AR HY review Flashcards
pH and CO2 deviate in the same direction (both up or both down) in which type of disorders?
metabolic acid/base disorders
pH and CO2 deviate in the opposite direction in which type of acid base disorders?
Respiratory acid base disorders
pH and CO2 both elevated seen in what type of disorder?
metabolic alkalosis
pH up and CO2 down in what type of disorder?
respiratory alkalosis (hyperventilation)
pH and CO2 both down in what type of disorders?
metabolic acidosis
pH down and CO2 up in what type of disorders?
respiratory acidosis (hypoventilation/CO2 retention)
Normal pH values
7.38-7.44
Normal blood gas CO2 levels
38-42
Normal serum bicarb levels:
23-28
24 is the value used to calculate delta bicarb (24 - delta gap)
- anion gap formula
- normal anion gap range
- Na - (Cl + HCO3)
- 7-13 (delta gap nl is 12
- urine anion gap formula
- UAG results interpretation
- (urine Na + urine K) - urine Cl
- positive = positively the kidneys causing acidosis
- negative = neGUTive, i.e. gut is causing acidosis
Things that cause decreased anion gap
excess proteins (e.g multiple myeloma)
proteins are usually negatively charged
Bartter syndrome features
- pH
- salt and water
- BP
- serum K+ level
- serum Cl- level
- serum Mg++
- Metabolic alkalosis (HCO3 high)
- salt (NaCl) and water loss
- BP: nl/low
- K: low serum (K loss in urine)
- Cl: low serum (Cl loss in urine)
- Mg: normal
Gitelman syndrome
- pH
- salt and water
- BP
- K+
- Mg+
Gitelman: most common inherited salt wasting disorder
- metabolic alkalosis (HCO3 high)
- salt (NaCl) and water wasting
- BP: nl/low
- K: low serum (K wasting in urine)
- Mg: low (wasting in urine)
Liddle syndrome
- pH
- salt and water
- BP
- K
- aldosterone
Liddle syndrome
- pH: metabolic alkalosis (HCO3 high)
- salt (NaCl) and water retention
- BP high (usually early onset
- K: low (urinary wasting)
- aldosterone: low (pseudohyperaldosteronism: ie BP high and K low like in high aldo; but aldo is low in reality)
Common causes of metabolic alkalosis
- volume depletion or diuretics (MCC)
- vomiting/NGT suction
- Hyperaldosteronism
- Cushing (hypercortisol)
- Licorice
- Bartter/Gitelman/Liddle
Common causes of NAGMA
- RTA
- diarrhea
- aggressive saline repletion
- early CKD
- ureterosigmoidostomy
AGMA with calcium oxalate crystals:
- likely ingestion
- complication
- Rx
- Ethylene glycol (glycolic acid/antifreeze)
- ATN (crystal induced)
- supportive care if sml osmolar gap, fomepizole for large gap or severe disease
ASA toxicity acid base response
early respiratory alkalosis (primary) followed by metabolic acidosis (secondary)
don’t forget tinnitus/hearing loss
Types of acidosis in DM patients and etiology
- AGMA = DKA
- NAGMA = RTA IV (hypoaldosteronism)
Cirrhotic patient: common acid base disturbance?
Respiratory alkalosis (often compensated with nearly nl pH)
d/t hyperventilation for unknown reasons
RTA type II
- location
- K
- stones
- etio
RTA type II
- proximal; HCO3+ resorption defect
- K: low/nl
- stones: maybe probably not
- etio: MM, topiramate, acetazolamide
RTA type I
- location
- K
- stones
- etio
RTA type I
- distal (collecting duct); H+ excretion defect
- K: low/nl
- stone: yes
- etio: SLE, Sjogren, amphotericin B, obstruction
RTA type IV
- location
- K
- stones
- etio
RTA type IV
- DCT, aldo deficiency or resistance
- K: high
- stones: no
- etio: DM or hypoaldosteronism
SIADH serum and urine trends
serum: LOW, urine: HIGH
serum: Na and Osm are low
urine: Na (>20) and Osm (usu > serum Osm) are high
Diabetes insipidus: types (2), DDAVP responsiveness, and lab trends
- Central DI: responsive to DDAVP, Na high/nl, urine Osm very low (<100), goes to > 300 with DDAVP
- Nephrogenic DI: not responsive to DDAVP, Na high/nl, urine Osm very low (<100) and stays that wasy after DDAVP
Psychogenic polydipsia/Beer potomania
lab trends and response to treatment
- Serum Na low
- Urine Na low (<20)
- Urine Osm low
- responds to water deprivation: urine Osm goes from < 100 to > 300
Too rapid of correction of chronic hyponatremia leads to what?
osmotic demyelination syndrom
sx: AMS, slurring speech, reguritating food, memory impairment
jockey/bodybuilder/runner: serum K is low: etio?
Diuretic abuse. Serum K is low, urine K is high (>20)
Hematuria with blood clots
likely bladder origin of pathology; get CT urography and urology consult
microscopic hematuria: benign etiologies
UA, fever, exercise, woman during menses, acute (minor) trauma
Hematuria: signs of glomerular etio:
- RBC casts
- dysmorpic RBCs
- elevated Cr
- HTN
- Edema
- low albumin
Microscopic hematuria: risk factors for serious etio
- >35 yo
- smoking
- exposure to benzene
- exposure to cyclophosphamide (alkylating agents)
- heavy non-narcotic analgesic use
- hx urologic disorder or dx (BPH, nephrolithiasis)
- recurrent UTIs
50y M routine physical, UA has 5 RBCs, no casts, no clots. wtd
repeat UA in 6 weeks
50y M routine physical, 5 RBCs persistently on multiple UAs, no casts, no clots. wtd
CT urography
(he is over 35 yo)
if CT is negative, refer for cystoscopy; if there are casts refer to nephro for renal bx
42y F with dysuria, post-void dribbling, and dyspareunia. dx?
urethral diverticulum
Nephrolithiasis
- recurr UTIs: a/w?
- prior malignancies/gout: a/w?
- malabsorbtion (IBC, CF, short gut): a/w?
- UTI: struvite stones
- malignancy/gout: uric acid stones
- malabsorption: calcium oxalate stones
Nephrolithiasis stone shapes
- cystine stones
- calcium oxalate
- struvite (Mg ammonium phosphate) stones
- uric acid stones
- acyclovir
- cystine: hexagon shape
- calcium: square envelope, or rods/dumbells
- struvite: coffin lids, staghorn
- uric acid: elongated hexagon
- acyclovir: needle shaped
Nephrolithiasis
- rx for small
- rx for large
- prevention
- Rx small (abt 5mm) should pass on own; increase fluid intake, tamsulosin
- Rx large (>10mm) require intervention
- Prevention: fluid intake, low Na diet (calcium stones), HCTZ, low meat diet, allopurinol (for uric acid stones)
Best way to decrease urinary calcium levels and prevent Ca oxalate stones?
HCTZ
low dietary calcium seems to have no benefit
35y M gross hematuria, hx of cough, fever, congestion, a week ago. Wears a hearing aid and has fam hx of hematuria. Cr 1.9, WBC normal. dx and path?
Alport syndrome; collage IV abnormality
Glomerular (nephrotic) diseases: 4 types
- minimal change
- FSGS focal segmental glomerular sclerosis
- MN membranous nephropathy
- MPGN membroproliferative nephropathy
Nephrotic syndrome features
- proteinuria: >3g/day
- hypoalbumiemia: causes edema
- loss of ATIII: thrombosis and PE
- hyperlipidemia and hyperlipiduria (fat bodies/casts in urine)
Nephrotic syndrome a/w low complement
membranoproliferative GN
FSGS etio and epidemiology
- African american
- HIV
- heroin
- sickle cell
Minimal change disease etio and epidemiology
- is mcc of nephrotic syndrome
- leukemia/lymphoma
- NSAIDS
- lithium
MPGN etio
- Hep B, Hep C
- cryoglobulinemia
- SLE, Sjogren
- syphilis
Nephrotic syndromes rx and out look
- MC: steroids, usually resolves
- MN: steroids, ⅓ get better, ⅓ same, ⅓ get worse
- FSGS: wt loss, HAART, steroids, 50% ESRD 5y
- MPGN: steroids, 50% ESRD or die in 5y
Systemic dz that causes nephrotic syndromes
- Diabetic nephropathy: usu co-occuring retinopathy
- Multiple myeloma
- Amyloidosis: Congo red dye: apple green with polarization
Conditions with low serum complement
- PSGN
- MPGN/cryoglobulinemia/Hep C
- SLE
- subacute bacterial endocarditis
- athreroembolism
Nephritic syndromes: HTN and hematuria
- PSGN
- IgA nephropathy
- RPGN
- Henoch-Schonlein/IgA vasculitis
PSGN vs IgA neprhitis
- PSGN: low complement (C3), and 1-3 weeks post URI
- IgA: nl complement, and < 1 week post URI
Young patient, palpable rash, arthralgia, GI symptoms. dx
Henoch-Schonlein/IgA vasculitis
supportive care to Rx
a/w linear IgG deposits
RPGN
The 4 pulmonary renal syndromes and features
- GPA: cANCA anti-PR3, URI involvement (otitis)
- eGPA: asthma, eosinophilia
- MPA Microscopic polyangiitis: pANCA anti-MPO no granulomas, less respiratory dz
- anti-GBM dz (Goodpasture): lower pulm dz, alveolar hemorrhage
Rx for the 4 pulm-renal syndrome
- GPA, eGPA, MP, and antiGBM
- rx steroids and cyclophosphamide, plasmapheresis for serious pulmonary hemorrhage
Large vessel vasculitis types (3)
- Takayasu arteritis
- GCA/temporal arteritis
- Behcet syndrome
- all have normal complement
- all may have prominent systemic symptoms
Medium vessel vasculitis types (2)
- PAN (testes pain is classic for)
- Behcet syndrome
- all have normal complement
- all may have prominent systemic symptoms
Small vasculitis types (7)
- MPA
- GPA
- eGPA (Churg-Strauss)
- IgA vasculitis (Henoch-Schonlein)
- Cryoglobulinemia
- a/w SLE or RA
- cutaneous leukocytoclastic angiitis
- all usu low complement and less likely systemic sx
TLS freatures vs rhabdo
- Ph > 4.5
- U > 8
- Ca < 7
- K > 6
- rhabdo has urine dipstick + for blood; TLS doesn’t
When to stop ACEi use
- > 30% incr in Cr after starting
- K > 5.5
NSAIDs and ACEi effects on kidney
- NSAIDS: constrict afferent arteriole
- ACEi: dilates efferent arteriole
ATN vs AIN: casts and etio
- ATN muddy brown casts
- ATN etio: aminoglycosides, contrast, rhabdo, TLS etc
- AIN WBC casts, peripheral eosinophils
- AIN etio: PPI, NSAIDS, abx, diuretics, phenytoin
CKD
- anemia Rx
- wtd for acidosis
- bone lesions (2nd hyperparathyroidism)
- complication of rx for #3
- anemia: EPO + iron, goal hgb 10-11
- if HCO3 < 22: give bicarb
- bones: Ca and vit D3
- adynamic bone disease likley if PTH < 100 or AlkP < 7
Post renal obstruction autodiuresis rx
Don’t replete volume lost with 1:1 ratio of IVF. Replace 50-75% of lost volume
Management of ESRD patient
- low Na, K, phos
- low water
- no calcium restriction
- no phos-based (FLEET) enema→ phos overload
ESRD pt with high Ca, phos and PTH: risk?
risk of calciphylaxis.
if Ca x phos > 70 increased risk
Pt renal insufficiency: how to increase nutritional status and slow rate of kidney decline?
keep serum bicarb > 22
Patient with short bowel syndrome: add what to diet to decrease risk of kidney stones?
calcium: added calcium decreases absorption of oxalate and helps prevent stones
Type of stone seen in RTA type I
Ca phosphate
type of stone seen in IBD or pt with hx of gastric bypass?
cystine stones
MCC recurrent nephrolithiasis?
idiopathic hypercalciuria
Lung nodule vs lung mass size
nodule < 30mm
mass > 30mm, increased risk of being malignant
Solid lung nodule < 6mm, wtd
- low risk pt
- high risk pt
Lung nodule < 6mm
- low risk: no f/u
- high risk: CT 6-12mo (smoker, female, elderly, fam hx)
Solid lung nodule 6-8mm, wtd
- low risk
- high risk
Solid lung nodule 6-8mm
- low risk: f/u 6-12mo; if no changed then again 18-24 mo
- high risk: same as above, 6-12mo then 18-24mo
High risk features of lung nodules
size > 30mm, spiculated, eccentric or low/no calcification
low risk features of lung nodules
size < 30mm, smooth border, central or popcorn calcification
Solid lung nodule > 8mm, wtd
either f/u CT in 3mo, or PET-CT, or Bx/resect
Ground glass or part solid nodule: f/u schedule
- < 6mm: no follow up for high or low ris
- 6-8mm: CT in 3-6mo for both high and low risk
FEV1 in COPD, asthma, restrictive lung diseases, bronchitis, etc
decreased in all lung diseases
FEV1/FVC abnormality in lung diseases
decreased in all obstructive diseases
normal in all restrictive lung diseases
DLCO in lung diseases
low COPD and intrathoracic restrictive dx
normal in all other obstructive and extrathoracic restrictive dz
Residual volume is low in what type of lung disease?
low in intrathoracic restrictive lung dz
high in all other lung dz
DLCO, TLC, and FEV1/FVC values in pulmonary embolism
- DLCO low
- TLC and FEV1/FVC are normal
DLCO is well above normal. Possible etiologies?
- alveolar hemorrhage
- CHF
- PDA/ASD/VSD
- polycythemia