Renal/Pulm/Acid-Base Flashcards

Question 1

Q

cor pulmonale

Answer

A

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

Question 2

Q

glomerulonephritis

Answer

A

PSGN - low serum C3

rapidly progressive glomerulonephritis
- crescent formation

idiopathic crescentic glomerulonephritis
- cell-mediated injury

lupus nephritis

Question 3

Q

acid-base disorders

Answer

A

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

Question 4

Q

non-cardiogenic pulm edema

Answer

A

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

Question 5

Q

acute cystitis and pyelonephritis in non-pregnant women

Answer

A

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

Question 6

Q

when would you give Na bicarb

Answer

A

salicylate tox, TCADs, metabolic acidosis (renal failure), hyperkalemia

Question 7

Q

anaphylaxis

Answer

A

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)

Question 8

Q

aspergillosis

Answer

A

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

Question 9

Q

airway obstruction

Answer

A

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)

Question 10

Q

interstitial cystitis

Answer

A

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

Question 11

Q

Goodpastures

Answer

A

anti-GBM abx, linear IgG deposition on IF

rapidly progressive GN or alveolar hemorrhage

Question 12

Q

mixed cryoglobulinemia

Answer

A

palpable purpura, proteinuria, hematuria

non-specific sxs - arthralgias, HSM, hypocomplementemia
membranoproliferative

circulating cryoglobulins

most pts will have underlying HCV infection - test for HCV antibodies

Question 13

Q

rhinitis

Answer

A

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

Question 14

Q

pulm auscultation findings

Answer

A

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

Question 15

Q

lupus

Answer

A

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

Question 16

Q

urinary incontinence in women

Answer

A

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

Question 17

Q

diuretics

Answer

A

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

Question 18

Q

hypovolemic hyponatremia and RAAS

Answer

A

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)

Question 19

Q

renal transplant

Answer

A

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

Question 20

Q

exercise-induced bronchoconstriction

Answer

A

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

Question 21

Q

electrolyte wasting

Answer

A

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

Question 22

Q

urinary incontinence in elderly

Answer

A

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

Question 23

Q

nephrotic syndrome

- 6 causes

Answer

A

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

Question 24

Q

alcohol withdrawal

Answer

A

agitation, tachy, HTN, mental status changes

Question 25

Q

urine dip

Answer

A

can only detect macroalbuminuria >300 mg/24hrs

Question 26

Q

nephrolithiasis

Answer

A

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

Question 27

Q

thiazide

Answer

A

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

Question 28

Q

acute oliguria

Answer

A

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

Question 29

Q

analgesic nephropathy

Answer

A

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

Question 30

Q

glomerular vs nonglomerular hematuria

Answer

A

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)

Question 31

Q

hyperkalemia

Answer

A

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

Question 32

Q

HTN and kidneys

Answer

A

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

Question 33

Q

diabetic autonomic neuropathy

Answer

A

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

Question 34

Q

hypokalemia

Answer

A

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

Question 35

Q

pulmonary embolism

Answer

A

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)

Question 36

Q

RTA

Answer

A

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

Question 37

Q

unilateral obstructive uropathy

Answer

A

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

Question 38

Q

ADH and aldosterone

Answer

A

ADH secreted with high serum osm and hypovolemia

aldosterone escape - escape from sodium-retaining effects of excess aldosterone
- by volume and/or pressure natriuresis

Question 39

Q

acute bronchitis

Answer

A

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

Question 40

Q

DLCO

Answer

A

low - anemia, PE, pulm HTN

high - pulm hemorrhage, polycythemia

nl - bronchitis, asthma, MSK disease

Question 41

Q

ILD

Answer

A

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

Question 42

Q

hypersensitivity pneumonitis

Answer

A

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

Question 43

Q

metabolic alkalosis

Answer

A

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

Question 44

Q

AKI

Answer

A

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

Question 45

Q

A1AT

Answer

A

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

Question 46

Q

RCC

Answer

A

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

Question 47

Q

anion gap

Answer

A

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

Question 48

Q

sarcoidosis

Answer

A

asx or can present with fatigue, weight loss, cough, dyspnea, or chest pain

CXR - bilateral hilar LAD

Question 49

Q

cough

Answer

A

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

Question 50

Q

pleural effusions

Answer

A

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

Question 51

Q

hemoptysis

Answer

A

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

Question 52

Q

hyponatremia

Answer

A

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

Question 53

Q

if a pt with multiple comorbidities dies in the next year, what will he die of?

Answer

A

1) CVD - general population and esp in dialysis pts

- ESRD is an independent risk factor for CVD

Question 54

Q

reactive airway disease

Answer

A

airway inflammation and bronchospasm –> wheezing or cough

Question 55

Q

uremia

Answer

A

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

Question 56

Q

bronchiectasis

Answer

A

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

Question 57

Q

IgA nephropathy v.s. PSGN

Answer

A

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

Question 58

Q

bladder cancer

Answer

A

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

Question 59

Q

pneumonia

CAP
atypicals
aspiration
other
recurrent pnas

Answer

A

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

Question 60

Q

OSA/OSH

Answer

A

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)

Question 61

Q

ASA OD

Answer

A

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&raquo_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)

Question 62

Q

benign recurrent hematuria

Answer

A

thin basement nephropathy - familial, isolated microscopic hematuria

Question 63

Q

V/Q mismatch

Answer

A

PE, PNA, pulm edema

hypoxemia with elevated A-a gradient

dead space - ventilated but not perfused

Question 64

Q

ESRD

Answer

A

5-yr survival of non-diabetics on dialysis - 30-40%

- 20% in diabetics

Answer 65

A

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

Answer 66

A

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

Answer 67

A

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

Answer 68

A

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

Answer 69

A

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

Answer 70

A

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

Answer 71

A

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

Answer 72

A

muddy brown, granular casts

BUN/Cr < 20:1, urine Na > 20 mEq/L and FeNa > 2%

causes - AGs, iodinated contrast dye, hypotension

Answer 73

A

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)

Answer 74

A

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

Answer 75

A

intraalveolar hemorrhage –> hypoxia –> hyperventilation –> resp alkalosis

Answer 76

A

pH = pK + log(c. base/acid)

pH = 6.1 + log(bicarb/0.03*PaCO2)

Answer 77

A

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

Answer 78

A

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

Answer 79

A

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

Answer 80

A

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

Answer 81

A

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

Answer 82

A

= 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

Answer 83

A

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

Answer 84

A

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

Answer 85

A

for increased intracranial pressure

Answer 86

A

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

Answer 87

A

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

Answer 88

A

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

Answer 89

A

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)

Answer 90

A

140-180 mg/dL (in practice, it is below 180)

SSI

Answer 91

A

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

Answer 92

A

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

Answer 93

A

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

Answer 94

A

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

Answer 95

A

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

Answer 96

A

hydralazine, procainamide, isoniazid

anti-histone abx are sensitive

Answer 97

A

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

Answer 98

A

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

Answer 99

A

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

Answer 100

A

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”

Answer 101

A

obstructive lung disease - progressive narrowing of medium and small bronchioles

wheezing

Brainscape's Knowledge GenomeTM

Renal/Pulm/Acid-Base Flashcards

Brainscape's Knowledge Genome^TM