9/24- Small Group Cases Flashcards
Case)
- 48 yo woman
- Hx of alcohol abuse
- Abdominal distention, swelling in feet/ankles, 15 kg weight gain, bilateral pitting edema to midcalf, hepatomegaly?, shifting abdominal dullness, multiple telangiectasia, and spider nevi, jaundiced; no asterixis
- Hyponatremia (130)
- BP 100/70
What is this describing?
Liver failure/cirrhosis
- Cirrhosis -> NO -> vasodilation -> perceived decrease in Na concentration -> ADH release….
What is the significance of her 24 hour urine sodium excretion? That is, what happens if she excretes less sodium than she is ingesting?
Net positive sodium balance
- Retaining sodium
- Sodium determines water balance; here -> edema
What pathophysiologic factors have led to her ascites and edema? Which hormone pathways are implicated?
Low effective circulating volume -> activation of RAAS system -> Na and thus water retention
- Low ECV also prompts PCT Na reabsorption Also non-osmotically-driven ADH release
- Further increases water reabsorption
Are the same factors responsible for the hyponatremia?
Yes
- Hyponatremic, but Na concentration depends on water volume; actually has high body Na content
- Principally due to ADH (from relatively low effective blood volume)
How would you treat this patient?
Loop diuretic
- Loop are the most effective for dealing with high volume
- Loop diuretics typically result in excretion of half sodium (causes hypernatremia)
- Loop diuretic causes water excretion > Na excretion (still causes decrease in total body Na but Na concentration will increase)
(Thiazide diuretics on the other hand cause hyponatremia?)
Fluid restriction
- Wan’t intake > free water excreted
Sodium restriction (1-2 g/day)
- Na follows water in the body
- More to do with edema/ascites rather than correcting sodium level
Calculate her creatinine clearance in ml/min (hint: UV / P).
Clearance = UcrVcr/Pcr
- U = 900mg/650mL
- V = 650 mL/d
- Pcr = 0.9 mg/dL
Thus, clearance = (900 mg/d)/(0.9 mg/dL)
= 1000 dL/day x 100 mL/dL / 1440 min/day ~ 69 mL/min
Her glucose is 70 mg/dl and BUN 6 mg/dl.
What is the calculated serum osmolarity?
- Normal serum gap
- What causes high serum gap
Calculated osmolarity = 2Na + BUN/2.8 + glucose/18
= 2(130) + 6/2.8 + 70/18 = 266
- Normal gap = 10
- High gap could be due to substance like ethanol/alcohol…
Fun fact: loop diuretics do not affect BP too much
(:
If patient has edema, what do we know about Na?
Total body sodium is high
How does BUN relate to osmolarity power/”effective osms”?
“Effective osms” = osmotically active solutes = 2Na + glucose/18
- Does NOT include BUN
- BUN freely crosses cell membranes (in contrast to Na and glucose)
Case 2)
- 55 yo female comes to ER with severe epigastric abdominal pain, N/V
- 2 wks intermittent right upper quadrant abdominal pain associated with fatty meals
- Light colored, fatty, foul smelling stools for 2 days
- Orthostatic hypotension
- Slightly high temp
- Slightly underweight
- Mucus membranes are dry
- Epigastric abdominal tenderness
- Decreased bowel sounds
- Jaundice
- Abdominal films show calcified densities in the RUQ
Setup
What is her total Na and ECV (decreased, normal, increased? What is the cause?
- Decreased ECV
- Decreased Na (Na is a marker for ECV)
- Hypovolemic (because ortho hypoTN, underweight, dry mucus membranes)
- Hypovolemia probably due to vomiting
What does BUN:creatinine ratio > 20 indicate?
Volume depletion
- Require IV fluids
What is the significance of her low urinary Na concentration?
- Kidney is avidly reabsorbing Na to try to compensate for volume depletion
What would be appropriate therapy for this patient?
- IV normal saline*
(should also correct metabolic acidosis, b/c urine Cl under 20)
- Antibiotics for infection
- Anti-emetics for nausea
- Pain medication
Case 3)
- 45 yo man with end-stage renal disease treated by hemodialysis
- Fell down the stairs and sustained a massive hematoma in left thigh and hip
- Brought to ER next day because weak and slow pulse
- Vital signs: BP 140/85, pulse 50, and normal temperature
- He had generalized weakness, was oriented, had a large bruise on his left thigh and hip
- There were no other obvious abnormalities that had not bee present on numerous prior examinations.
- EKG: wide QRS complex and bradycardia (HR under 60)
What is causing the wide QRS complex and bradycardia?
Hyperkalemia
Side note: How do you tell the difference between saline responsive/non-responsive metabolic acidosis?
Urine chloride
- Low urine chloride indicates saline responsive (< 20)
What caused the hyperkalemia?
- Rhabdomialysis (?)
- Bruise itself causes hematoma, resulting in RBC lysis and K release
- ESRD, so can’t effectively excrete K
What is the plan for treatment?
- Calcium gluconate: stabilize the membrane
- Insulin D50: insulin causes intracellular movement of glucose and K; give D50 (dextrose) to prevent hypoglycemia
- Beta agonists: big dose of inhaled albuterol increases Na/K/ATPase and shifts K into cells
- K binding resins if long time to dialysis (binds K in gut and excreted in stool)
- IV Lasix (loop diuretic): K wasting but don’t anything if pt is anuric
- Dialysis, but takes ~ 2 hrs to set up and this is an emergency
What is this patient’s anion gap?
AG = Na - (Cl + HCO3)
Total serum CO2 is equivalent to bicarb!!!
= 135 - (96 + 18) = 21 High AG
What could be causing this patient’s high AG?
- Possibly lactic acidosis
- Uremia
Case 4)
- 22 yo female admitted through ER after losing consciousness at home
- Severe occipital headache and vomited twice
- VS: BP 120/80, HR 50, normal temp, RR 22
- Stiff neck, pupils PERRLA
- Neuro exam showed response only to deep pain, upward plantar response, increased DTRs
- Lumbar puncture revealed grossly bloody spinal fluid
- Condition stabilized but she remained comatose
- On day 4, her urine output increased to 6 L/day and her BP was 60/40
What in her labs is most concerning?
Severe hypernatremia
What is causing this pt’s hypernatremia?
Central Diabetes Insipidus
- Decrease in urine output
- Sodium through the roof
What are the main causes of DI?
Central:
- Meningitis/CNS infections
- Head trauma
- CVA
- Sarcoidosis
- Hypoxic encephalopathy
Nephrogenic:
- Inherited genetic mutations
- Hypocalcemia and hypokalemia may induce this?
- Obstruction causing effacement of collecting ducts
Calculate serum osmolality on day 2
Osmolality = 2Na + BUN/2.8 + glucose/18
= 2(171) + 36/2.8 + 120/18 = 361.6
What is the water deficit on day 4?
Pt was 60 kg on day 1 and 54 kg on day 4
- Water deficit = 6 kg!
List the characteristics of an ideal indicator for the msmt of glomerular filtration.
What are the advantages/disadvantages of endogenous creatinine for the measurement of GFR?
- Freely filtered
- No reabsorption or secretion
- Not synthesized or metabolized
- Physiologically inert
- Easily measured**
- Not affected by hemodynamics**
Creatinine Advantages:
- Freely filtered
- Physiologically inert
- Easy
- Pretty reliable indicator of GFR in steady state
Creatinine Disadvantages:
- Slightly secreted (PCT); results in overestimation of GFR
- Not reliable indicator of GFR if changing (only in steady state)
What can you say about GFR is someone’s creatinine is increasing?
Nothing! Only good marker in steady state
Case 6)
- 35 yo female presents with headaches, weakness, lethargy, and polyria
- She’s on no meds
- No family illnesses
- BP 160/95, HR 75
- Absence of increased JVP, no edema
What stands out?
- Hypertensive
- Hypokalemia
- High bicarb
What is the acid-base disturbance?
Why is the PaCO2 48 mmHg?
Metabolic alkalosis
- High pH
- High bicarb (total serum CO2)
- High PaCO2
Are the acid-base values internally consistent (Henderson equation)
[H] = 24 PaCO2/HCO3 = 24(48)/(35)
= 33 nmol/L
This is equal to the given [H+], so internally consistent!
What is the significance of the urine chloride (25 mmol/L)?
Saline unresponsive-ish (responsiveness considered urine Cl under 20; typically due to volume depletion)
What are some causes of elevated urine Cl in metabolic acidosis?
Which is probable in this case?
- Hyperaldosterone-type state
- Severe hypokalemia (under 2)
- Diuretic use
- Bicarbonate loading (tablets, baking soda…)
This case could be hyperaldo state as indicated by high BP (order aldosterone and renin labs)
Case 7)
- 38 yo male alcoholic rodeo star brought to ER
- Increasing lethargic throughout the day
- Vital signs: BP 110/80, HR 100, R 20 and deep
- Weighs 75 kg
- Responsive only to pain, but can move all extremities
- Large tender liver
- Exam otherwise unremarkable What is notable?
- Really low PaCO2 and pH
- Elevated BUN and creatinine
What do these urine analysis findings suggest?
Oxalate crystal (envelope-shaped)
What is the acid-base disturbance?
Probable etiologies?
This is AG metabolic acidosis
- A: aspirin
- M: methanol
- U: uremia
- D: DKA
- P: paraldehyde
- I: ischemia/infarcct
- L: lactic acidosis
- E: ethanol glycol/ethylene
- S: sepsis/starvation
What is the anion gap?
AG = Na - (Cl + HCO3) = 138 - (100 + 8) = 30?
What is the bicarbonate deficit?
Formula = TBW x (HCO3nl - HCO3msrd)
- TBW = BW x 0.6
- Formula: (75 x 0.6)(24-8) = 720 mmol
Case 8)
- Pt has new diagnosis of HTN What stands out?
- Hypokalemia
- High bicarb
- Venous pH is high (should be more acidic)
What is the acid base abnormality?
Metabolic alkalosis
What hormone *typically* causes the urinary potassium to be 40 mmol/L?
Aldosterone
The pt gives a positive FHx of HTN in his father and his grandfather, both of which began at a young age. You check renin and aldosterone levels, and those are normal. What is the most likely diagnosis?
Liddell’s syndrome
- Always active ENaC channels
- Entry of Na into cells results in negative lumen
- Electrochemical gradient favors K exit from cell into lumen, resulting in high urine K
Case 9)
- 22 yo Asian male pt comes to your office with dark urine for one day
- It is not painful and there is no foul odor
- He is drinking a normal amt of water (1-2 L/day)
- He believes he has had episodes of dark urine in the past
- For the past few days, he has had a runny nose and low-grade fevers
What is notable?
- Blood in urine
- RBC casts
- Normal albumin and complement
- Mildly elevated creatinine (decreased renal function)
Explain the pathophysiology that causes RBCs casts to appear in the urine?
Glomerular abnormality/leakage allows RBCs into tubular space
- Tam-Horsfall protein?
What syndrome is this?
Nephritic syndrome
- Hematuria
- RBC casts
- Normal albumin
- No notable edema
- Higher creatinine/decreased GFR
How does nephritic syndrome result in higher creatinine/decreased GFR?
Nephritic syndrome injures vessel, causing reactive vasoconstriction, reduced filtration SA and resultingly decreased GFR
The timing of the dark urine with his upper respiratory infection suggests what common disease?
IgA Nephropathy
- If it was 3-ish weeks later, could be post-infectious glomerulonephropathy
What do you expect to find on IF on his kidney biopsy (IgA Nephropathy)?
IgA deposits in mesangium
Does post-infectious GN have normal or low complement?
Low complement in post-infectious GN
Case 10)
- A 5 yo boy is brought by his parents to evaluate sudden onset of pretibial edema within the past 1 wk
- The boy was previously healthy
- No FHx of kidney disease
- Exam is remarkable for the absence of increased JVP and generalized anasarca
What do these findings indicate?
Nephrotic syndrome
- High protein (9 g/day)
What would you expect to see on the kidney biopsy?
Expect minimal change disease
- LM: no changes
- EM: podocyte effacement
- IF: negative
