UWorld 1 Flashcards
How does the kidney compensate for respiratory alkalosis?
The kidneys retain H ions and excrete increased amounts of bicarb in an attempt to normalize the serum pH. The increased bicarb in the urine increases urine pH
Renal transplant dysfunction in early postop period
Manifests as oliguria, HTN, and increased Cr/BUN. It can be explained by a number of causes:
1) Ureteral obstruction - renal US would show this as dilated calyces
2) Acute rejection - bx of transplant shows heavy lymphocyte infiltration and vascular involvement with swelling of the intima. Normal serum cyclosporine. Transplant feel tender. Tx is IV steroids.
3) Cyclosporine toxicity - No graft tenderness. The transplant’s function is usually restored when the dose of cyclosporine is decreased.
4) Vascular obstruction
5) Acute tubular necrosis - give IV diuretics
MRI and renal bx can be employed in conducted the ddx.
Normal acid-base status
1) pH 7.35-7.45
2) HCO3 22-28
3) PaCO2 33-45
DKA on ABG
Anion gap metabolic acidosis with low PH, low bicarb and compensatory (respiratory compensation) fall in PaCO2 due to Kussmaul breathing via chemoreceptor response (rapid, deep breathing/hyperventilation).
Typical symptoms of DKA (very brief)
Usually in type 1 DM. Polyuria, polydipsia, nausea, vomiting and abdominal pain that may mimic a surgical abdomen.
When should metformin be avoided?
Do not give to acutely ill patients with acute renal failure, liver failure or sepsis. These all increase risk of lactic acidosis.
What is one feared renal complication of cocaine overdose?
Nearly 20% of cocaine overdoses are complicated by rhabdo (marked elevations in serum CPK, high K, urine dipstick positive for blood but no RBCs on microscope - this is due to myoglobin in urine). CPK levels above 20000 is associated with acute renal tubular necrosis due to myoglobinuria.
Risk of rhabdo-induced renal failure is decreased with aggressive hydration. Mannitol and urine alkalinization may also help.
Rifampin urine changes
Rifampin causes red to orange discoloration of body fluids including urine, saliva, sweat and tears. It can also cause discoloration of soft contact lenses.
Get a UA. Absence of significant changes on UA (proteinuria, hematuria, and sterile pyuria) essentially rules out renal TB or TB-associated glomerulopathy) - remember they may have TB if they are on rifampin to begin with so the UA is just making sure there isn’t some TB complication.
First generation H1 antihistamines
Diphenhydramine, chlorpheniramine, hydroxysine. They all also have significant anticholinergic effects (at muscarinic receptors of the parasympathetic nervous system), which can manifest as dryness of eyes, dryness of the oral mucosa and respiratory passages, or urinary retention.
Urinary retention caused by anticholinergic agents results from failure of detrussor muscle contraction and (to lesser extent) impaired bladder sphincter relaxation, both of which are controlled by parasympathetic input from the pelvic splanchnic nerves.
Elderly men, who are likely to have some degree of underlying urinary obstruction due to BPH are at increased risk of developing urinary retention due to anticholinergic agents.
Most common causes of respiratory acidosis
Usually caused by respiratory suppression.
1) Narcotic OD
2) Neuro diseases causing airway muscle weakness
3) COPD
Classic causes of metabolic acidosis
MUDPILES (anion gap)
1) Methanol
2) Uremia
3) DKA
4) Paraldehyde
5) INH
6) Lactic acidosis
7) Ethylene glycol
8) Salicylates
Non-anion gap
1) Diarrhea
2) RTA
Most common causes of metabolic alkalosis
1) Vomiting
2) Hyperaldosteronism
3) Volume contraction
Common causes of respiratory alkalosis
Hyperventilation due to:
1) Pneumonia
2) High altitude
3) Salicylate intox
Brief overview of metabolic alkalosis
Causes: Saline responsive 1) Vomiting 2) Gastric suctioning 3) Diuretics 4) Laxative abuse 5) Decreased oral fluid intake (volume depletion)
Saline resistant
1) Primary hyperaldosteronism
2) Cushing’s Syndrome
3) Severe hypoK (less than 2)
Clinical presentation
1) Volume depletion - easy fatigability, postural dizziness, muscle cramps
2) HypoK - muscle weakness, arrhythmias
3) Urine Chloride - less than 20 is saline responsive. More than 20 is saline resistant.
Tx
1) Treat underlying cause to reverse generation phase in all cases
2) Saline-responsive: Also give NS to correct maintenance phase
Metabolic alkalosis pathophys
MA is due to an underlying disorder producing excess bicarb (generation phase) combined with a process preventing renal bicarb excretion (maintenance phase). MA is further classified as saline responsive or resistant. The generation phase in saline responsive form can be due to urinary or GI Hydrogen loss (diuretics, vomit) or decreased oral intake. Maintenance phase (hypovolemia) prevents the normal kidney from excreting the excess bicarb in the urine.
The kidneys perceive a decreased effective arterial blood volume from the underlying etiology (vomiting with volume depletion) and increase renin and aldosterone release. This leads to sodium reabsorption, K excretion, and H excretion. There is also decreased HCO3 excretion.
If the history cannot reveal the cause of the MA, urine Cl can help. Saline-resistant MA has excess mineralocorticoid causing H and K loss and increased Na retention leading to increased extracellular volume. The kidneys respond by excreting both Na and Cl to result in high urine Cl
Saline-responsive MA has low serum Cl due to hypovolemia and hypochloremia.
Treatment for both types focuses on the underlying cause to reverse generation and increase renal bicarbonate excretion. In saline responsive MA, saline restores arterial volume, corrects hypochloremia and increases urinary bicarb excretion
Membranoproliferative glomerulonephritis (type 2)
Nephrotic range proteinuria and hematuria. Dense intramembranous deposits that stain for C3 is characteristic.
It is caused by IgG antibodies (this is unique) called C3 nephritic factor directed against C3 convertase of the alternate complement pathway. These antibodies reacting with C3 convertase lead to persistent complement activation and kidney damage.
Note: This glomerulonephritis is NOT caused by circulating immune complexes. Those are SLE, PSGN, etc.
What drugs can stimulate hypothalamic ADH production and cause SIADH?
1) Carbamazepine
2) Cyclophosphamide
3) SSRIs like fluoxetine
Glomerular vs non-glomerular causes of hematuria
Glomerular
1) Microscopic is more than gross hematuria
2) Causes include glomerulonephritis and basement membrane disorders (Alport)
3) Presents with nonspecific or no symptoms. Can have nephritic syndrome (HTN, oliguria, elevated Cr)
4) UA shows blood AND protein. RBC casts, dysmorphic RBCs
Non-glomerular (more common)
1) Gross is more than microscopic hematuria
2) Can be caused by kidney stones. Cancer (renal cell, prostate). PCKD. Infections (cystitis). Papillary necrosis. Renal infarction.
3) Presents with dysuria or symptoms of urinary obstruction (flank pain, renal or ureteral colic, anuria)
4) UA shows blood but NO protein. Normal appearing RBCs.
Proteinuria and transient gross hematuria following acute pharyngitis.
Think IgA nephropathy. This is the most common GN in adults. It is typified by hematuria starting within 5 days of an URI or pharyngeal illness. AKA synpharyngitic GN.
Causes of papillary necrosis
This is sloughing of renal papilla. A rare cause of non-glomerular hematuria. May be seen with long term acetaminophen abuse but not with light-intermittent use.
NSAID is the trick.
1) NSAIDs
2) Sickle Cell Disease
3) Analgesic abuse
4) Infection (pyelonephritis)
5) Diabetes mellitus
Tubular origins of hematuria
Acute tubular necrosis is characterized by acute azotemia following a hypotensive or nephrotoxic injury. Patients may have dark or cola urine, but significant hematuria is uncommon.
Tubulointerstitial nephritis causes microscopic hematuria associated with elevated Cr and variable proteinuria. Most commonly linked with certain meds like ABx, NSAIDs and diuretics.
SIADH very brief clinical markers
Hypotonic hyponatremia with euvolemia.
Low plasma osmolality (less than 280) with high urine osmolality (more than 100-150) is diagnostic.
Preferred modality for diagnosing a ureteral stone
Ultrasound or noncontrast CT (US is preferred, esp in patients with a low likelihood of an alternative diagnosis and who are pregnant)
