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119 Cards in this Set
- Front
- Back
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How does the body maintain K homeostasis post-meal?
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Na-K ATPase (insulin sensitive) transports K into cells
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What upregulates Na-K ATPase?
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Insulin, catecholamines, and high K
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What can cause K to shift out of the cells?
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NON-ANION GAP Acidemia (H and K get switched around)
Hyperosmolarity (Glucose drags water drags K out of cells - unless you have a big anion gap which means anion went in with H, keeps K inside) Massive cell lysis (tumor or rhabdomyolisis) - K will leak out of dying cells |
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What can cause K to shift into the cells?
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Massive cell production (B12 shots for anemia)
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Where does the majority of K regulation in the nephron occur?
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At the CCD by two cells
***Principal cell - the star of the show, transports K out of CCD Intercalated cell ensures that you keep that K |
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There are 3 effects on principal cells by aldosterone. Describe them, and whether they enable active or passive transport of K
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1) increase activity of Na reabsorption from filtrate - PASSIVE
2) increase activity of K secretion into filtrate - PASSIVE 3) Upregulate Na/K ATPase in the apical membrane - ACTIVE |
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What will encourage K secretion from principal cells into filtrate?
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-High K concentration
-Aldosterone*** (goes up with High K) -High distal Na delivery from filtrate -Alkalotic or anionic filtrate (results from high Na delivery from filtrate because Cl left behind) -High urine flow |
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What would a K serum of 7.0 do to aldosterone production?
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INCREASE - aldosterone is sensitive to high K. Will increase Na reabsorption which will favor K secretion at principal cells
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What do intercalated cells do with potassium?
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Reabsorb it in exchange for H+
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82-year-old woman with mild chronic kidney disease admitted with a hip fracture and is now post-op day #2.
You, the nephrologist, are called for a consult for hyperkalemia. Past Medical History: Hypertension, stable chronic kidney disease with stable GFR 30-40 ml/min Medication: Aspirin 325 mg daily, oxycodone 10 mg q 6 hrs prn and ½ NS with 20 mEq KCl @100 cc/hr. Exam: T:98 P:66 BP: 135/80 100% on 2L NC Gen: NAD, frail-appearing CV: RRR Lungs: CTAB Abd: soft, n/t, n/d Ext: warm, no edema Skin: clear, no rashes Na: 144 K: 6.2 Cl:105 HCO3:24 BUN:20 Cr:1.5 Increase physical therapy sessions so that the patient can leave the hospital sooner. In the meantime, stop checking labs. Stop potassium-containing fluids and put her on a K+-restricted diet. Start lisinopril (an ACE-Inhibitor). Increase the rate of her fluids. |
-Stop potassium fluids and put on K restricted diet
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76-year-old woman with history of hypertension, diabetes brought to the ED by her family after she was found in bed and lethargic. The patient had been feeling ill with fever, cough and minimal PO intake X 5 days.
Past Medical History: Hypertension, coronary artery disease, and hyperlipidemia Medication: Lisinopril 40 mg daily, Spironolactone 25 mg daily, Amlodipine 10 mg daily, Lipitor 40 mg daily Social History: Lives alone, widow, no longer drives, lifetime non-smoker, no ETOH Physical Exam: T:101.7 P:115 BP: 87/40 100% on RA Gen: Lethargic, ill-appearing HEENT: dry mucous membranes CV: Tachy, RR, no murmurs Lungs: ronchi rt upper lung field Abd: soft, non-tender, no masses, +bowel sounds Ext: warm, no edema Skin: no rashes, decreased skin turgor Labs: Na: 136 K:7 Cl:104 HCO3 :27 BUN:30 Cr:1.1 CXR: RUL infiltrate Which of the following caused hyperkalemia? Lisinopril Spironolactone Volume Depletion All of the above |
-All of the above
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Volume depletion can contribute to hyperkalemia by:
Causing constipation and decreased GI excretion of K+ Causing extracellular shift of K+ Volume depletion has nothing to do with hyperkalemia Decreasing delivery of Na+ and H2O to the cortical collecting duct |
Decreasing delivery of Na+ and H2O to the cortical collecting duct
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19-year-old woman with type 1 diabetes presenting with 3 days of fatigue, nausea, and weakness. She also reported polyuria, polydypsia and blurry vision. After a lengthy interview by a skilled medical student she admitted that, in an effort to lose weight, she stopped taking her insulin four days ago.
Medical History: Type 1 diabetes diagnosed at age 7. Erratic compliance w/insulin. Multiple hospitalizations for DKA. Depression. Medication: Celexa 40 mg daily, Lantus 45 units qhs, humalog sliding scale with meals Social History: No tobacco or ETOH. Unemployed, lives with mother and sister. Physical Examination: T:98.7 P:100 BP:100/60 100% on RA Gen: Lethargic HEENT: dry mucous membranes CV: Tachy, RR Lungs: CTAB Abd: soft, n/t, n/d, no masses Ext: no edema Labs: Na: 133 K:7.2 Cl:100 HCO3:15 Glucose: 760 BUN:35 Cr:1.2 Anion Gap: 18 (high) pH: 7.25 pCO2: 30 PO2:98 The patient’s hyperkalemia is driven by cellular shift from: Lack of insulin decreasing Na-K-ATPase activity High extracellular osmolarity Metabolic Acidosis A and B A, B and C |
A and B (not C because she has a big anion gap - not pushing K out of cells)
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What are the symptoms of HyperK?
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Weakness, paralysis, cardiac arrhythmias
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How should you treat someone with HyperK?
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BUY TIME:
EKG, Calcium; Insulin + Glucose, Bicarb, Beta agonist (like dobutamine or epinephrine, but not albuterol - takes 7X asthma dose), SHED K: Kayexalate, IVF, diuretics, dialysis, |
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What is the most appropriate therapy to correct a DKA patient’s hyperkalemia?
IV Calcium Lisinopril Insulin Insulin + glucose Insulin followed by kayexalate |
Insulin, sugar is already high
Kayex unnecessary because cause is all DKA. Correct that and it will work itself out |
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What (apart from lower intake) is usually a cause of HypoK?
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Diarrhea/laxative abuse
Aldosterone releasing adenoma or adrenal hyperplasia Increased urinary flow Anions in collecting duct |
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What is Bartter's syndrome?
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A defect in NaK2CL transporter in thick ascending limb of loop causes loss of Na K and CL, just like a loop diuretic (furosemide)
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Why does vomiting deplete K?
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Some in gastric juices, and lower intake;
but mostly loss of H/CL causes excess of bicarb (negative) which pulls K out at principal cells. Volume depletion also causes aldosterone increase and K loss |
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Most likely the patient with DKA will end up needing
Hemodialysis to remove K+ Diuretics to encourage K+ excretion K+ replacement to correct total body depletion Nothing more than insulin |
K+ replacement to correct total body depletion
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Which of the following laboratory results would you expect in a subject taking acetazolamide?
Na 140, K 3.5, Cl 112, HCO3 18 Urine pH 4.5 Na 140, K 3.5, Cl 112, HCO3 18, Urine pH 7 Na 140, K 3.5, Cl 98, HCO3 18, Urine pH 7 Na 140, K 3.5, Cl 98, HCO3 18, Urine pH 4.5 Na 140, K 3.5, Cl 98, HCO3 24, Urine pH 7 |
Answer B: Na 140, K 3.5, Cl 112, HCO3 18, Urine pH 7
Carbonic anhydrase inhibitors cause bicarbonate loss by inhibiting bicarbonate conversion and leading to bicarbonaturia which alkalinizes the urine. Augmented chloride reabsorption raises the serum chloride, leading to a “hyperchloremic” metabolic acidosis with a normal anion gap. |
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Which of the following diuretic classes would most likely cause hyponatremia?
Loop diuretics Thiazides K-sparing Carbonic anhydrase Osmotic |
Thiazides
Loop diuretics impair BOTH urinary concentration and dilution Thiazides only work on urinary dilution, most likely to cause hypoNa |
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What affect to NSAIDs have on diuretics?
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Block augmented excretion of salt by diuretics
They also block PG effects on the afferent arteriole (normally dilates), constricting AE and decreasing GFR. |
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What diuretic mimics the effects of Gitelman's syndrome?
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Thiazides
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Mr. Aquavit is a 70 year-old man with CHF, peripheral edema, and pulmonary rales. His urine osmolality is 600 mOsm/Kg. He is given 40 mg of furosemide intravenously and experiences an increased urine flow.
What would you anticipate would the urinary findings after furosemide administration? Increased sodium excretion and increased osmolality Decreased sodium excretion and decreased osmolality Increased sodium excretion and decreased osmolality Decreased sodium excretion and increased osmolality Increased sodium excretion and unchanged osmolality. |
Increase Na excretion and decreased osmolality - increases free water loss because it's right before the diluting segment where Na will be pulled out but not water
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A 40 year old woman presents to your office with complaints frequent and large volume urine output. She often must get up at night to pass urine and usually keeps a glass of water at her bedside. She acknowledges that she is always thirsty and drinks at least 2 gallons of water per day.
Past medical history is notable for bipolar disorder for which she has been taking lithium carbonate therapy. Measured 24 hour urine volume is 12 liters and the serum sodium concentration is 147 mM. Which one of the following is the most likely diagnosis? Psychogenic polydipsia Nephrogenic diabetes insipidus Central (neurogenic) diabetes insipidus Impaired thirst and lack of water intake Salt-wasting nephropathy |
Answer – b, nephrogenic diabetes insipidus
The patient’s disorder is due to an impaired nephron response to ADH which is caused by long-term lithium use |
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Your patient shows signs of diabetes insipidus. Which one of the following tests would you perform to make the diagnosis?
Water load test Water deprivation test with ADH administration Salt loading test Measurement of free water excretion Measurement of urine volume |
Answer: Water deprivation with ADH
If central, urine output will decrease If nephrogenic, urine output will continue to be high |
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A medical student volunteers to the following experiment. On a normal diet of sodium and water, he ingests 1 liter of water over a twenty minute period. During the next 3 hours urine is collected and measured for volume. On the following day, he undergoes the identical study but substutes 1 liter of normal saline.
Which volume is excreted faster? Water Saline |
Water
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How do you calculate serum osmolarity?
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NaX2+Glucose/18 + BUN/2.8
**Na is mosm/L, Glucose is mg/dl, BUN is mg/dl |
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Mr. Abercrombie is a 70 year-old with heart failure with the following studies:
PNa 128, BUN 28, Glucose 90 Urine flow (V) 1 ml/min, Uosm 542 What is the calculated plasma osmolality? 291 281 271 310 300 |
271
=128*2+28/2.8+90/18 |
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How do you calculate free water clearance?
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Ch20 = V(1 - Uosm ÷ Posm)
Urine flow (1 - (urine osmolarity/plasma osmolarity)) |
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Mr. Abercrombie is a 70 year-old with heart failure with the following studies:
PNa 128, BUN 28, Glucose 90 Urine flow (V) 1 ml/min, Uosm 542 Is there: free water clearance or absorption? |
Absorption
1ml/min *(1-542/271) = -1 Net reabsorption |
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What two processes constantly increase H+ concentration?
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Ingestion of protein, and metabolism of carbohydrate and fat
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What is the Henderson equation for determining H+ concentration from CO2 pressure and HCO3 concentration?
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H+ = 24 (pCO2) / (HCO3)
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You are in the emergency room and an unidentified man, who appears to be in his twenties, is brought to the critical care area after passing out at a bar. An arterial pH is done and is 7.28. The pO2 is 97 mmHg and the pCO2 is 36 mmHg. The HCO3- level is 31 mEq/L. What is the acid base disturbance?
metabolic acidosis metabolic alkalosis respiratory acidosis respiratory alkalosis a mixed acidosis and alkalosis the lab values must be incorrect. |
Answer: F
Acid-base disorders are defined because CO2 is high or bicarb is low. pCO2 was low, and bicarb was high. |
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What three organ systems regulate the H+ concentration in blood?
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Kidneys, GI, Lungs
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Describe the movements of H+ and HCO3 in the upper and lower GI tracts
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In the stomach, H+ goes into the lumen while bicarb is pumped in capillaries
In the jejunum, ileum and cecum, bicarb is secreted into the lumen while H+ is extracted back into the capillaries |
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What does the enzyme CA do in the proximal tubule?
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It breaks H2CO3 down to CO2 and water, instead of letting it deprotonate
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How is bicarb handled in the proximal tubular cells?
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reabsorbs bicarb filtered at the glomerulus
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What role do the alpha-intercalated cells of the collecting duct play in acid-base regulation?
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alpha-intercalated cells allow reabsorption of bicarb from H2CO3 that has donated a proton to a dietary acid to be excreted (i.e. H2PO4)
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What role do the distal tubular cells play in acid-base regulation?
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Secrete H+ into the tubular lumen and regenerate bicarb
-Stimulated by aldosterone |
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What conditions would cause a respiratory acidosis?
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ANYTHING THAT DEPRESSES VENTILATION, DUE TO
1) Lung disease -Pneumonia, PEdema, COPD, Respiratory failure 2) CNS disease -Drug overdose, CVA, trauma or bleeding 3) Neuromuscular diseases -Chest wall deformities, MD, myasthenia gravis, Guillain Barre |
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What conditions would cause a respiratory alkalyosis
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HYPERVENTILATION, DUE TO:
1) Anxiety, pregnancy (PG), asthma/PEmbolus, early pneumonia, aspirin OD |
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More information comes in about your patient, who was found passed out in a bar having drank "a lot". He apparently combined the use of heroin and benzodiazepines, then fell from a balcony, sustained head injuries, and is now apneic and unresponsive. You repeat the lab values. Which of the following represents his likely lab tests?
pH 7.00, pCO2 100 mmHg, HCO3- 20 mEq/L pH 7.00, pCO2 20 mmHg, HCO3- 10 mEq/L pH 7.60, pCO2 20 mmHg, HCO3- 20 mEq/L pH 7.60, pCO2 100 mmHg, HCO3- 50 mEq/L |
pH 7.00, pCO2 100 mmHg, HCO3- 20 mEq/L
-High PCO2 because he can't breath off CO2 |
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What conditions give rise to metabolic acidosis?
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BICARB LOSS:
-GI - Diarrhea, infections or inflammation -Kidneys - proximal renal tubular acidosis (T2) LOW BICARB PRODUCED -Distal renal tubular acidosis (T1) -Hypoaldosteronism, adrenal insufficiency, ACEIs/ARBs INCREASED ACID IN ECF: -DKA, Lactic, aspirin, methanol, EG -Failure to excrete dietary acid in RF |
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What is the cutoff for a high anion gap?
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Greater than 12 - DKA, Lactic acidosis, ingestion and renal failure
Less than 12 - Diarrhea, tubular acidosis and hypoaldo |
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A 27 year old woman shows up in your clinic for an initial visit. She has a history of hypertension and complains of fatigue. Lab tests show an arterial pH of 7.28, a pCO2 of 31 mmHg, and a HCO3- of 15 mEq/L. The Na+ is 129 mEq/L, and the Cl- is 88 mEq/L. Which of the following is the likely explanation for her acid base abnormality?
Chronic kidney disease An aldosterone producing tumor Pregnancy Diarrhea |
Chronic kidney disease
Can't be aldosteronism because would have high bicarb Can't be pregnancy because she has acidosis (pregnancy leads to alkalemia) Can't be diarrhea because she has a big anion gap (diarrhea gives normal anion gap) |
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Which of the following organ systems give rise to metabolic alkalosis:
GI, Renal, Pulmonary |
Renal only, either from
1) lowered filtration at glomerulus 2) increased synthesis at the proximal tubule 3) increased reabsorption at the CD alpha intercalated cells |
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What would hyperaldosteronism lead to in terms of acid-base regulation?
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Increased reabsorption of bicarb reabsorption at the distal tubule
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What can look like hyperaldosteronism, but is not primary aldosteronism?
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Glucocorticoid excess (Exogenous steroids, adrenal hyperplasia)
Bilateral RAS, Na or Cl depletion |
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A 79 year old woman has congestive heart failure and hypertension and is on digoxin and the diuretics furosemide and metolazone. You see her in follow up, and you obtain labs which show: arterial pH 7.58, pCO2 44 mmHg, HCO3- 40 mEq/L. What explains the abnormal pH ? (More than one choice may be correct)
Hypoventilation Increased urinary loss of chloride Increased serum levels of aldosterone Decreased renal filtration of bicarbonate Increased ingestion of bicarbonate |
Both loss of Cl and increased serum aldosterone
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A 82 year old woman with a history of vascular disease is admitted to the surgical intensive care unit with abdominal pain. Her arterial pH is 7.08 and the pCO2 is 36 mmHg. The Na+ is 130 mEq/L, the K+ is 5.8 mEq/L, the Cl- is 94 mEq/L, and the HCO3- is 10 mEq/L. The lactate level is 9 mEq/L (elevated).
What is the acid base disorder? |
Metabolic acidosis, probably secondary to ischemia
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A 82 year old woman with a history of vascular disease is admitted to the surgical intensive care unit with abdominal pain. Her arterial pH is 7.08 and the pCO2 is 36 mmHg. The Na+ is 130 mEq/L, the K+ is 5.8 mEq/L, the Cl- is 94 mEq/L, and the HCO3- is 10 mEq/L. The lactate level is 9 mEq/L (elevated).
What is the acid base disorder? |
Two disorders: metabolic acidosis is the primary problem, but there is a problem with respiratory compensation: one would expect the pCO2 to decrease to 23 mmHg—it is higher than that, there is inadequate respiratory compensation, so the patient also has a respiratory acidosis.
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A 59 year old man has a history of severe chronic obstructive pulmonary disease due to heavy smoking. He also has a history of alcohol abuse, and has been vomiting daily for the past two weeks. His pH is 7.32, his pCO2 is 74 mmHg, and his Na+ is 142 mEq/L, Cl- is 92 mEq/L, and the HCO3- is 40 mEq/L.
What is the acid base disorder? |
Two disorders. The primary disorder is a respiratory acidosis (high H+, high pCO2). But one would expect an increase of 10 mEq/L in the HCO3- (to 34 mEq/L). The HCO3- is higher than that, so the patient must have a respiratory acidosis and a metabolic alkalosis.
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A 15 year old girl with diabetes out of control and severe vomiting. pH is 7.34, pCO2 is 33 mmHg, Na+ is 140 mEq/L, K+ is 5.4 mEq/L, Cl- is 98 mEq/L, and HCO3- is 18 mEq/L.
What is her primary acid/base disorder? Bonus points for any other disorders |
The patient has a primary metabolic acidosis (low pH, high H+, low HCO3-. The anion gap is 24 mEq/L (an increase of about 14 mEq/L) but the drop in the HCO3- is only 6 mEq/L. This can only happen if the initial HCO3- was higher than 24 mEq/L; so the patient has a combined metabolic acidosis and metabolic alkalosis.
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A 12 year old girl with diabetes out of control and severe diarrhea. pH is 7.34, pCO2 is 24 mmHg, Na+ is 140 mEq/L, K+ is 3.1 mEq/L, Cl- is 114 mEq/L, and HCO3- is 10 mEq/L.
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The patient has a primary metabolic acidosis (low pH, high H+, low HCO3-. The anion gap is 16 mEq/L (an increase of about 4 mEq/L) but the drop in the HCO3- is much higher: 14 mEq/L. This can only happen with a combined anion gap metabolic acidosis and nonanion gap metabolic acidosis.
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A 79 year old man is a patient of yours. He has osteoarthritis and has been chronically taking large doses of analgesics. He has become nauseated and has been vomiting. He comes to the ER, where his pH is 7.42, his Na+ is 128 mEq/L, K+ is 3.5 mEq/L, Cl- is 80 mEq/L, HCO3- is 20 mEq/L. The pCO2 is 52 mmHg. Does he have any of the following acid base disorders, and if so, which one(s)?
Metabolic acidosis J. C and D Metabolic alkalosis K. A, B, and C Respiratory acidosis L. A, B, and D Respiratory alkalosis M. B, C, and D A and B N. A, C, and D A and C A and D B and C B and D |
B and C
High CO2 from ASA intox = RESP ACID Low Urine Cl from vomiting secondary to ASA = MET ALK |
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40 yo female with poorly controlled diabetes mellitus with urinary incontinence x 1 year. Voids 1-2 times/day, has trouble urinating, and strains to void. PVR (postvoid residual) 300 ml.
Is this a storage or emptying problem? What does her diabetes have to do with her voiding problems? |
Emptying problem - diabetic neuropathy means she's not feeling the urge to void when she normally would. Leading to overflow incontinence
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What can increased voiding pressures lead to?
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Trabeculation - hypertrophy and decreased compliance
Eventually transmitted to kidneys and can lead to renal failure |
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What can a CVA, pontine tumor, MS or Parkinson's lead to in terms of urinary continence? Be specific.
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Reflex voiding - brain no longer able to exert control over detrussor means frequency (detrussor hyperreflexia)
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40 yo male with h/o herniated L3-L4 disk, on chronic narcotic pain meds with urinary incontinence, erectile dysfunction, fecal impaction, & numbness in perineum. Voids 1-2 times/day, has trouble urinating and strains to void. PVR 300 ml.
Does he have a bladder storage or emptying problem? |
Bladder emptying problem = ACUTE URINARY RETENTION
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50 yo male fell from ladder, T-12/L-1 vertebral fracture which was repaired surgically 6 months ago, still with complete urinary retention except for stress incontinence, fecal impaction, numbness in perineum, and erectile dysfunction.
Does he have a storage or emptying problem? |
BOTH - Conus medullaris injury to low thoracic or high lumber results in
Bladder emptying and storage problem ACUTE URINARY RETENTION STRESS URINARY INCONTINENCE (SUI) |
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25 yo male s/p complete C5-C6 spinal cord injury 1 week ago with complete urinary retention
Does he have a storage or emptying problem? |
Emptying problem = spinal shock results in urinary retention
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25 yo male s/p complete C5-C6 spinal cord injury who had complete urinary retention
He now starts to void spontaneously 1 month after injury Continuous leakage day and night Leaks every 30 minutes or so Diaper dependent & developing sacral decubitus ulcer New onset headaches and HTN since started leaking Febrile UTI’s and PVR 200 ml Is this a storage or emptying problem? |
Both - Hyperreflexia with detrussor-sphincter dyssynergia
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What can Hyperreflexia with DSD lead to?
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Vesicoureteral reflux, eventually hydronephrosis
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What is BPH, a storage or emptying problem?
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Emptying problem, but can also be a storage problem when bladder becomes irritated and becomes overactive
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What is TURP used for?
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BPH - transurethral resection of prostate
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What do bladder cancer and UTIs cause in terms of voiding?
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A storage problem - OAB
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What can men suffer from following radical prostatectomy in terms of voiding, or women after many children, and is it a storage or emptying problem?
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Stress incontinence, a storage problem due to incompetent sphincter
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What are the priorities for treating someone with ASA poisoning?
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ABC(d) - airway, breathing, circulation, dextrose
GI decontamination with activated charcoal dialysis or hemoperfusion acetylcysteine for acetaminophen naloxone if opioid intoxication suspected tox screenings in selected patients |
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Why do people die of aspirin poisoning?
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-CNS injury or depression, with secondary respiratory failure
-CV toxicity, with secondary hypotension -Direct tissue hypoxia/mitochondrial toxicity |
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Where is aspirin mainly metabolized?
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Hepatic, with saturable metabolic pathways
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What happens to aspirin half-life at higher doses?
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Increases, as metabolic pathways become saturated
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What level of aspirin toxicity would induce tinnitus, vomiting, and mild hyperpnea?
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Mild
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What level of aspirin toxicity would induce lethergy/excitability, severe hyperpnea and fever?
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Moderate
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What level of aspirin toxicity would cause metabolic acidosis?
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Severe, and in addition severe hyperpnea and possibly coma
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Why would you get metabolic acidosis with ASA poisoning?
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1) Metabolites are organic acids
2)Uncouples oxidative phosphorylation which increases metabolic rate, causing: -heat -increased CO2 production -increased cardiac output -increased glucose use, eventually low glucose -LACTATE |
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Would ASA cause an anion gap acidosis?
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Yes - via lactate, Beta hydroxybutyrate and acetoacetate
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ASA poisoning can cause respiratory alkylosis via CNS poisoning, and can cause metabolic acidosis via uncoupling oxidative phosphorylation or the metabolite products of ASA.
What age group is likelier to experience alkylosis instead of acidosis? |
Adults and children older than 12.
Babies up to 4 tend to get acidotic. |
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Why would you want to alkalinize urine for ASA poisoning?
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ASA is a weak acid, and the more alkaline the environment, the likelier it is to be ionized - a form that cannot cross biological membranes.
More alkaline urine = greater ASA excretion |
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Apart from administering bicarb, what is a great way to alkalinize urine for ASA poisoning
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Administer acetazolamide (diamox), a carbonic anhydrase inhibitor which will prevent reabsorption of bicarb
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What happens to GFR in acute tubular injury?
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Decreases, subsequent to loss of polarity of tubule cells, moving NaKATPase to the apical membrane and shedding Na. Increased sodium is sensed by JGA and leads to afferent constriction
Also decreased NO and PGI cause constriction |
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Describe 1 of the 2 changes visible here indicative of tubular injury
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Hyaline cast formation
Dilated tubules |
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What urine finding is indicative of tubular injury?
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Oliguria
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How do you differentiate a bladder cystitis from pyelonephritis?
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Kidney infection shows systemic clinical signs (fever, malaise, flank pain)
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What is shown here?
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Acute Pyelonephritis with neutrophilic infiltrate cellular cast formation
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When would you expect someone to get a polyoma pyelonephritis?
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Immunocompromised - as in a kidney allograft transplant
Important to biopsy and find these viral cell changes (arrow) indicative of polyoma, because treatment is to lower immunosupression. If patient is experiencing transplant rejection, need to INCREASE immunosupression |
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When would you see this sort of kidney?
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Chronic pyelonephritis
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When would you get a "thyroidization" of the kidney?
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In chronic pyelonephritis. Tubules are dilated with eosinophilic casts
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What is the time course for drug-induced interstitial nephritis?
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2 weeks post exposure
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What drugs can cause acute interstitial nephritis, pictured here?
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Penicillins, NSAIDs, allopurinol, cimetidine, etc.
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How does analgesic nephropathy differ from drug-induced interstitial nephritis?
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Analgesic nephropathy is due to chronic use (10-20 years) of aspirin, acetaminophen, caffeine, usually multiple taken
Drug-induced IN is acute |
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How do analgesic nephropathys appear on gross examination of kidneys.
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As papillary necrosis. Columns spared.
Clinically present with with stones, UTIs, headache, HTN, sometimes renal colic from shed papillae |
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What kinds of kidney injury can NSAIDs cause?
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-Renal failure due to inhibition of prostaglandin afferent vasodilation
-Minimal change disease -Membranous glomerulonephropathy |
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What can aristocholic acid, found in some herbal remedies for snake bites, RA and gout, cause in kidneys?
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Renal failure with prominent fibrosis and no inflammatory infiltrate
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What other disease might you expect someone with this nephropathy to have?
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Gout - uric acid stone formation
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What does a patient with this kidney, Bence-Jones proteinuria and Tamm-Horsfall glycoproteinuria in formed casts probably have?
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Multiple myeloma
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What are the vast majority of urinary calculi formed from?
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Calcium and phosphate (70%)
Struvite (magnesium aluminum phosphate) (20%) |
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What type of collagen is GBM made of?
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Collagen Type IV- many autoimmune diseases target this
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What cells produce the GBM?
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Podocytes
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What are mesangial cells continuous with?
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Capillary lumen - don't have to cross a basement membrane to get from one to the other
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Would you get lymphoproliferation in nephritis or nephrotic syndrome?
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Nephritis
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What pattern of glomerulonephropathy exhibits both nephritic and nephrotic signs?
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Membranoproliferative GN
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What do circulating levels of immune complex tell you about the probable cause of a GN?
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Low circulating immune complex favor Mesangial pattern of injury (i.e. IgA, Mesangial Prolif Lupus Nephritis)
High circulating immune complex favor endothelial pattern of injury (i.e. Post-Strep) |
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What kind of GN follows a membranoproliferative pattern of injury?
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Hep C and Membranoproliferative LN
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What kinds of deposits cause epithelial (podocyte side) patterns of injury?
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Complement, and cations which favor the anionic GBM
Ex: Membranous nephropathy |
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What immune factor lines the capillary wall in post-strep GN?
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Lumpy bumpy granules of IgG gradually replaced by Complement (C3-5)
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What do you notice about this glomerulus?
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It is very full and packed - proliferative GN subsequent to strep infection
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When do you get IgG and C3 deposition on capillary endothelial?
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In PSGN
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How do IgG and IgA deposits causing GN differ in terms of location?
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IgG deposits on capillary wall, IgA results in mesangial proliferation (really leukocyte deposition)
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Based on the location of this deposition, what would you expect the clinical picture of this patient to include?
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Mesangial IgA deposits, might have accompanied an upper respiratory infection. Probably has had episodes like this before.
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What 3 diseases might this pattern of GN be?
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Really bad IgA GN (that has become rapidly progressive)
Goodpasture's (anti-GBM antibodies) Pauci-Immune (no immune complex deposits) |
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What are ANCA (anti-neutrophil cytoplasmic bodies) in neutrophils associated with in terms of glomerulonephropathy?
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Pauci-immune GN, associated with systemic vasculidity and characterized by crescentic pattern of proliferation
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What is shown here?
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A segmental necrotizing GN associated with fibrin (red)
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In what disease can you expect immune complexes in the endothelium, mesangium and epithelium?
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Global Lupus Nephritis
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What is the finding characteristic for minimal change nephrosis?
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Effacement of podocytes - visible only on SEM
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What is pictured here, and what can cause it?
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Focal Segmental Glomerulosclerosis
-reflux nephropathy, steroid dependence or resistance |
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What is pictured here, and what is the target in this disease?
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Membranous nephropathy, target is a phospholipase that is targeted, and the complex deposits in the subendothelial space of the GBM
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What are these lesions typical of?
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Diabetic GN - thickened basement membrane and nodular lesions.
Capillaries can become huge as podocytes no longer able to maintain glomerular structure |
