitol
serum osm = 2*Na + glu/18 + BUN/2.8
SPECIFIC FEATURES:
serum osm > 290 – marked hyperglycemia, advanced renal failure
urine osm <100 - primary/psychogenic polydipsia, malnutrition (beer drinkers potomania)
urine sodium <25
- no - SIADH, adrenal insufficiency, hypothyroidism
- yes - volume depletion, CHF, cirrhosis
general tx - 3% saline, serial measurements of electrolytes
- serum sodium 6-8 meq/L in first 24hrs (or 0.5 meq/L/hr)
- if you correct too quickly - risk of osmotic demyelination (water quickly moves out of the brain –> disruption of cellular metabolic activity –> subsequent cell damage)
SIADH (euvolemic hyponatremia) - small cell lung cancer/pneumonia, carbamazepine, cyclophosphamide, SSRIs, CNS disturbance, pain/nausea
- euvolemic - so urine Na will be elevated (>40 meq/L), urine will be concentrated
- also low serum uric acid, serum K is normal, normal acid-base status
- risk is cerebral edema
- tx - fluid restriction and salt tablets for mild symptoms
–> 3% saline for severe hyponatremia - less than 8 meq/L increase over first 24hrs (note - need fluid infusion to be greater than urine osm)
–> NS (0.9%) = 300 mosm/kg H2O
if a pt with multiple comorbidities dies in the next year, what will he die of?
1) CVD - general population and esp in dialysis pts
- ESRD is an independent risk factor for CVD
reactive airway disease
airway inflammation and bronchospasm –> wheezing or cough
uremia
signs/sxs typically develop at BUN of >100
but BUN level is not used to dx - signs/sxs are used to dx
uremic encephalopathy is indication for urgent HD (lactulose is used to treat hepatic encephalopathy)
uremic coagulopathy
- plt dysfunction, bleeding time prolonged, aPTT and PT will be normal
- ecchymoses, epistaxis, more severe complications can occur (but dont occur as often due to advent of dialysis)
note - GI bleed can cause elevated BUN
- metabolism of blood proteins –> urea
bronchiectasis
infection + impaired bacterial clearance
- causes - CF (pseudomonas infection, upper lung lobe involvement), A1AT (lower lobe emphysema), airway obstruction (cancer), rheumatic disease (RA, Sjogren), toxic inhalation, chronic prior infection (aspergillosis, mycobacteria), immunodeficiency (hypogammaglobulinemia)
dyspnea, cough, rhinosinusitis, hemoptypsis, crackles, wheezing
- obstructive lung disease
airway thickening - tram-track and ring signs on CXR
evaluation
- initial dx - HRCT scan chest
- Ig quantification
- test for CF and sputum culture
- PFTs
IgA nephropathy v.s. PSGN
preceding URI
IgA nephropathy
- usu within 5d of URI, more common in young adult men
- recurrent gross hematuria
- NL serum complements
- bx - mesangial IgA deposits
- benign, possible RPGN or nephrotic syndrome
PSGN - delayed
- 10-21 d after URI, more common in kids, adults can be asymptomatic or develop acute nephritic syndrome
- gross hematuria
- LOW C3, elevated anti-streptolysin O/anti-DNAse B
- bx - subepithelial humps (C3 complement)
- good prognosis, possible CKD in adults
bladder cancer
painless hematuria
RFs - age, cigarette smoking, exposure to industrial chemicals, cyclophosphamide, FHx
USPSTF recommends against screening for bladder cancer due to low incidence and poor PPV of current screening tests
pneumonia
- CAP
- atypicals
- aspiration
- other
- recurrent pnas
CAP - majority bacterial, viral, fungal
- orgs - S pneumo, H flu, Legionella, M pneumo
- physical exam has <50% sensitivity - if you suspect, get CXR (dx requires CXR with infiltrate)
- flu - would present with fever and URI sxs
- CURB-65- 65+, confusion, BUN > 20, RR > 30, BP < 90/60 (0 outpatient, 1-4 floor, >4 ICU)
- outpatient, healthy - macrolide or doxy
- inpatient floor - cef + azithro or FQ
- inpatient ICU - cef + azitrho or cef + FQ
- high risk pts should be discharged with flu and pneumococcal vaccinations
ATYPICALS
- Mycoplasma pna - cold agglutinins (though these are not used for dx)
ASPIRATION
predisposing conditions
- altered consciousness impairing cough reflex (dementia, drug intoxication), dysphagia (stroke, neurodegen), GERD
- NG, ET tubes
- protracted vomiting
- large-volume tube feeds in recumbent position
occurs days after aspiration event
location - posterior segments of R upper lobes and superior segments of lower lobes
tx - anaerobic (oropharyngeal bac) coverage = clinda, augmentin
compare to pneumonitis - which is due to direct lung injury from gastric acid and will present few hours after event
- supportive tx
OTHER eosinophilic PNA - gradual onset - pts will present with asthma-like sxs - exam - diffuse wheezes and inspiratory crackles - peripheral eosinophilia
PCP - CD4 < 200
cryptogenic organizing PNA - bilateral ground glass infiltrates
OTHER FEATURES:
in PNA - there is V/Q mismatch
- in consolidative process - shunting occurs (V = 0, alveoli are filled with inflammatory exudate but are still perfused), increasing FiO2 will NOT correct hypoxemia
after a single episode of PNA - in pts >50, get CXR in 6-12 wks to assess for malignancy
parapneumonic effusion
- exudative effusions (require more investigation than transudative) - protein ratio > 0.5, LDH ratio > 0.6, LDH >2/3 ULN
- if you have low glucose in an effusion - means there is a high level of bacteria/leukocytes (RA, empyema, malignancy, TB, lupus, esophageal rupture)
- sterile exudate in the setting of pna - glucose >60, WBC < 50K, tx with abx
- bacterial invasion of pleural space - glucose < 60, WBC >50L, negative gram stain and culture (due to low bacterial counts), abx and drain
- empyema - will have pos gram stain and culture, abx and drainage
RECURRENT
same region of lung:
- local airway obstruction - extrinsic bronchial compression (neoplasm, adenopathy), instrinsic bronchial compression (foreign body, bronchiectasis)
- recurrent aspiration - seizures, alcohol/drug use, GERD, dysphagia
different region of lung: due to immunodeficiency, sinopulmonary disease, non-infectious (vasculitis, BOOP)
work-up: 1) CT, 2) bronch and bx
OSA/OSH
restrictive lung disease patterns
OSA
- daytime sleepiness, impaired concentration, and morning headaches, sexual dysfunction
- relaxation of pharyngeal muscles –> closure of airway - factors are tonsillar hypertrophy, excessive soft tissue, short mandible
- loud snoring with periods of apnea
- sequela include systemic HTN (which will improve with tx of OSA), pulm HTN, and RHF
- dx - get nocturnal polysomnography
- -> apnea - cessation of breathing >10 sec
- -> hypopnea - drop in SaO2 by >4%
- -> 5 events are diagnostic - note - PFTs will NOT aid in dx because the obstruction is transient
OSH - fatigue, DOE in pts with morbid obesity
- BMI > 30
- chronic (daytime and nighttime) hypoxia and hypercapnia –> increased bicarb RT (and Cl excretion) –> decreased ventilatory response to increased CO2… (cant breathe, wont breathe)
- chronic hypoxia –> pulm HTN and cor pulmonale (because lung vasculature constricts when there is low O2 tension, hypoxic vasoconstriction)
- work-up includes TSH, sleep study
- tx - PPV (first-line), weight loss, avoidance of sedative meds, respiratory stimulants (acetazolamide, last resort)
ASA OD
tinnitus, fever, tachypnea, GI upset
1) respiratory alkalosis - stimulates the respiratory center in the medulla
2) AG metabolic acidosis
- increased production and decreased renal excretion
- uncouples oxidative phosphorylation - lactic acidosis, low bicarb
- Winter’s formula for resp compensation of met acidosis: PaCO2 = 1.5*HCO3 + 8 +/- 2
end result - pH is usu in normal range
- start tx early - because pt will reach a point where acidosis»_space; ability to blow off CO2
note - if pt only had metabolic acidosis and appropriate resp compensation –> pH would be acidic (compensatory processes dont perfectly correct the pH to normal)
benign recurrent hematuria
thin basement nephropathy - familial, isolated microscopic hematuria
V/Q mismatch
PE, PNA, pulm edema
hypoxemia with elevated A-a gradient
dead space - ventilated but not perfused
ESRD
5-yr survival of non-diabetics on dialysis - 30-40%
- 20% in diabetics
renal artery stenosis
renovascular HTN should be treated with ACEis or ARBs (+ additional agents prn)
unilateral renal artery stenosis
- ACEI –> dilates the glomerular efferent arterioles
- no rise in Cr
bilateral renal artery stenosis - fall in GFR –> rise in Cr (acceptable is <30%)
- ACEIs are sometimes contraindicated but can still be used with close renal function monitoring - due to their long term renoprotective effects
revascularization - has NOT been proven superior to medical managment
- reserved for pts refractory to medical therapy, HF, or recurrent flash pulmonary edema
rhabdomyolysis
risk factors - immobilization, cocaine abuse (vasoconstriction –> diffuse ischemia, seizures, hyperpyrexia, toxic effect on myocytes)
causes ATN - due to excessive filtered myoglobin
other hint - urine dipstick positive for blood but no blood on microscopy
tc - aggressive hydration, mannitol, urine alkalinization
asthma
intermittent asthma - albuterol prn
- attacks <2d/wk and nighttime awakenings <2x/mo
persistent asthma - treated based on mild-mod-severe
- frequency of daytime sxs and nighttime awakenings
- albuterol prn AND
1) low dose ICS (beclomethasone, fluticasone)
2) low dose ICS + LABA (salmeterol), or medium dose ICS or theophylline (PDEi)
3) medium-dose ICS + LABA
4) high dose ICS + LABA (add omalizumab for pts with allergies)
5) high dose ICS + LABA + short course oral corticosteroid (add omalizumab for pts with allergies) - summary - start with ICS, add LABA, for most severe disease add oral corticosteroids
- high dose ICS for long times can cause the same systemic effects as oral corticosteroids
patients whose condition is well controlled for 3 mo should be considered for step-down
asthma exacerbation
- trigger - viral infection (will have leukocytosis due to stress and not infection)
- decreased breath sounds, prolonged expiration, diffuse wheezing, lung hyperinflation
- mild-mod - inhaled SABAs (reverses airflow obstruction) –> may need to escalate to systemic corticosteroids
- severe asthma exacerbations - SABA + ipratroprium (potentiates bronchodilation) + systemic corticosteroids –> give 1x mag sulfate if pt shows no improvement
- increased respiratory drive and hyperventilation - when you seen a nl-elevated PaCO2 –> that means that pt has respiratory muscle fatigue and is unable to blow off the necessary CO2
- signs of impending resp failure - elevated PaCO2, decreased breath sounds, absent wheezing, decreased MS, hypoxia with cyanosis –> intubate
- severe hypoxemia (PaO2 < 60) - rare in acute asthma exacerbation
ASA-exacerbated asthma - cough, asthma, refractory chronic rhinosinusitis and nasal polyposis in a pt with NSAID use
- termed a pseudo-allergic reaction to NSAIDs
- another sign - facial flushing within 30 min-3hrs after NSAID ingestion
- briefly: ASA and NSAIDs block COX1 and 2 (blocks production of pro and anti-inflammatory PGs), shunts metabolites to LOX and LT pathway (LTS are all pro-inflammatory)
- tx - manage underlying asthma and chronic rhinosinusitis, avoid NSAIDs, LT inhibitors
pts can have comorbid GERD and asthma
- px - sore throat, morning hoarseness, worsening cough at night, need for albuterol inhaler after meals
- trial of PPI
LABA monotherapy has been shown to increase asthma-related mortality
inhaled cromolyn (mast cell stabilizer), zafilukast - asthma only
familial hypocalciuric hypercalcemia
AD- due to mutation of Ca-sensing receptor
- highER calcium concentrations are required to suppress PTH release
- increased reabsorption of Ca in renal tubules
asymptomatic hypercalcemia
- high-nl PTH
- low urine Ca
v.s. primary hyperparathyroidism - which will also have high PTH, but urine Ca will also be high
ankylosing spondylitis
other sxs - enthesitis (pain over bony prominences), acute anterior uveitis (unilateral), IBD, aortic regurg
restrictive PFTs
- FRC and RV are nl/increased due to fixed rib cage
- if there is overlying pulmonary fibrosis - FRC, LC, and RV are reduced
chronic renal disease
broad casts - occur in dilated tubules of enlarged nephrons (undergone compensatory hypertrophy in response to reduced renal mass)
waxy casts - also in chronic renal disease
ADPKD
HTN, palpable bilateral abdominal masses, microhematuria
- NO proteinuria
note - R kidney is easier to palpate because it lies lower than the L
complications - intracranial berry aneurysms, hepatic cysts, valvular disease, colonic diverticula, abd wall and inguinal hernia
ATN
muddy brown, granular casts
BUN/Cr < 20:1, urine Na > 20 mEq/L and FeNa > 2%
causes - AGs, iodinated contrast dye, hypotension
ARDS
fever, respiratory distress, hypoxemia, bilateral opacities
associated with infections, trauma, massive transfusion, pancreatitis
- lung injury –> release of proteins, inflammatory cytokines, neutrophils into alveolar space –> alveolar collapse and diffuse alveolar damage –> shunting, increased physiologic dead space, impaired gas exchange, decreased lung compliance
- PaO2/FiO2 <300 mm Hg
- increased A-a gradient
will also have increased pulmonary arterial pressure - hypoxic vasoconstriction, destruction of lung parenchyma, and compression of vascular structures (PAP in mechanically ventilated pts)
PaO2 goal - 55-80 mm Hg (88-95%)
ways to improve low PaO2 - increase FiO2 or PEEP
- high PEEP approaches may improve mortality in pts with severe ARDS
- want FiO2 <60% - higher increases the risk of O2 tox (generation of pulmonary free radicals)
- permissive hypercapnia
- avoid overdistending alveoli (LTVV, 6 mL/kg ideal body weight) - improves mortality
note - ways to change PaCO2 is TV and RR
- increasing TV increases peak inspiratory pressure (and risk of barotrauma)
hypercalcemia
bones, groans, moans, psych overtones
pts are typically volume depleted - due to hypercalcemia-induced nephrogenic DI and decreased oral intake
severe >14, or symptomatic
- immediate - NS hydration + calcitonin (avoid loops unless pt is volume overloaded)
- long-term - bisphosphonate (onset takes 2-4 days)
moderate - 12-14
- usu no tx
asx or mild < 12 - no tx
- avoid thiazides, Li, volume depletion, and prolonged bed rest
causes
- squamous cell cancer of lung - BUT have to correct electrolyte abnormalities before contrast imaging
- MM - pancytopenia, get bone marrow bx
- hypercalcemia of malignancy gets worse with time - start on bisphosphonates
other tx
- glucocorticoids inhibit 1,25-vitamin D to be activated by mononuclear cells in lungs and LNs - can be used to treat excessive vitamin D intake, granulomatous disease, lymphomas
pulmonary contusions
intraalveolar hemorrhage –> hypoxia –> hyperventilation –> resp alkalosis
Henderson-Hasselbalch eqn
pH = pK + log(c. base/acid)
pH = 6.1 + log(bicarb/0.03*PaCO2)
renal cysts
simple - thin smooth wall, homogenous, no contrast enhancement, asx
- reassurance
- other notes - infection is rare
malignant cystic mass
- thick, irregular wall
- multilocular, septae, heterogenous
- contrast enhancement
- sxs
- f/u imaging and referral to urology
obstructive vs restrictive lung disease
obstructive
FEV1 < 80%
FEV1/FVC <70%
FVC - nl-decreased
restrictive
FEV1 > 80%
FEV1/FVC >70%
FVC < 80%
- *FEV1/FVC**
- low = obstructive disease –> get DLCO –> nl or increased in asthma, decreased in COPD
- nl-high (and low VC) = restrictive disease –> get DLCO –> normal in chest wall dysfunction (OHS, myasthenia, ALS), decreased in ILD
pos bronchodilator response (>12% in FEV1) = asthma
- this means there was complete reversibility of the obstruction with bronchodilators
- DLCO in asthma is nl-increased (severe asthma) - it is nl-low in COPD
acute urinary RT
elderly post-op pt with agitation and lower abdominal (suprapubic) tenderness
- risk factors - male, old, BPH, hx of neuro dz, surgery
- opioids, anesthetics, and anticholinergics can precipitate AIUR
1) bladder ultrasound >300 mL of urine –> foley and UA
- if you cant do bladder ultrasound –> directly to foley
mediastinal mass
anterior mediastinum - thymoma, teratoma, thyroid, thoracic aorta, terrible lymphoma
- hoarseness, horners, facial and UE edema
- get CT
middle mediastinum -
bronchogenic cyst, tracheal tumors, percardial cyst, lymphoma, LN enlargement, aortic enlargement of arch
- get CT
posterior mediastinum - neurogenic tumors (meningocele, enteric cysts, lymphoma, diaphragmatic hernias, esophageal tumors, aortic aneurysms)
- get MRI
urgent hemodialysis indications
A - acidosis <7.1 (refractory to medical therapy)
E - electrolytes
- hyperkalemia with EKG changes
- K > 6.5 refractory to medical therapy
Ingestion - toxic alcohols, salicylate, Li, sodium valproate, carbamazepine
- Li >4 OR L > 2.5 + tox sxs (seizures, depressed mental status) or inability to excrete (renal dz, decompensated HF)
O - volume overload refractory to diuretics
U - symptomatic encephalopathy, pericarditis, bleeding
- asterixis is seen in hepatic encephalopathy, uremic encephalopathy (advanced renal failure), and CO2 retention
hypernatremia
= net loss of free water
- less common than hyponatremia
- occurs in debilitated or inds with altered levels of consciousness (NM disorder pts, these pts will also have dysphagia)
sxs - lethargy, AMS, irritability, seizures, muscle cramps and weakness, decreased DTRs
- ASSESS VOLUME STATUS*
- etiologies overlap
HYPOvolemic hypernatremia
- dehydration, renal losses, GI upset, excess sweating
tx
1) isotonic (0.9% NS saline, LR) IVFs (to return Na slowly back to normal)
2) can switch to 5% dextrose preferred (or 1/2 NS) once volume deficit has been restored
- rate of correction - 0.5 meQ/L/h
- 1/2 NS and 5% dextrose are hypotonic - DONT use because they will lower Na too rapidly (risk is cerebral edema)
HYPERvolemic hypernatremia - due to exogenous Na intake and mineralocorticoid excess
- tx - 5% dextrose in water (D5W)
EUvolemic hypernatremia - DI
- complete v.s. partial - complete is urine osm < 300 mOsm/kg (often less than 100 mOsm/kg), partial is a higher urine osm
- central
- nephrogenic - hypercalcemia, severe hypokalemia, tubulointerstitial renal disease, meds (Li, demeclocycline, foscarnet, cidofovir, ampho B)
- correct with free water supplementation
hypertrophic osteoarthropathy
digital clubbing is accompanied by sudden-onset arthopathy (of hand and wrists)
but issue is in lungs - get CXR to evaluate for underlying lung disease (cancer, TB, bronchiectasis, emphysema)
associated with adenocarcinoma
cyanide tox
cause - combustion of wool or silk, metal extraction in mining, and sodium nitroprusside
CN - inhibits oxidative phosphorylation
flushing (cherry-red color), cyanosis occurs later
CNS - headache, AMS, hyperreflexia (CN accumulation)
CV - arrhythmias
Respiratory - tachypnea followed by respiratory depression, pulm edema
GI - upset
renal - metabolic acidosis (from lactic acidosis), renal failure
tx - sodium thiosulfate
mannitol
for increased intracranial pressure
crystal-induced AKI
kidney rapidly excretes drug into renal tubules but drug has low solubility in tubules
- easily precipitates in renal tubules –> intratubular obstruction –> direct renal tubular tox
causes - acyclovir, sulfonamides, methotrexate, ethylene glycol, protease inhibitors, uric acid (needle shaped crystals, tumor lysis syndrome)
px - usu asx or nonspecific sxs, AKI < 7d of starting drug
- UA will show hematuria, pyuria, crystals
- increased risk with volume depletion and CKD
d/c drug, volume repletion, loop
acute interstitial nephritis
drugs - b-lactams, cephalosporins, cipro, PPIs, sulfonamides
- usu 5d after starting drug
less commonly due to infection
occurs 7-10 d after drug exposure
- can also have skin rash (maculopapular rash), arthralgias, eosinophilia, eosinophiluria, and pyuria
d/c the offending drug
- dont give steroids because they may hasten the recovery but may aggravate the underlying infection
COPD
distant heart sounds due to hyperinflated lungs
acute exacerbation - increased dyspnea, increased cough, sputum production
- exam - wheezing, JVD during expiration (due to increased thoracic pressure)
- URI is the most common trigger, 50% of exacerbations are due to bacterial pathogen
- sputum cultures NOT recommended - difficulty isolating a single pathogen
- tx - O2 (88-92%, PaO2 60-70mm Hg), inhaled bronchodilators, systemic glucocorticoids (improves outcomes), abx (for 2+ sxs or if needing mechanical vent), oseltamivir (if flu),
–> if ventilatory failure -
try CPaP/BiPaP (preferred to intubation in mild-mod exacerbation, pts with COPD are harder to extubate, if all else fails then intubate)
- empiric abx - azithro, FQs, or augmentin for 3-7d
- roflumilast - PDEi, has anti-inflam properties, used as maintenance tx in pts with hx of COPD exacerbations
O2-induced CO2 RT in COPD
- pts with COPD are chronic CO2 retainers - have hypoxic vasoconstriction, high affinity for CO2 (Haldane effect), and increased RR
- -> hypoxic vasoconstriction = destruction of alveoli –> hypoxia and hypercapnia –> hypoxic vasoconstriction and blood flow is redirected to alveoli with better SA - when O2 is administered –> vasodilation in lungs (V/Q mismatch because dead space is being perfused), decreased CO2 uptake from tissues (due to now decreased CO2 affinity), and decreased RR –> CO2 RT
- AMS and seizures due to CO2 RT
ipratropium inhalers + b-agonists - added bronchodilator effect
LABA = maintenance therapy
decreased mortality - smoking cessation and long-term supplemental O2 therapy
Wegners
granulomatosis with angiitis
small and medium vessel vasculitis
ENT + pulm + renal insufficiency
- chronic sinusitis and otitis - ulcerations
- lower respiratory tract involvement with tracheal narrowing and ulcerations and cavitations
- active urine sediment, rapidly progressive GN
- skin - livedo reticularis, non-healing ulcers
- systemic sxs
dx - first ANCA (this is a serum autoantibody, c-ANCA is usu pos)
- HIV can increase the chance of getting a false positive ANCA - test for HIV first
- confirm with bx - skin (leukocytoclastic vasculitis), kidney (pauci-immune GN), lung (granulomatous vasculitits)
tx - corticosteroids and immunomodulators (MTX, cyclophosphamide)
what is the target blood glucose level for acutely ill pts
140-180 mg/dL (in practice, it is below 180)
SSI
lung cancer
solitary nodule - <3cm nodule, no associated LN enlargement
- most incidentally discovered SPN are benign
- high risk features - age, size, smoking cessation and quit date, irregular contour
- 1) usu found on CXR –> 2) look for previous CXR and stability –> if no previous imaging or growth –> CT –> work-up accordingly
high malignancy risk - surgical excision
low-intermediate risk - proceed by nodule size
- greater than 8 mm –> FDG-PET or bx –> excise if suspicious for malignancy or serial CTs if not suspicious
- less than 5-8 mm - serial CTs
- less than 4mm and low malignancy risk - no follow-up
infectious granulomas are responsible for the majority of benign solitary pulm nodules - BUT important to rule out cancer
if nodule has been stable over 2-3 yrs –> reassurance, no further work-up
- nodule with ground-glass appearance - more likely to be malignant, repeat assessment annually
small cell - rapid growth, will present with metastatic disease
- SIADH, ACTH production
squamous cell - hypercalcemia
- vs sarcoid - bilar LAD, erythema nodosum
bronchogenic carcinoma - asbestos exposure
- asbestos = pleural plaques
- bronchogenic carcinoma more common than pleural mesothelioma
- bronchogenic carcinoma and asbestosis can present similarly - progressive dyspnea, bibasilar, end-inspiratory crackles, clubbing
- -> asbestosis presents 20-30yrs after the exposure, honeycombing, bilateral pleural thickening
pancoast tumor - squamous cell, lung adeno
- inferior brachial plexus involvement - ulnar nerve dist
- Horners (sympathetic chain, hoarseness, SVC, weight loss
multiple nodules - mets
lower urinary tract sxs
initial eval - UA, PSA
- get Cr if patient has significant sxs or additional risk factors - hypertension, diabetes
acutely elevated Cr –> renal ultrasound to assess for obstruction
- cath pts with hydronephrosis
peripheral edema
increased capillary hydrostatic pressure
- heart failure
- primary renal Na retention - renal disease (acute nephritic syndrome) and drugs
- venous obstruction - cirrhosis, venous insufficiency
with renal disease:
primary glomerular damage –> decreased GFR –> volume overload –> fluid RT and increased BP
decreased capillary oncotic P
- protein loss - nephrotic syndrome, protein-losing enteropathy
- decreased albumin synthesis - cirrhosis, malnutrition
increased capillary permeability
- burns, trauma, sepsis
- allergic reactions
- ARDS
- malignant ascites
lymphatic obstruction/increased interstitial oncotic pressure - malignant ascites, hypothyroidism, LN dissection
primary adrenal insufficiency
causes - autoimmune, infections (Tb, HIV, disseminated fungal), hemorrhagic infarct, metastatic cancer (lung), granulomatous disease
acute - shock, N&V
- hypoNa, hyperKa, hyperCa, normal AG acidosis (H + retention)
- eosinophilia
chronic
- fatigue, weakness, anorexia and weight loss
- GI sxs
- hyperpigmentation or vitilgo
- hypotension, hyponatremia, hyperkalemia, normal AG acidosis, hyperCa
- anemia, eosinophilia
dx - measure ACTH and serum cortisol with high dose ACTH stim test
- primary adrenal insufficiency
- secondary - brain issue
NPPV vs intubation
indications - COPD exacerbation, cardiogenic pulm edema, acute respiratory failure, to facilitate early extubation
contraindications
- medically unstable - CP arrest, pH < 7.10, ARDS, non-respiratory organ failure
- inability to protect airway - uncooperative or agitate, inability to clear secretions/high aspiration risk
- mechanical issues - recent esophageal anastomosis, facial or neuro surg/trauma, upper airway obstruction
drug-induced lupus
hydralazine, procainamide, isoniazid
anti-histone abx are sensitive
hepatorenal syndrome
cause - pts with cirrhosis and ESLD develop splanchnic arterial dilation and decrease in vascular resistance (due to portal HTN)
–> RAAS –> renal vasoconstriction, decreased perfusion, and GFR
risk factors - advanced cirrhosis with portal HTN and edema
precipitating factors
- most common causes - GI bleed, SBP
- reduced renal perfusion, vomiting, sepsis, excessive diuretic use
- reduced glomerular pressure and GFR - NSAID use (constricts afferent arterioles)
dx
- renal hypoperfusion
- FeNA < 1% (or urine Na < 10 mEq/L)
- no tubular injury, RBCs, protein, or casts in urine
- no improvement in renal function with fluids
tx - hepatic recovery
- splanchnic vasoconstrictors (midodrine, octreotide, norepi) and albumin can be used in the interim
- dialysis is of limited benefit - but may be used as a bridge to liver transplantation
- note - pts who are unlikely to have a quick recovery will not be candidates for liver transplant
theophylline
tox - theophylline has narrow therapeutic index
- metabolized by liver - affected by liver disease or drugs (abx like cipro)
- CNS stimulation (headache, insomnia, seizures), GI upset, arrhythmias
tumor lysis syndrome
severe electrolyte abnormalities
- elevated phos, K, and uric acid (released from lysed cells)
- decreased Ca - because phosphate binds Ca
AKI - due to uric acid/Ca- phosphate
px - N&V, muscle cramps, seizures, tetany
tx - continuous tele (risk of arrhythmias)
- aggressive electrolyte monitoring/tx
ppx - IV fluids, allopurinol
airway pressures
peak airway pressure = resistive pressure + plateau pressure
- plateau pressure = elastic pressure + PEEP
increases in resistive pressure can occur due to - bronchospasm, mucus plug, ET obstruction
decreased pulm compliance - pulm edema, atelectasis, PNA, right mainstem intubation, atelectasis, pneumothorax
intrinsic or auto PEEP
- normally end-expiratory pressure should be = Patm
- in pts with COPD, alveoli cant empty completely so there will be an “auto PEEP”
bronchiolitis obliterans
obstructive lung disease - progressive narrowing of medium and small bronchioles
wheezing
