What metabolic abnormality does diarrhea cause?
Non-anion gap metabolic acidosis due to bicarb loss in the intestine
Metabolic alkalosis with a low urine chloride (less than 20)
Typically due to ECF loss due to vomiting or NG suctioning which leads to increased renal chloride and sodium reabsorption and increased urinary H+ and K+ excretion
In contrast, current diuretic use will have high urine chloride
Both are saline – responsive
Metabolic alkalosis with high urine chloride that are saline – unresponsive
Bartter and Gitelman syndromes
If hypervolemic: access mineralocorticoid activity: primary hyperaldosteronism, Cushing disease, Ectopic ACTH production
How does obstructive uropathy present?
Flank pain, low volume void with or without occasional high-volume voids
If bilateral or if patient has one kidney can cause renal failure
In contrast interstitial nephritis presents with fever, rash, AKI, eosinophiluria with WBC casts
How to prevent uric acid stones
Hydration, alkalinize the urine with potassium citrate, allopurinol, low purine diet
In contrast, hydrochlorothiazide is used in calcium stones, decreases urinary calcium excretion
Renal changes in hypertension
Intimal thickening and luminal narrowing of renal arterioles with evidence of sclerosis, progressive decrease in renal blood flow and GFR
Renal changes in multiple myeloma
Obstruction of the distal and collecting tubules by large Laminated casts of Ben’s – Jones proteins, also, amyloid deposition and infiltration of kidneys by plasma cells
Renal changes in analgesic abuse
Typically tubulointerstitial disease: focal glomerulosclerosis
Winters formula and how to interpret
(1.5 x HCO3-) + 8 +/- 2 should equal PaCO2 if just compensating for metabolic acidosis
If lower than expected, there is a respiratory alkalosis as well, as seen in ASA toxicity
Appropriate compensation for metabolic alkalosis
Rise in PaCO2 by 0.7 mmHg for every 1 rise in serum HCO3-
acute respiratory acidosis and alkalosis compensation
Rise in HCO3 by 1 for every ^10 in PA CO2
Alkalosis: decrease in HCO3 by 2 for every 10 decrease in PaCO2
PH in aspirin toxicity
Typically within normal range, mixed respiratory alkalosis and metabolic acidosis
If it was a primary metabolic acidosis with respiratory compensation, pH would still be acidic, not in the normal range
Abnormal hemostasis in patient with chronic renal failure or is due to?
Platelet dysfunction: prolonged bleeding time but normal PT, PTT, platelet count
Treat with DDAVP: increases factor VIII: von Willebrand multimers
Others: cryoprecipitate, conjugated estrogens
Drugs associated with SIADH
What will you see on labs?
SSRIs, carbamazepine, NSAIDs
Low serum osmolality– less than 275, high urine osmolality – +100, elevated urine sodium concentration- +40
Dilute blood, inappropriately concentrated urine, patient should look euvolemic
nephrotic range proteinuria and hematuria with C3 deposits in GBM
membranoproliferative GN, type 2
persistent activation of alternative complement pathway
PSGN has C3 and IgG deposits
worsening renal function in chronic hepatitis pt, lack/minimal hematuria, RBC, protein, or granular casts, no improvement with fluids, think?
hepatorenal syndrome: cirrhotic pts develop splanchnic vasodilation and decreased SVR which activates RAAS and decreases renal perfusion
risk factors: GIB, SBP, vomiting, sepsis, diuretics, reduced GFR (NSAIDs)
tx: splanchnic constrictors: octreotide, NE, midodrine, albumin, liver transplant
Immobility, mutism, stupor, in a psych patient think?
How to treat?
Catatonia, treat with benzo’s – lorazepam, if refractory, ECT
Cauda equina versus conus medullaris syndrome
Cauda equina: LMN, saddle anesthesia, asymmetric motor weakness, hyporeflexia, LATE onset bowel/bladder dysfunction
conus medullaris: LMN/UMN (still part of the spinal cord) perianal anesthesia, symmetric motor weakness, hyperreflexia, EARLY bowel/bladder dysfunction
FAT RN, Think? How to treat?
TTP, treat with plasma exchange
Pheochromocytoma versusthyroid storm in surgical patient receiving anesthesia
Pheo: severe hypertension, tachycardia, pallor (catecho-vasoconstriction)
Thyroid storm: less acute, almost all patients will have pyrexia
Difficulty initiating swallowing, feeling of something stuck in throat, right lower lobe pneumonia, think? How to work up?
Oropharyngeal dysplasia – in contrast to esophageal dysphasia
Videofluoroscopic modified barium swallow: evaluate swelling mechanics, degree of dysfunction, severity of aspiration
If esophageal: should not cause difficulty initiating swallowing, would do motility studies and endoscopy
Characteristics of uremia
Metabolic acidosis, fluid overload, encephalopathy, hyperkalemia, pericarditis
Manifestations of renal failure besides uremia
Anemia: loss of EPO
Low calcium: kidney converts 25 to 1, 25 vit D
Osteodystrophy, secondary hyperparathyroidism, Hyperphosphatemia, hypermagnesiumia
Bleeding, infection, itching
Atherosclerosis and hypertension: MCC of death in dialysis patients is cardiac
Endocrinopathy: anovulation, low testosterone, ED
Treatment of hyperphosphatemia in ESRD
Correct calcium – corrects PTH, So less phis released from bones: calcium acetate, calcium carbonate
Phosphate binders: Sevelamer, Lanthanum
What lab values in TTP/HUS? How to treat?
Thrombocytopenia, PT and PTT are normal
Most cases of HUS will resolve, plasmapheresis if severe
plasmapheresis for TTP, it’s not a choice use FFP, steroids and platelet transfusions do not help
Polycystic kidney disease presentation and associations
MCC?
Pain, hematuria, stones, infection, hypertension
Liver cysts, ovarian cysts, MVP, diverticulosis, cerebral aneurysms
MCC of death: renal failure from recurrent episodes of pyelonephritis and nephrolithiasis
How do high glucose levels change sodium levels?
For every 100 mg/dL or a glucose above normal, there is a 1.6 mEq/L decrease in sodium
So a glucose of 500 will have a sodium that is about 8 below normal, i.e. 127 when it’s actually 135
What can cause SIADH?
Any lung or brain disease: small cell cancer
SSRIs,sulfonylureas, vincristine, cyclophosphamide, TCAs
Moderate versus severe hyponatremia presentation and treatment
Moderate: minimal confusion, NS and loop diuretic
Severe: lethargy, seizures, coma; hypertonic sailing, vaptans -ADH antagonist
Demeclocycline for chronic SIADH
In SIADH, NS without a diuretic makes it worse
What conditions have a normal anion gap metabolic acidosis? Why is the gap normal?
RTA, diarrhea, think hard ass
Gap is normal because the chloride level rises: hyperchloremic metabolic acidosis
In contrast, increase gap in ethylene glycol or methanol poisoning or lactic acidosis as these conditions are anionic and drive down the chloride level
RTA 1
Distal tubule, bicarb cannot be generated, so acid is not secreted into the tubule urine pH is above 5.5,calcium phosphate kidney stones
Amphotericin, SLE, Sjogren’s
Diagnosed with acid administration, urine will stay basic
Treat with bicarb
RTA 2
Proximal, decreased ability to reabsorbed bicarb, eventually becomes so depleted urine pH will become less then 5.5, is higher at first (variable)
Amyloidosis,MM, Fanconi syndrome, acetazolamide, heavy metals
Diagnosed with giving bicarb, kidneys can’t reabsorb and urine will get more basic
Treat with thiazide diuretics which caused volume depletion which enhances bicarb re-absorbtion
Both type 1 and 2 are hypokalemic
RTA 4
Diabetes, decreased amount/affect of Aldo, high urine sodium
Urine pH less than 5.5, hyperkalemia
Diagnosed with urinary salt loss, treat with fludrocortisone which is a steroid with mineral corticoid effects
How to distinguish between diarrhea and RTA as a cause of normal anion gap metabolic acidosis
Calculate the urine anion gap:
UAG = Na+ minus Cl-
And RTA, less Cl- is excreted as less H+ is excreted, so +UAG
And diarrhea, kidneys compensate by excreting more H+ and Cl- (Hypochloremic metabolic acidosis) so UAG is negative
Meds to help pass kidney stones
Nifedipine and tamsulosin
Kidney stone treatment bigger than 5mm
Lithotripsy less than 2-3 cm if halfway up ureter, if halfway down, basket removal
Bigger than 2 cm: surgery with stent placement
Treatment for urge incontinence
Anticholinergics: oxybutynin, tolterodine, solfenacin, dariferancin
Best initial therapy for HTN
Thiazides, CCBs, ACEs/ARBs
Best initial therapy for HTN crisis
Labetolol, nitroprusside
Then: enalapril, CCBs (diltiazem, verapamil), esmolol, hydralazine
65-year-old with pneumonia, dramatic leukocytosis, hepatosplenomegaly, cervical lymphadenopathy, think? How to diagnose?
CLL
diagnosed with flow cytometry – showing a clonality of mature B cells
Do not need LN biopsy
Acting out dreams, remember dreams think
REM sleep behavior disorder
lupus anticoagulant is paradoxical how
is actually PRO-thrombotic (misnomer)
BUT causes a paradoxically prolonged PTT +/- PT ex vivo
preferred treatment for specific phobias
behavior therapy
benzos appropriate only once in a while
eye movement desensitization and reprocessing therapy for PTSD
MCC of congenital hypothyroidism
thyroid dygenesis: aplasia, hypoplasia, ectopic gland
in contrast, defective synthesis is more rare (AR)
transplacental TSH-receptor Abs (mom has Graves) leads to hyperthyroidism
ARDS vs fluid overload/CHF
ARDS: bilateral pulmonary infiltrates with increased FiO2 requirement (<300 ratio)
fluid overload CHF will have JVD, cardiomegaly or S3
exposure and outcome measured at same time (“snapshot study”) think?
cross-sectional study
pathophys of digital clubbing
megakaryocytic skip normal fragmentation process in lung and get trapped in fingertips and release PDGF and VEGF that cause tissue hypertrophy and cap perm and vascularity
how is bronchiectasis different from bronchitis? how to dx?
recurrent infections, more sputum, bacterial (instead of viral) infection, requires abx
dx: high resolution CT
carbohydrate (lactulose, glucose) breath test used for?
bacterial overgrowth (i.e. small intestine) measures production of H+ by intestinal flora
liver vs RH failure
RHF: murmur, ^JVP, b/l peripheral edema, hepatojugular reflux
liver: ascites, splenomegaly (liver may be any size) +/- asterixis, spider agiomas, etc., +/- pleural effusion