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STEP1 > RENAL: BOARDS AND BEYOND > Flashcards

RENAL: BOARDS AND BEYOND Flashcards

1
Q

ECG Findings in Hyperkalemia

A

Tall, “peaked” T-waves in the anterior and lateral precordial leads (V3-V6).

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2
Q

Serum Potassium Levels:
Normal: 3.5 - 5.0 mEq/L
Peaked T-waves: Serum potassium > 5.5 mEq/L
Severe Hyperkalemia: Typically > 7 mEq/L

A

Potassium Levels and T-wave Changes

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3
Q

Severe Hyperkalemia Effects

A

Potential ECG Changes:
- QRS widening
Arrhythmias such as:
- Sinus bradycardia
- AV block
- Bundle branch block
- Sinus arrest

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4
Q

Peaked T-waves are commonly tested in association with hyperkalemia on exams (such as Step 1).

A

Exam Relevance

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5
Q

Does not typically cause ECG changes.

A

Hyponatremia

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6
Q

Causes prolongation of QT interval

A

Hypocalcemia

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7
Q

Causes a shortened QT interval.

A

Hypercalcemia

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8
Q

May cause flattened T-waves and the presence of U-waves.

A

Hypokalemia

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9
Q

Abnormal levels of magnesium can significantly impact both potassium and calcium levels in the body.

A

Effects of Magnesium on Potassium and Calcium

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10
Q
  • The CaSR is a membrane protein receptor on chief cells in the parathyroid gland.
  • It detects low levels of calcium and triggers the release of parathyroid hormone (PTH).
A

Role of the Calcium-Sensing Receptor (CaSR)

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11
Q
  • Magnesium is essential for the proper functioning of the CaSR.
  • Severe magnesium depletion (hypomagnesemia) leads to impaired CaSR function.
A

Magnesium’s Influence on CaSR

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12
Q

Reduced PTH release due to abnormal CaSR function can lead to hypocalcemia (low calcium levels).

A

Consequence of Impaired CaSR Function

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13
Q

Precipitation of calcium-fatty acid salts can occur with fat necrosis. Although small areas of fat necrosis will not cause hypocalcemia, pancreatitis can cause diffuse necrosis of the peripancreatic fat which can lead to

A

Hypocalcemia.

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14
Q

Hypercalcemia can cause

A

Polyuria

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15
Q

Slightly reduced magnesium mimics calcium and stimulates the CaSR, leading to PTH release and resulting in mild hypercalcemia.

A

Slightly Low Magnesium:

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16
Q

Continuous Nebulized Albuterol

A

Albuterol is a beta-2 agonist used for bronchodilation in respiratory conditions.

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17
Q

Systemic Effects of Albuterol

A

Although intended to act locally in the lungs, large amounts can cause systemic effects, including hypokalemia.

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18
Q

Mechanism of Hypokalemia with Beta-Agonists

A

Beta-agonists, like albuterol, cause potassium to shift into cells, leading to decreased serum potassium levels.

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19
Q

Other Causes of Potassium Shifts

A
  • Insulin: Promotes potassium entry into cells.
  • Alkalotic States: Increased pH can also cause potassium to shift into cells.
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20
Q

Causes of Hypokalemia

A

Mechanisms:
Intracellular Shifts: Due to beta-agonists, insulin, or alkalosis.
Loss of Total Body Potassium:
- Excessive diuresis (use of diuretics).
- Diarrhea.

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21
Q

Aldosterone and Hypokalemia

A

States with high aldosterone levels increase renal potassium secretion, contributing to hypokalemia.

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22
Q

Certain drugs can cause hyponatremia by causing the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Common drugs include

A

Anti-epileptics (i.e. carbamazepine) and anti-neoplastic agents (i.e. cyclophosphamide).

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23
Q

Hypernatremia can be seen with drug-induced diabetes insipidus. Typically implicated drugs include

A

Lithium and amphotericin B.

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24
Q

Hyperkalemia is a common side effect of

A

Potassium-sparing diuretics (i.e. spironolactone, amiloride) and ACE inhibitors.

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25
Q

Hypocalcemia can occur with a variety of different drugs including

A

Bisphosphonates and long-term proton pump inhibitor use.

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26
Q

Clinical Manifestations of Hypocalcemia

A
  • Perioral and acral paresthesias (tingling around the mouth and in hands/feet).
  • Tetany (muscle twitching).
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27
Q

Etiologies of Hypocalcemia

A
  • Hypoparathyroidism
  • Renal Failure
  • Certain Medications
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28
Q

Chelation and Hypocalcemia

A

Chelation of calcium can lead to hypocalcemia when substances bind to calcium ions.

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29
Q

Blood Transfusions and Hypocalcemia

A
  • Blood transfusions contain citrate, which acts as an anticoagulant.
  • Large amounts of citrate can chelate calcium, leading to citrate-induced hypocalcemia.
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30
Q

Hypokalemia and hyperkalemia present with

A

Arrhythmias and muscle weakness.

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31
Q

Hypercalcemia presents with

A

Polyuria, nephrolithiasis, bone pain, abdominal pain, and altered mental status.

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32
Q

Hyponatremia presents with

A

Nausea, vomiting, headache, altered mental status, and seizures/coma if severe.

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33
Q

Hypokalemia in Hypomagnesemia

A

In the setting of hypomagnesemia, hypokalemia may persist until magnesium levels are corrected.

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34
Q

Importance of Magnesium Replacement

A

Always replace magnesium first in cases of hypokalemia with hypomagnesemia, as potassium levels will not improve with low magnesium.

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35
Q

Mechanism of Magnesium and Potassium Interaction

A
  • Magnesium normally inhibits the ROMK potassium channel in the renal collecting duct.
  • Low magnesium removes this inhibition, leading to excess potassium secretion into the urine.
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36
Q

Is the proper step after magnesium is repleted.

A

Replacing potassium

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37
Q

In cases in which the kidney is suspected to be responsible for an electrolyte abnormality, urinary electrolytes can be measured. Alcoholics typically develop electrolyte abnormalities through

A

Poor nutrition and gastrointestinal losses.

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38
Q

Differential Diagnosis for Hypocalcemia

A

Key Causes:
- Hypoparathyroidism
- Renal Failure
- Pancreatitis
- Vitamin D Deficiency
- Hypomagnesemia

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39
Q

Chronic Kidney Disease and Hypocalcemia

A

Abnormal renal function (elevated BUN and creatinine) suggests chronic kidney disease, which can cause hypocalcemia and hyperphosphatemia.

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40
Q

Role of 1α-Hydroxylase

A

Key Mechanism:
- Proximal tubular cells in the kidney contain 1α-hydroxylase, responsible for producing active vitamin D.
- Without active vitamin D, calcium absorption from the GI tract is impaired.

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41
Q

Consequences of Poor Renal Function

A
  • Inadequate excretion of phosphate leads to hyperphosphatemia.
  • This results in hypocalcemic hyperphosphatemia.
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42
Q

Parathyroid Hormone (PTH) Response

A

Low calcium levels lead to elevated PTH, but poor renal function prevents restoration of calcium-phosphate homeostasis.

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43
Q

Acute pancreatitis can cause hypocalcemia through saponification of peripancreatic fat. Necrosis frees fatty acids from triglycerides in adipose tissue. Free fatty acids bind calcium, forming insoluble salts in a process called

A

Saponification.

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44
Q

Causes of Hypercalcemia

A

Hypercalcemia can have various etiologies. Incidental hypercalcemia in a middle-aged female often indicates primary hyperparathyroidism.

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45
Q

Primary Hyperparathyroidism

A

Most common cause of “outpatient” hypercalcemia in healthy, younger patients.
Phosphate levels may be low, but often remain at the low end of normal range.

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46
Q

Etiology of Primary Hyperparathyroidism

A

Key Causes:
- Parathyroid Adenoma (80%)
- Parathyroid Hyperplasia (15-20%)
- Parathyroid Carcinoma (<1%)

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47
Q

Surgical Management: Hyperparathyroidism

A

Patients who are good surgical candidates typically undergo removal of the hyperfunctioning parathyroid gland.

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48
Q

Patients with primary hyperparathyroidism may not exhibit significant past medical history or presenting symptoms.

A

Incidental findings are common.

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49
Q

Is the most likely cause of hypercalcemia found in older, hospitalized patients.

A

Malignancy

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50
Q

Can cause hypercalcemia through excess bone turnover.

A

Hyperthyroidism

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51
Q

Can cause hypercalcemia, however, this patient denies taking any supplements.

A

Hypervitaminosis D

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52
Q
  • Occurs due to significant blood loss, often in trauma situations.
  • Characterized by decreased effective circulating volume (ECV) and decreased cardiac output.
A

Hypovolemic Shock Overview

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53
Q

Abdominal Findings in Trauma

A
  • Abdominal bleeding can irritate the peritoneal lining.
  • Symptoms include rebound tenderness and guarding.
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54
Q

Physiological Response to Hypovolemic Shock

A
  • Increased sympathetic tone.
  • Activation of the renin-angiotensin-aldosterone system (RAAS).
  • Resulting actions: renal salt and water retention, vasoconstriction.
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55
Q

Differential Diagnosis for Low ECV

A
  • Similar findings in cardiogenic shock, cirrhosis, and heart failure.
    Key difference: Cirrhosis and heart failure patients have increased total body water despite low ECV.
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56
Q

Response to Increased Effective Circulating Volume

A
  • Patients with increased ECV show decreased sympathetic tone and RAAS activity.
  • This is a normal physiological response to maintain homeostasis.
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57
Q

Hypervolemia in Cirrhosis

A
  • Patients develop excess total body water.
  • Physical exam findings: ascites and peripheral edema.
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58
Q

Pathophysiology of Cirrhosis

A
  • Begins with hepatic fibrosis and elevated portal venous pressures.
  • Portal hypertension leads to splanchnic and peripheral vasodilation.
  • Results in low systemic vascular resistance.
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59
Q

Hemodynamic Changes in Cirrhosis

A
  • Low peripheral resistance due to increased vasodilatory molecules.
  • Development of portosystemic collateral shunts contributes to changes.
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60
Q

Effects of Vasodilation in Cirrhosis

A
  • Decreased effective circulating volume (ECV).
  • Activation of the renin-angiotensin-aldosterone system (RAAS).
  • Leads to volume retention and hypervolemia.
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61
Q

Hyponatremia in Cirrhosis

A
  • Result of low ECV and non-osmotic release of antidiuretic hormone (ADH).
  • Excess free water retention due to high ADH activity.
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62
Q

Hyponatremia and Small-Cell Lung Carcinoma

A

Recent diagnosis of small-cell lung carcinoma is associated with hyponatremia.
- Consistent with SIADH (syndrome of inappropriate anti-diuretic hormone secretion).

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63
Q

Mechanism of SIADH

A
  • Elevated antidiuretic hormone (ADH) levels despite low serum sodium.
  • Causes water retention, leading to hyponatremia.
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64
Q

Renin-Angiotensin-Aldosterone System (RAAS) in SIADH

A
  • RAAS is down-regulated due to water retention.
  • Results in sodium and water excretion, helping maintain volume status.
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65
Q

Volume Status in SIADH

A
  • Patients with SIADH have normal volume status.
  • No evidence of volume contraction (dry mucous membranes, low blood pressure) or volume expansion (rales, edema, ascites).
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66
Q

Can develop hyponatremia secondary to the non-osmotic release of ADH. In this situation, low volume status is the driving force for ADH release, which can result in an increased total body free water relative to total body sodium (i.e. low total body water but excess total body water relative to sodium), and therefore hyponatremia.

A

Patients with hypovolemia from various causes (i.e. renal loss, gastrointestinal loss, bleeding) c

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67
Q

Heart Failure and Cardiac Output

A
  • Heart failure results in poor cardiac output.
  • Leads to low effective circulating volume (ECV).
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68
Q

Activation of Compensatory Mechanisms in Heart Failure

A
  • Low ECV triggers activation of the sympathetic nervous system.
  • Renin-angiotensin-aldosterone system (RAAS) is also activated.
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69
Q

Volume Retention in Heart Failure

A
  • Activation of compensatory mechanisms results in volume retention.
  • Patients become hypervolemic despite low ECV.
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70
Q

Discordance Between Volume Status and Effective Circulating Volume

A
  • In heart failure, elevated volume status is not reflected in ECV.
  • Healthy hearts would show increased ECV with similarly increased volume.
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71
Q

Diarrhea and Fluid Loss

A
  • Diarrhea results in loss of both water and electrolytes.
  • Can lead to decreased total body water and sodium.
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72
Q

Serum Sodium in Gastrointestinal Loss

A
  • Low-normal serum sodium indicates isotonic fluid loss.
  • Total body water and sodium decrease proportionally, maintaining normal serum sodium.
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73
Q

Assessment of Total Body Sodium

A
  • Normal serum sodium does not indicate normal total body sodium.
  • Total body sodium is assessed through clinical volume status.
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74
Q

Indicators of Hypovolemia and Hypervolemia

A

Hypovolemia: dry mucous membranes indicate low total body sodium.
Hypervolemia: ascites and peripheral edema indicate high total body sodium.

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75
Q

SIADH and Body Sodium/Water Status

A
  • SIADH leads to increased total body water and normal total body sodium.
  • Normal serum sodium can coexist with excess water in this condition.
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76
Q

Diabetes Insipidus (DI) Overview

A
  • Characterized by polydipsia (increased thirst) and hypernatremia.
  • Results from the kidneys’ inability to retain free water.
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77
Q

Causes of Diabetes Insipidus

A

Central DI: Lack of ADH production (can be idiopathic or due to neurologic insult).
Nephrogenic DI: Renal tubular resistance to ADH.

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78
Q

Nephrogenic DI and Medications

A

Can be caused by drugs, notably lithium (used in bipolar disorder).
- Leads to resistance to ADH, resulting in excessive free water excretion.

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79
Q

Clinical Presentation of Nephrogenic DI

A
  • Symptoms include polydipsia and hypernatremia.
  • Urinary osmolarity will be low due to inability to concentrate urine.
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80
Q

Diagnostic Indicators of DI

A
  • Hypernatremia indicates water loss exceeds intake.
  • Low urinary osmolarity suggests nephrogenic DI.
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81
Q

Occurs when massive excess free water is consumed. This may be a complication of psychiatric disorders but causes hyponatremia not hypernatremia through excess free water intake.

A

Psychogenic polydipsia

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82
Q

Refers to hyponatremia among alcoholics through excessive free water intake, as beer is electrolyte poor.

A

Beer potomania

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83
Q

Hyperaldosteronism can rarely cause hypernatremia, but more commonly leads to

A

Hypokalemia

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84
Q

Hypernatremia Overview

A
  • Common in elderly patients, especially during acute illnesses.
  • Characterized by elevated serum sodium levels.
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85
Q

Causes of Hypernatremia

A
  • Often due to inadequate water intake.
  • Can occur with excessive fluid loss (e.g., from diarrhea, sweating).
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86
Q

Management of Hypernatremia

A
  • Treatment involves hypotonic fluid supplementation.
  • Options include oral free water, 5% dextrose in water, or 0.45% NaCl (half-normal saline).
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87
Q

Correction Rate for Hypernatremia

A
  • Sodium should not be lowered faster than 12 mEq/L/day.
  • No more than 1 mEq/L/hour to prevent cerebral edema.
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88
Q

Cerebral Adaptation in Hypernatremia

A
  • The brain adapts by accumulating organic osmoles to minimize fluid loss.
  • Rapid correction of hypernatremia can lead to cerebral edema as osmoles are slow to leave cells.
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89
Q

Risks of Rapid Correction of Hypernatremia

A
  • Rapid sodium correction can cause CNS fluid shifts and edema.
  • Slow correction is essential to prevent complications.
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90
Q

Extreme hypermagnesemia can put patients at risk for respiratory depression and cardiac arrest. The clinical scenario where magnesium can reach levels this high is in the management of patients with ? with magnesium infusion therapy.

A

Preeclampsia/eclampsia

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91
Q

Central pontine myelinolysis is associated with rapid correction of

A

Hyponatremia

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92
Q

Is a rare condition in which tissues become calcified due to high serum levels of calcium and phosphate.

A

Calciphylaxis

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93
Q

SIADH Overview

A
  • Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) results in elevated ADH levels.
  • Leads to water retention, concentrated urine, and hyponatremia.
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94
Q

Common Causes of SIADH

A
  • Medications: Carbamazepine is a notable cause.
  • CNS disturbances: Stroke, trauma.
  • Paraneoplastic disorders: Small cell lung cancer.
    Lung pathology and postoperative states.
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95
Q

Urinary Findings in SIADH

A
  • Urine osmolarity is elevated (normal range: 50–1200 mOsm/kg).
  • Urinary sodium concentrations are usually high due to retained water.
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96
Q

Urine Sodium Levels

A
  • Urine sodium <20 mEq/L indicates high sympathetic nervous system (SNS) and RAAS activity (sodium reabsorption).
  • In SIADH, urine sodium is typically high because ADH causes water retention without activating SNS or RAAS.
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97
Q

Symptoms of Hyponatremia

A
  • Nonspecific symptoms: Altered mental status, headache, nausea.
  • Severe cases can lead to neurological complications.
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98
Q

Management of Hyponatremia

A
  • Initial treatment: Free water restriction.
  • Hypertonic saline can be used for severe hyponatremia.
  • Monitor sodium levels to avoid rapid correction, which can cause central pontine myelinolysis.
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99
Q

Risk of Rapid Sodium Correction

A
  • Rapid correction of sodium levels can lead to serious neurological complications.
  • Gradual correction is essential for safe treatment.
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100
Q

Primary Polydipsia Overview

A
  • Also known as psychogenic polydipsia.
  • Characterized by excessive consumption of free water.
  • Often associated with psychiatric disorders or hypothalamic lesions.
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101
Q

Mechanism of Primary Polydipsia

A
  • Abnormal thirst response leads to excessive water intake.
  • ADH (antidiuretic hormone) release is suppressed due to high free water levels.
  • Results in maximally dilute urine production.
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102
Q

Effects on Serum Sodium

A
  • Hyponatremia may develop if free water intake exceeds renal excretion capacity.
    Sodium levels decrease as water dilutes serum sodium.
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103
Q

Management of Primary Polydipsia

A
  • Treatment involves free water restriction.
  • Goal is to reduce fluid intake to allow sodium levels to normalize.
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104
Q

Clinical Considerations

A
  • Monitor for symptoms of hyponatremia: headache, confusion, seizures.
  • Important to differentiate from diabetes insipidus, where ADH is ineffective.
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105
Q

Causes of Hyponatremia in Gastrointestinal Illness

A
  • Volume depletion due to diarrhea leads to sodium loss.
  • Non-osmotic release of ADH occurs, causing renal free water retention.
  • Hyponatremia can develop if water intake exceeds water losses.
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106
Q

Mechanisms of Hyponatremia

A

GI sodium loss + renal water retention = hyponatremia.
- Patients may consume free water to combat thirst, worsening hyponatremia.

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107
Q

Urine Concentration in GI Illness

A
  • Elevated ADH activity causes urine to become concentrated.
  • Despite concentrated urine, urinary sodium may be low due to volume depletion.
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108
Q

Role of SNS and RAAS

A
  • Activation of the sympathetic nervous system and renin-angiotensin-aldosterone system in response to volume depletion drives sodium reabsorption.
  • Results in low urinary sodium concentration, even in the presence of elevated ADH.
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109
Q

Clinical Implications

A
  • Important to monitor electrolytes in patients with GI illnesses.
  • Educate patients about maintaining electrolyte intake, especially if experiencing diarrhea.
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110
Q

Hypernatremia Differential Diagnosis

A
  • Excess free water loss (renal, gastrointestinal, pulmonary).
  • Diabetes insipidus (DI) is characterized by polyuria and polydipsia.
  • Other causes: primary hyperaldosteronism, excess glucocorticoids.
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111
Q

Types of Diabetes Insipidus

A

Central DI: Decreased ADH production (pituitary issue).
Nephrogenic DI: Renal resistance to ADH.
Both types lead to dilute urine and hypernatremia.

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112
Q

Water Deprivation Test

A
  • Differentiates between central and nephrogenic DI.
  • Patients with DI will not concentrate urine with water restriction.
  • Healthy individuals will show increased urine osmolality.
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113
Q

Desmopressin Administration

A
  • Desmopressin is an ADH analog.
  • An increase of >50% in urine osmolality indicates central DI.
  • No significant change suggests nephrogenic DI.
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114
Q

Clinical Implications of DI

A
  • Recognize symptoms: polyuria, polydipsia, hypernatremia.
  • Appropriate testing (water deprivation, desmopressin) is crucial for diagnosis.
  • Manage underlying causes and ensure proper hydration.
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115
Q

Definition of Pseudohyponatremia

A
  • Mild hyponatremia with normal serum osmolality.
  • A laboratory artifact rather than a true electrolyte disturbance.
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116
Q

Differentiating Hyponatremia

A

True Hyponatremia: Decreased serum osmolality correlating with low sodium levels.
Pseudohyponatremia: Normal serum osmolality despite low sodium levels.

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117
Q

Causes of Pseudohyponatremia

A
  • Occurs with very high protein levels (e.g., multiple myeloma).
  • Also associated with hyperlipidemia.
  • Increased solids in plasma lead to underestimation of sodium concentration.
118
Q

Laboratory Measurements

A
  • Sodium is an osmole; low sodium should decrease serum osmolality in true hyponatremia.
  • Normal osmolality indicates no true disturbance in body water vs. sodium balance.
119
Q

Clinical Relevance

A
  • Recognizing pseudohyponatremia is crucial to avoid unnecessary treatments.
  • Assess the clinical context and consider potential causes of elevated protein or lipids.
120
Q

Causes of Hyponatremia

A
  • Likely caused by SIADH associated with small cell lung carcinoma.
  • SIADH leads to water retention and dilutional hyponatremia.
121
Q

Treatment for Severe Hyponatremia

A
  • Hypertonic saline is used for treatment.
  • Caution is needed to avoid rapid correction.
122
Q

Guidelines for Sodium Correction

A
  • Correct sodium no faster than 0.5 mEq/L/hr.
  • Maximum increase of 8 mEq/L over 24 hours to prevent osmotic demyelination syndrome (ODS).
123
Q

Osmotic Demyelination Syndrome (ODS)

A
  • Caused by rapid fluid shifts out of glial cells, leading to cellular damage.
  • Clinical symptoms may develop days after sodium correction.
124
Q

Clinical Manifestations of ODS

A
  • Symptoms include dysarthria, dysphagia, altered mental status, and paraparesis.
  • Severe cases may lead to “locked-in syndrome,” where the patient is conscious but cannot move or speak.
125
Q

Prognosis of ODS

A
  • Neurologic deficits are typically irreversible.
  • Emphasizes the importance of careful management of sodium levels.
126
Q

What are the key features and management for acute uncomplicated cystitis?

A

This patient shows classic UTI symptoms (dysuria, increased urinary frequency) with positive leukocyte esterase on urinalysis. She can be diagnosed with acute uncomplicated cystitis and started on empiric therapy (e.g., trimethoprim-sulfamethoxazole, nitrofurantoin). It’s generally unnecessary to isolate the organism before starting treatment.

127
Q

Mechanism of Proteinuria in MCD

A
  • Loss of heparan sulfate from the basement membrane.
  • Heparan sulfate is negatively charged, contributing to the charge barrier that repels albumin.
128
Q

Components of the Glomerular Filtration Barrier

A
  • Composed of endothelial cells, basement membrane, and podocyte foot processes.
  • Filtration is restricted by both charge and size selectivity.
129
Q

Characteristics of Proteinuria in MCD

A
  • Causes “selective proteinuria,” primarily losing albumin.
  • Unlike other nephrotic syndromes, where both structural and charge components are lost.
130
Q

Comparison of Nephrotic Syndromes

A
  • MCD leads to selective loss of albumin.
  • Other causes of nephrotic syndrome typically result in a broader spectrum of protein loss.
131
Q

Urine Dipstick and Hematuria

A
  • A dipstick showing large amounts of blood suggests hematuria.
  • Urine microscopy showing no red blood cells contradicts the dipstick results.
132
Q

Interpretation of Urine Dipstick

A
  • Urine dipsticks detect hemoglobin and myoglobin, reporting them as “blood.”
  • Presence of myoglobin can occur without red blood cells in urine.
133
Q

Myoglobin in Urine

A
  • Myoglobin is filtered into urine, leading to a positive dipstick for blood.
  • Typically indicates muscle breakdown rather than kidney bleeding.
134
Q

Rhabdomyolysis

A
  • Involves breakdown of myocytes, releasing muscle contents into circulation.
  • Common causes include trauma, leading to myoglobinuria and dark urine.
135
Q

Clinical Presentation of Rhabdomyolysis

A
  • Symptoms may include dark urine, muscle pain, and weakness.
  • Urine may test positive for blood due to myoglobin presence.
136
Q

Urine Dipstick for Blood

A

A positive dipstick indicates the presence of heme, typically from hemoglobin in red blood cells.
- Urine microscopy is needed to confirm the source of blood.

137
Q

Dysmorphic Red Blood Cells

A
  • Dysmorphic red blood cells indicate glomerular bleeding.
  • Red blood cells become misshapen as they pass through the nephron lumen.
138
Q

Red Blood Cell Casts

A
  • Presence of red blood cell casts in urine confirms glomerular source of bleeding.
  • Indicates damage to the glomerular filtration barrier.
139
Q

Lupus and Glomerulonephritis

A
  • Lupus can cause glomerulonephritis due to immune complex deposition.
  • This leads to disruption of the glomerular filtration barrier and bleeding.
140
Q

Urinary Findings in Lupus Glomerulonephritis

A
  • Patients with lupus may exhibit dysmorphic red blood cells and red blood cell casts in urine.
    These findings are indicative of glomerular inflammation and damage.
141
Q

Nephrolithiasis is a possible cause of hematuria, which can result from bleeding at the site of stone impaction. Possible sites include the

A

Renal calyces or the ureters.

142
Q

Nephrotic Syndrome Overview

A
  • Characterized by edema and proteinuria >3.5 grams in 24-hour urine collection.
  • Common causes include HIV (focal segmental glomerulosclerosis) and hepatitis C (membranous nephropathy).
143
Q

Pathophysiology of Edema in Nephrotic Syndrome

A
  • Loss of protein decreases plasma oncotic pressure.
  • Fluid shifts from capillaries to tissue beds lead to edema.
144
Q

Response to Edema in Nephrotic Syndrome

A
  • Decreased intravascular volume activates the renin-angiotensin-aldosterone system (RAAS).
  • RAAS activation causes sodium and water retention, worsening edema.
145
Q

Effects of RAAS Activation

A
  • Increases total body water.
  • Contributes to the cycle of edema formation in nephrotic syndrome.
146
Q

Membranous Nephropathy Overview

A
  • A cause of nephrotic syndrome.
  • Characterized by significant proteinuria and edema.
147
Q

Hypercoagulable State in Nephrotic Syndrome

A
  • Increased risk of thrombosis, including renal vein thrombosis.
  • Mechanisms include urinary loss of antithrombin and low plasminogen activity.
148
Q

Renal Vein Thrombosis Symptoms

A
  • Often asymptomatic but may present with flank pain and hematuria.
  • Right-sided thrombosis can lead to varicocele due to venous backup.
149
Q

Varicocele and Renal Vein Thrombosis

A
  • Right-sided varicoceles are rare and usually caused by retroperitoneal pathology.
  • Renal vein thrombosis has a strong association with nephrotic syndrome.
150
Q

Membranoproliferative Glomerulonephritis (MPGN) Overview

A
  • Characterized by hematuria, red blood cell casts, and variable proteinuria.
  • Can present as nephritic syndrome, nephrotic syndrome, or both.
151
Q

Diagnostic Confirmation of MPGN

A

Renal biopsy is the best confirmatory diagnostic test.
Pathologic findings specific to MPGN will be observed on biopsy.

152
Q

Common Etiologies of Type I MPGN

A
  • Most commonly associated with hepatitis B or C infections.
  • Screening for viral hepatitis is essential in patients with risk factors.
153
Q

Indications for Hepatitis Screening

A
  • IV drug use is a key risk factor for hepatitis screening.
  • One-time hepatitis C screening recommended for all “baby boomers” (born 1945-1965).
154
Q

Importance of Hepatitis Screening

A
  • High prevalence of asymptomatic hepatitis C among older adults due to historical infection control issues.
  • Early detection can aid in management and prevent complications.
155
Q

Type II Membranoproliferative Glomerulonephritis (Dense Deposit Disease) Overview

A
  • Characterized by renal failure and unique pathology findings.
  • Pathology includes dense deposits along the basement membrane.
156
Q

Electron Microscopy Findings in Type II MPGN

A
  • Continuous, dense deposits observed in the glomeruli and tubules.
  • Complement deposition without significant immunoglobulin detected on immunostaining.
157
Q

Pathophysiology of Type II MPGN

A
  • Related to C3 nephritic factor, an antibody that stabilizes C3 convertase.
  • Results in excessive complement activation and deposition in the glomerular basement membrane.
158
Q

Complement Levels in Type II MPGN

A
  • Patients typically present with low plasma complement levels.
  • Ongoing complement activation leads to depletion of complement in the serum.
159
Q

Clinical Presentation of Dense Deposit Disease

A
  • Renal failure as a common manifestation.
  • May present with features of nephritic syndrome or nephrotic syndrome.
160
Q

Results in hyaline material deposited throughout the glomeruli on light microscopy.

A

Renal amyloidosis

161
Q

Antibodies against podocyte phospholipase A2 are seen in

A

Idiopathic membranous nephropathy.

162
Q

Antibodies against glomerular basement membrane collagen are seen in

A

Goodpasture’s disease.

163
Q

Type I Membranoproliferative Glomerulonephritis (MPGN) Overview

A
  • Can present with features of both nephritic and nephrotic syndromes.
  • Characterized by renal biopsy findings showing mesangial and endothelial proliferation.
164
Q

Clinical Features of Type I MPGN

A
  • Symptoms may include hypertension and worsening renal failure.
  • Laboratory findings often include red blood cell casts and dysmorphic red blood cells (indicative of nephritic syndrome).
165
Q

Proteinuria in Type I MPGN

A
  • Protein levels can be in the nephrotic range (greater than 3.5 g/24 hours).
  • This contributes to edema and other features associated with nephrotic syndrome.
166
Q

Nephritic vs. Nephrotic Syndrome in MPGN

A
  • Nephritic syndrome: Characterized by hematuria, hypertension, and renal impairment.
  • Nephrotic syndrome: Characterized by significant proteinuria, hypoalbuminemia, and edema.
167
Q

Diagnosis of Type I MPGN

A

Confirmed through renal biopsy.
Immunofluorescence may show complement and immunoglobulin deposition.

168
Q

IgA Nephropathy Overview

A
  • A common cause of glomerulonephritis, particularly in young adults.
  • Characterized by the presence of IgA deposits in the mesangial region of the glomeruli.
169
Q

Clinical Presentation of IgA Nephropathy

A
  • Often presents with hematuria following an upper respiratory infection.
  • Patients may report previous episodes of similar hematuria.
170
Q

Urinalysis Findings in IgA Nephropathy

A
  • Urinalysis typically shows red blood cells, proteinuria, and red cell casts.
  • Findings are consistent with nephritic syndrome.
171
Q

Diagnosis of IgA Nephropathy

A

-Confirmed by kidney biopsy.
- Biopsy reveals mesangial IgA deposits, often with accompanying mesangial hypercellularity.

172
Q

Pathophysiology of IgA Nephropathy

A
  • Impaired clearance of IgA leads to deposition in the kidneys.
  • Associated with abnormal immune responses, particularly following infections.
173
Q

Post-Streptococcal Glomerulonephritis (PSGN) Overview

A
  • Occurs 2-3 weeks after a streptococcal infection (pharyngitis or skin infection).
  • Characterized by sudden onset of hematuria, proteinuria, and hypertension.
174
Q

Laboratory Findings in PSGN

A
  • Low complement levels, particularly C3.
  • Elevated antistreptolysin O (ASO) titers indicating recent streptococcal infection.
175
Q

Pathological Findings in PSGN

A
  • Biopsy shows subepithelial humps of C3 complement.
  • Commonly presents with red blood cell casts.
176
Q

Differentiating IgA Nephropathy from PSGN

A
  • IgA nephropathy often presents within days of an upper respiratory infection.
  • PSGN has a delayed onset (2-3 weeks) after streptococcal infection.
177
Q

Key Clinical Features of IgA Nephropathy

A
  • Frequent episodes of hematuria, especially after infections.
  • Typically, normal complement levels; diagnosis confirmed with mesangial IgA deposits on biopsy.
178
Q

Alport’s Syndrome Overview

A
  • Genetic disorder characterized by hematuria, sensorineural hearing loss, and visual disturbances.
  • Associated with progressive renal failure and nephritic syndrome.
179
Q

Pathophysiology of Alport’s Syndrome

A
  • Caused by mutations in type IV collagen, essential for the glomerular basement membrane.
  • Defects lead to compromised kidney function, hearing loss, and ocular issues.
180
Q

Inheritance Pattern: Alport’s Syndrome

A

Typically X-linked inheritance (80% of cases), affecting males more severely.
Females with one mutated gene may have hematuria but usually experience milder symptoms.

181
Q

Clinical Features of Alport’s Syndrome

A

Renal: Hematuria, progressive renal failure.
Audiological: High-pitched sensorineural hearing loss.
Ocular: Worsening visual acuity.

182
Q

Diagnosis of Alport’s Syndrome

A
  • Family history often present.
  • Renal biopsy may show characteristic changes in the glomerular basement membrane.
183
Q

Lupus Nephritis Overview

A

Patients with lupus may develop renal failure due to various mechanisms, including diffuse proliferative glomerulonephritis, membranous nephropathy, and RPGN.

184
Q

Rapidly Progressive Glomerulonephritis (RPGN)

A
  • Characterized by a rapid decline in renal function (often within weeks).
  • Pathological hallmark: crescent formation in glomeruli composed of fibrin.
185
Q

Pathology of RPGN

A
  • Crescents in RPGN consist of fibrin and inflammatory cells (macrophages, T-cells).
  • Immune complex deposition leads to breaks in the glomerular basement membrane, allowing for inflammatory infiltration.
186
Q

Clinical Presentation of RPGN in Lupus

A
  • Rapid decline in renal function over weeks.
  • Symptoms may include edema, hypertension, and signs of acute kidney injury.
187
Q

Treatment of RPGN

A
  • Treatment typically involves immunosuppressive therapy and plasmapheresis.
  • Renal replacement therapy (dialysis or kidney transplant) may be required due to severe renal failure.
188
Q

Key Differences in Lupus Nephritis Types

A
  • RPGN presents with rapid progression and crescentic changes.
  • Other types (like diffuse proliferative glomerulonephritis) may progress more slowly and have different histological findings.
189
Q

Post-Streptococcal Glomerulonephritis Overview

A
  • Occurs 2-3 weeks after a streptococcal throat or skin infection.
  • Common symptoms: hematuria, decreased urine output.
190
Q

Symptoms and Lab Findings: Post-Streptococcal Glomerulonephritis

A
  • Presents with nephritic syndrome: hematuria, proteinuria, hypertension, and edema.
  • Laboratory findings include low complement levels and elevated anti-streptolysin O (ASO) and anti-DNase B titers.
191
Q

Pathogenesis of PSGN

A
  • Immune complexes form and deposit in the glomerular basement membrane.
  • This leads to inflammation and significant complement activation and fixation.
192
Q

Complement Levels in PSGN

A
  • Low complement levels (especially C3) due to consumption during the immune response.
  • Monitoring complement levels can aid in diagnosis and assessing disease activity.
193
Q

Differential Diagnosis: PSGN

A

Important to differentiate PSGN from other forms of glomerulonephritis like IgA nephropathy, which typically presents differently and may follow upper respiratory infections.

194
Q

Treatment of PSGN

A

Supportive care: managing hypertension and edema.
Most patients recover spontaneously; severe cases may require more intensive management.

195
Q

Goodpasture’s Disease Overview

A
  • Characterized by renal disease and hemoptysis.
  • Caused by auto-antibodies against the alpha-3 chain of type IV collagen.
196
Q

Goodpasture’s Disease Clinical Presentation

A
  • Commonly presents with nephritic syndrome: hematuria, red cell casts, dysmorphic red cells, and nephritic-level proteinuria (< 3.5 g/24-hour collection).
  • Pulmonary symptoms include dyspnea and hemoptysis due to alveolar hemorrhage.
197
Q

Goodpasture’s Disease Urinalysis Findings

A
  • Urinalysis shows red blood cell casts and dysmorphic red blood cells.
  • Proteinuria typically falls under nephritic levels (< 3.5 g/24 hours).
198
Q

Goodpasture’s Disease Laboratory Findings

A
  • Elevated serum creatinine indicates renal failure.
  • Presence of anti-glomerular basement membrane (GBM) antibodies supports the diagnosis.
199
Q

Goodpasture’s Disease Epidemiology

A
  • Most frequently seen in young adult males.
  • Can occur in the context of previous viral infections or exposure to certain toxins.
200
Q

Goodpasture’s Disease Treatment Options

A
  • Treatment includes immunosuppressive therapy (e.g., corticosteroids, cyclophosphamide).
  • Plasmapheresis may be indicated to remove circulating antibodies.
201
Q

Auto-antibodies to DNA occur at part of

A

Systemic lupus erythematosus.

202
Q

Antibodies against the phospholipase A2 receptor are found in many patients with

A

Idiopathic membranous nephropathy.

203
Q

Auto-antibodies against Smith antigens may occur in patients with systemic lupus erythematosus (SLE) or mixed connective tissue disease. Smith antigens are nuclear proteins. These autoantibodies are highly specific for SLE but occur in only about

A

30% of patients

204
Q

Nephrotic Syndrome Overview

A
  • Characterized by progressive periorbital and peripheral edema, possible abdominal ascites, and pleural effusions.
  • Urinalysis shows significant proteinuria and fatty bodies.
205
Q

Minimal Change Disease in Children

A
  • Most common cause of nephrotic syndrome in children under six.
  • Triggered by inflammatory cytokines leading to effacement of foot processes in podocytes.
206
Q

Triggers for Minimal Change Disease

A
  • Often follows upper respiratory infections, recent vaccinations, or Hodgkin lymphoma.
  • These triggers release cytokines that contribute to the disease process.
207
Q

Histopathology of Minimal Change Disease

A
  • Light microscopy typically shows normal glomeruli.
  • Effacement of foot processes is seen on electron microscopy, not light microscopy.
208
Q

Acute Renal Failure and Symptoms

A
  • Elevated serum creatinine indicates acute renal failure.
  • Symptoms can include malaise and confusion.
209
Q

Nephrotic Syndrome Indicators

A
  • Fatty casts and significant proteinuria suggest nephrotic syndrome.
  • Common in various conditions, including HIV-related diseases.
210
Q

HIV and Nephrotic Syndrome

A
  • The most common cause of nephrotic syndrome in HIV patients is focal segmental glomerulosclerosis (FSGS).
  • Approximately 75% of HIV patients with nephrotic-range proteinuria have FSGS upon biopsy.
211
Q

Collapsing Variant of FSGS

A
  • HIV-associated FSGS is often referred to as the “collapsing variant.”
  • Characterized by widespread collapse and sclerosis of glomeruli.
  • Leads to rapidly progressive kidney failure.
212
Q

Renal Amyloidosis Secondary to Multiple Myeloma

A

Laboratory Findings: Renal failure and nephrotic range proteinuria.
Biopsy Results: Renal biopsy reveals glomerular deposition of hyaline material staining positive with Congo red, indicative of amyloid.
Microscopic Findings: Diffuse deposition of amorphous eosinophilic material in the mesangium and capillary loops.

213
Q

Association with Multiple Myeloma

A

Symptoms: Patient presents with hypercalcemia and focal back pain, suggestive of multiple myeloma.
Pathophysiology: Abnormal clonal proliferation of plasma cells in multiple myeloma can lead to AL amyloidosis.
Complications: Amyloidosis can cause various end-organ complications, including significant renal impairment.

214
Q

What are the key features and causes of primary membranous nephropathy (MN)?

A

MN presents as nephrotic syndrome, primarily affecting non-diabetic males. Approximately 75% of cases are idiopathic, with secondary causes including systemic lupus erythematosus, hepatitis B/C, syphilis, malignancies, and certain drugs (e.g., gold, penicillamine).

215
Q

What is the pathophysiology of primary MN and how is it diagnosed?

A

Idiopathic MN is caused by auto-antibodies against podocyte proteins, particularly the phospholipase A2 receptor. Diagnosis is increasingly made via serum antibody testing due to its high specificity, often reducing the need for renal biopsy.

216
Q

What is minimal change disease, and what are its classic features in children?

A

Minimal change disease is the most common cause of nephrotic syndrome in children, characterized by podocyte foot process effacement. Patients typically present with edema, proteinuria, and normal renal function.

217
Q

How does minimal change disease affect podocytes?

A

In minimal change disease, the foot processes of podocytes become effaced, leading to significant proteinuria.

218
Q

What is renal papillary necrosis, and what are its common causes?

A

Renal papillary necrosis is characterized by acute onset of asymptomatic gross hematuria, often presenting with white flecks in urine. Common causes include sickle cell disease, pyelonephritis, NSAID use, and diabetes mellitus, all of which can lead to renal ischemia.

219
Q

How does renal papillary necrosis typically present, and what symptoms are associated with it?

A

It typically presents with painless gross hematuria and may show sloughed necrotic tissue in urine. The condition is usually asymptomatic unless necrotic tissue causes urinary obstruction.

220
Q

What are the typical clinical findings associated with acute interstitial nephritis (AIN)?

A

AIN commonly presents with acute kidney injury (elevated serum BUN and creatinine), low-grade fever, and a maculopapular rash, usually developing 1-3 weeks after exposure to certain medications.

221
Q

What are common causes of AIN and how is it managed?

A

Common causes include sulfa drugs, penicillins, cephalosporins, rifampin, NSAIDs, and proton pump inhibitors. Management primarily involves discontinuing the offending drug, and corticosteroids may be used in severe cases.

222
Q

What is the typical presentation and cause of acute tubular necrosis (ATN)?

A

ATN often follows hemorrhagic shock or surgery, leading to ischemia of the kidneys. This results in necrosis of tubular epithelial cells, sloughing off, and the formation of “muddy brown” casts.

223
Q

How can you differentiate between ATN and pre-renal azotemia based on lab findings?

A

ATN typically presents with a BUN/Cr ratio <20 and FeNa >3%, indicating intrinsic renal damage. In contrast, pre-renal azotemia usually shows a BUN/Cr ratio >20 and FeNa <1%, reflecting preserved tubular function.

224
Q

What electrolyte abnormalities are commonly associated with acute tubular necrosis (ATN)?

A

Typical findings in ATN include elevated BUN (uremia), hyperkalemia, and elevated anion gap metabolic acidosis.

225
Q

What occurs during the recovery phase of ATN regarding urinary output and electrolyte levels?

A

As tubular function recovers, patients may experience polyuria, leading to hypokalemia due to increased potassium excretion. They are also at risk of losing electrolytes like calcium and magnesium.

226
Q

What condition can develop from severe renal hypoperfusion during obstetric emergencies, and what are its characteristic findings?

A

Diffuse cortical necrosis can occur, characterized by a pale (white) outer cortex of the kidney, instead of the normal red/dark brown appearance.

227
Q

What are the potential causes and risks associated with diffuse cortical necrosis in pregnant patients?

A

It can arise from hypoperfusion due to obstetric catastrophes like placental abruption or amniotic fluid embolism, often accompanied by disseminated intravascular coagulation (DIC) and vasospasm. This condition has a high mortality rate due to rapid progression to anuria and uremic death.

228
Q

What is a key clinical indicator of post-renal obstructive kidney injury in a patient with an enlarged prostate?

A

Severely increased BUN and creatinine levels, along with symptoms such as decreased urine output and abdominal distension.

229
Q

What is the most important next step in managing a patient with post-renal obstructive kidney injury?

A

Place a bladder (Foley) catheter to bypass the obstruction and allow urine to drain, which can lead to rapid improvement in renal function.

230
Q

Why is diuresis important in heart failure exacerbations?

A

Diuresis is needed to restore normal volume status in hypervolemic states caused by heart failure.

231
Q

What can occur if too much volume is removed during diuresis in heart failure patients?

A

Excessive diuresis can lead to decreased effective circulating volume, reduced renal perfusion, and pre-renal acute kidney injury (AKI), indicated by an increased BUN/Cr ratio (e.g., 25).

232
Q

How does volume loss due to conditions like viral gastroenteritis lead to pre-renal acute kidney injury (AKI)?

A

Volume loss causes low renal perfusion, activating the renin-angiotensin-aldosterone system (RAAS). The kidneys retain sodium and water in response, resulting in decreased urinary sodium concentration (FeNa ≤ 1%) and elevated urine osmolality, as the urine becomes concentrated to preserve volume.

233
Q

How can you differentiate pre-renal azotemia from acute tubular necrosis (ATN) in volume-depleted patients?

A
  • Pre-Renal Azotemia: Characterized by low FeNa (≤ 1%), indicating effective sodium reabsorption and preserved urine osmolality as the kidneys concentrate urine to retain water and sodium.
  • Acute Tubular Necrosis (ATN): Features elevated FeNa (> 2-3%), indicating impaired sodium reabsorption due to tubular damage. Urine sodium concentration rises, and urine osmolality decreases because the tubules cannot effectively concentrate urine.

Both conditions can arise from hypoperfusion, but the urinary electrolytes help distinguish them based on their responses to low volume status.

234
Q

What complications are associated with uremia due to end-stage chronic kidney disease (CKD)?

A

Uremia can lead to pericarditis, encephalopathy, asterixis, and platelet dysfunction. Elevated BUN levels are linked to these complications, as uremic toxins impair platelet function, causing abnormal bleeding despite normal platelet counts and coagulation times (PT/PTT).

235
Q

How can platelet dysfunction in uremia be managed?

A

Management strategies include:

  • Hemodialysis: Often improves bleeding symptoms by reducing uremic toxins.
  • Desmopressin: Can be used to rapidly enhance platelet function if immediate correction is needed.

Platelet dysfunction typically manifests as bruising and superficial bleeding.

236
Q

What are the clinical features of uremic pericarditis?

A

Clinical features include:

  • Positional chest pain that is pleuritic and worsens when lying down.
  • Possible presence of a pericardial friction rub on auscultation.
  • Electrocardiogram (EKG) findings are often unremarkable, lacking the classic changes seen in other types of pericarditis (like PR depression or diffuse ST elevation).
  • Echocardiography typically reveals a pericardial fluid collection.
237
Q

How is uremic pericarditis managed?

A

The management of uremic pericarditis includes:

Urgent Dialysis: This is indicated and leads to rapid relief of symptoms and reduction in the size of the effusion.

238
Q

How does sodium balance manifest in a kidney donor?

A
239
Q

What happens to the fractional excretion of sodium (FENa) after nephrectomy?

A

After nephrectomy, her GFR decreases due to reduced nephron mass, leading to a lower amount of sodium filtered. Despite unchanged sodium excretion, the decrease in filtered sodium results in an increased FENa. For example, if her filtered load drops from 24,000 mEq/day to 14,000 mEq/day, her FENa increases from 0.4% to 0.7% to maintain sodium balance, illustrating that FENa rises after kidney donation.

240
Q

What does a urine gram stain showing gram-positive cocci suggest in UTI?

A

The presence of gram-positive cocci in the urine gram stain likely indicates Staphylococcus saprophyticus, a common cause of UTI, especially in sexually active young women.

241
Q

What should be avoided in a patient with a sulfa allergy being treated for a UTI?

A

Trimethoprim-sulfamethoxazole (TMP-SMX) should be avoided due to its sulfa content.

242
Q

What are appropriate alternative treatments for a UTI in a patient with a sulfa allergy?

A

Suitable alternatives include ciprofloxacin (a fluoroquinolone), amoxicillin-clavulanate, or an oral 2nd generation cephalosporin.

243
Q

What is vesicoureteral reflux, and what risks does it pose to children?

A

Vesicoureteral reflux is a structural defect where the ureters are abnormally inserted into the bladder, causing urine to reflux from the bladder back into the ureters. This condition increases the risk of recurrent urinary tract infections, pyelonephritis, hydronephrosis, and potential renal failure if not corrected.

244
Q

What is the gold standard screening test for vesicoureteral reflux?

A

The gold standard is the voiding cystourethrogram (VCUG), a fluoroscopic imaging test where contrast is injected into the urethra to check for abnormal ascent into the ureters.

245
Q

What is sterile pyuria, and what does it indicate?

A

Sterile pyuria is the presence of white blood cells in the urine (indicated by microscopy and positive leukocyte esterase) without bacterial growth on culture. It often suggests an underlying infection or inflammation, particularly from sexually transmitted diseases (STDs) like chlamydia and gonorrhea.

246
Q

What is the best test to evaluate sterile pyuria in sexually active patients?

A

The best test is an endourethral swab PCR for chlamydia and gonorrhea, as these are the most likely STDs associated with sterile pyuria. Other potential causes to consider include herpes virus, fungi, parasites, and tuberculosis.

247
Q

What is a renal abscess, and how does it typically develop?

A

A renal abscess is a complication of pyelonephritis, usually caused by the same organism responsible for the original infection. It presents with persistent fever, flank pain, and leukocytosis, often with a lack of improvement despite antibiotic treatment.

248
Q

How is a renal abscess diagnosed and treated?

A

Diagnosis is confirmed via CT imaging, which shows a walled-off renal or perinephric cavity. Treatment includes continued antibiotic therapy along with percutaneous or surgical drainage of the abscess.

249
Q

What are the key features and complications of adult onset polycystic kidney disease (ADPKD)?

A

ADPKD is an autosomal dominant disorder characterized by bilateral renal cysts, often presenting with hypertension, renal insufficiency, or hematuria. Extra-renal complications include hepatic cysts, cerebral “berry” aneurysms, cardiac valvular disease (e.g., mitral valve prolapse), and colonic diverticula.

250
Q

What are some significant extra-renal complications associated with ADPKD?

A
  • Hepatic Cysts: Usually asymptomatic and benign.
  • Cerebral Aneurysms: Can rupture, leading to subarachnoid hemorrhage; elective screening is considered for some patients.
  • Cardiac Valvular Disease: Commonly mitral valve prolapse.
  • Colonic Diverticula: Increased risk due to diverticulum formation.
251
Q

What is multicystic dysplastic kidney and its cause?

A

Multicystic dysplastic kidney is a condition characterized by a cystic kidney without normal renal tissue, caused by abnormal interaction between the ureteric bud and metanephric mesenchyme. This disruption prevents normal differentiation and leads to dysplastic connective tissue instead of functional renal tissue.

252
Q

What are the clinical implications of multicystic dysplastic kidney in a fetus?

A

The affected kidney is nonfunctional, but the remaining normal kidney usually hypertrophies to compensate, allowing the baby to remain asymptomatic. If both kidneys are affected, there is a risk for Potter syndrome, characterized by oligohydramnios and related complications.

253
Q

What is medullary cystic kidney disease and what are its key features?

A

Medullary cystic kidney disease is an autosomal dominant condition often presenting with teenage-onset gout and a family history of renal disease. Despite its name, it typically shows no cysts on renal ultrasound, and urinalysis is usually normal. In severe cases, kidneys may appear shrunken.

254
Q

How does medullary cystic kidney disease affect renal function and what is its alternate name?

A

The condition is characterized by abnormal functioning of tubular and interstitial cells, leading to issues with urine concentration, but the glomerular filtration barrier remains intact, resulting in no hematuria or proteinuria. It is increasingly referred to as “autosomal dominant tubulointerstitial kidney disease” due to this pathophysiology.

255
Q

What are the key features of an uncomplicated renal cyst?

A

An uncomplicated renal cyst is well-demarcated, homogeneous, thin-walled, and typically small (less than 3 cm). These characteristics indicate a low risk for malignancy.

256
Q

When evaluating an incidental renal cyst, what should be considered regarding its nature and associated symptoms?

A

Isolated cystic lesions are generally benign and unlikely to be associated with genetic cystic syndromes. Mild hypertension in such cases may be due to pain from other conditions (e.g., bowel obstruction) and not necessarily indicative of kidney disease.

257
Q

What role does acetazolamide play in preventing high altitude illness?

A

Acetazolamide is used as prophylaxis for high altitude illness by inhibiting carbonic anhydrase, which reduces bicarbonate formation and helps counteract respiratory alkalosis caused by hyperventilation at high altitudes.

258
Q

How does acetazolamide affect arterial pH in the context of high altitude?

A

By lowering serum bicarbonate levels, acetazolamide decreases arterial pH, which helps mitigate the respiratory alkalosis that occurs due to lower arterial oxygen pressure and hyperventilation at high altitudes.

259
Q

What is a major risk associated with high-dose loop diuretic therapy in heart failure patients?

A

Patients receiving high-dose loop diuretics (typically >240 mg/hour) are at risk for ototoxicity, which can manifest as decreased hearing, tinnitus, or deafness.

260
Q

How does ototoxicity occur with loop diuretics?

A

Ototoxicity is believed to result from disruption of ion transporters in the inner ear, leading to abnormal endolymph secretion and structural damage in the inner ear, especially when high doses are used or when combined with other ototoxic agents like aminoglycosides.

261
Q

What are key components of managing large intracerebral hemorrhage?

A

Management includes elevating the head of the bed, sedation, blood pressure control, and possibly administering mannitol to reduce intracerebral pressure.

262
Q

How does mannitol reduce intracerebral pressure in patients with intracerebral hemorrhage?

A

Mannitol increases plasma osmolality, drawing fluid out of the intracerebral compartment into the vasculature, thereby lowering intracerebral pressure. It is also used in other conditions with elevated intracranial pressure, such as head trauma or brain tumors.

263
Q

What are the first-line medications for treating essential hypertension according to current guidelines?

A

Thiazide diuretics, ACE inhibitors, and calcium channel blockers.

264
Q

Why is hydrochlorothiazide the best choice for a patient with a history of recurrent calcium oxalate nephrolithiasis?

A

Hydrochlorothiazide promotes diuresis and increases calcium absorption in the distal tubule, reducing the likelihood of calcium oxalate stone formation.

265
Q

What is diuretic resistance in the context of chronic loop diuretic therapy for heart failure?

A

Diuretic resistance refers to the need for higher dosages of loop diuretics over time to achieve adequate diuresis due to compensatory mechanisms in the nephron.

266
Q

What are the primary mechanisms contributing to diuretic resistance in patients with heart failure?

A

1) Increased sodium reabsorption in unaffected nephron areas due to elevated renin-angiotensin-aldosterone system activity and sympathetic tone.
2) Poor furosemide secretion in the proximal tubule due to low cardiac output, which impairs drug activity in the thick ascending limb.

267
Q

What are the key findings and causes of rhabdomyolysis in this patient?

A

The patient shows elevated creatine kinase levels, dark urine, and acute kidney injury, likely due to muscle compression from restraints. High-risk scenarios include psychotic agitation, coma with immobilization, and substance use (e.g., alcohol, amphetamines, PCP).

268
Q

What electrolyte abnormalities are associated with rhabdomyolysis?

A

Rhabdomyolysis leads to hyperkalemia and hyperphosphatemia due to the release of potassium and phosphate from damaged muscle cells. Hypocalcemia occurs due to calcium deposition in necrotic tissues. Calcium levels typically normalize over time.

269
Q

What are the key symptoms and causes of McArdle disease?

A

McArdle disease is characterized by lifelong exercise intolerance, myalgias, weakness, dark urine, and elevated creatine kinase levels. It is a genetic glycogen storage disease caused by myophosphorylase deficiency, leading to impaired glycogen breakdown in muscle cells, especially during exercise.

270
Q

How does McArdle disease affect muscle function during exercise?

A

In McArdle disease, glycogen cannot be effectively utilized by muscle cells, leading to stress and potential rhabdomyolysis during prolonged exercise. Symptoms typically manifest in adolescence or early adulthood, as muscle cells struggle to generate energy from stored glycogen.

271
Q

What are the key clinical features of a bladder rupture following trauma?

A

Key features include abdominal pain, rebound tenderness, a seatbelt-shaped bruise, and red urine. Urinalysis typically shows a positive heme test and red blood cells on microscopy, indicating hematuria.

272
Q

How does a bladder rupture lead to peritoneal signs and hematuria?

A

A bladder rupture allows urine and blood to leak into the peritoneum, causing irritation and signs of peritonitis (e.g., rebound tenderness and abdominal pain). Hematuria results from trauma to the bladder, leading to blood in the urine.

273
Q

What is a common cause of nephrolithiasis in patients undergoing chemotherapy, and why?

A

Uric acid stones are common in patients undergoing chemotherapy, particularly for malignancies like lymphoma. Chemotherapy causes cell death, releasing purines that are metabolized to uric acid, leading to hyperuricemia and precipitation of uric acid crystals.

274
Q

How are uric acid stones diagnosed, and what imaging technique is preferred?

A

Uric acid stones are diagnosed using a CT scan, which can visualize most stone types, including uric acid stones, which are not visible on plain X-ray. CT is preferred for its accuracy in identifying stone composition and location.

275
Q

What is a key treatment strategy for uric acid stones?

A

Urinary alkalinization is an effective treatment for uric acid stones, as it can dissolve the stones. This contrasts with other stone types, which typically require surgical intervention or must pass on their own.

276
Q

What is a staghorn calculus, and what causes it?

A

A staghorn calculus is a large kidney stone that conforms to the renal collecting system, primarily caused by magnesium-ammonium-phosphate (struvite). Struvite stones form in alkaline urine due to upper urinary tract infections from urease-producing organisms like Proteus and Klebsiella.

277
Q

What urinalysis findings and risk factors are associated with struvite stones?

A

Struvite stones are associated with alkaline urine (pH > 7) and commonly present with a urine pH of 8.2. Risk factors include conditions that predispose to urinary infections, such as neurogenic bladder and urinary reflux.

278
Q

What is the most common cause of kidney stones and what type of crystals are typically seen in urine microscopy for this condition?

A

The most common cause of kidney stones is calcium oxalate, which comprises approximately 70% of stones. Urine microscopy typically reveals envelope-shaped crystals characteristic of calcium oxalate.

279
Q

In a patient with first-time nephrolithiasis, what condition is often associated with elevated urinary calcium levels and normal serum calcium levels?

A

The patient likely has idiopathic hypercalciuria, which is a common cause of calcium oxalate stone formation.

280
Q

What are the key lifestyle modifications recommended for prophylaxis against recurrent nephrolithiasis?

A
  • Increase daily fluid intake to over 2 L/day.
  • Follow a low sodium diet to decrease calcium reabsorption.
  • Increase intake of citrate (fruits/vegetables) to inhibit stone formation.
  • Avoid high dietary protein, as it raises the risk of stones.
  • Reduce dietary sources of oxalate (e.g., beans, chocolate, certain fruits/vegetables).
281
Q

How does a low sodium diet help prevent recurrent kidney stones?

A

A low sodium diet reduces activity of the renin-angiotensin-aldosterone system, which decreases proximal tubule sodium and calcium reabsorption, leading to less calcium in the urine and a lower risk of stone formation.

282
Q

Anormal calcium diet is recommended

A

1200 mg/day

283
Q

What is the common metastatic pattern of renal-cell carcinoma (RCC)?

A

RCC commonly metastasizes to the lungs and bones, spreading hematogenously via the venous system.

284
Q

How does the metastatic spread of renal-cell carcinoma differ from most solid tumors?

A

Unlike most solid tumors that spread via lymphatics, RCC spreads hematogenously through the venous system. Other solid tumors that spread this way include follicular thyroid cancer, hepatocellular carcinoma, and choriocarcinoma.

285
Q

Rarely presents with multiple bilateral nodules.

A

Primary lung malignancy

286
Q

Renal Cell Carcinoma Presentation and Risk Factors

A

Presentation: New-onset hematuria, often asymptomatic.
Classic Triad: Flank pain, flank mass, and hematuria (present in only 10% of patients).
Common Presentation: Nonspecific signs or asymptomatic hematuria.

287
Q

Renal Cell Carcinoma and Erythropoiesis

A

Elevated Hemoglobin/Hematocrit: May indicate erythropoietin production by the tumor, leading to erythrocytosis.
Risk Factor: Cigarette smoking is a major risk factor for renal cell carcinoma.

288
Q

Schistosoma haematobium and Bladder Infection

A
  • Infection Type: Chronic bladder infection with the trematode Schistosoma haematobium.
  • Geographic Endemic Areas: Middle East and Africa, including Egypt.
  • Diagnosis: S. haematobium eggs, identifiable by urine microscopy.
289
Q

Schistosoma haematobium and Bladder Cancer Development

A
  • Cancer Risk: Infection raises the risk of developing squamous cell carcinoma of the bladder.
  • Pathogenesis: Chronic infection deposits eggs in the bladder, causing irritation and inflammation.
  • Progression: Inflammation triggers squamous metaplasia of transitional epithelium, similar to Barrett’s esophagus. Continued irritation leads to squamous dysplasia and may progress to squamous cell carcinoma.
290
Q

Tuberous Sclerosis - Neurocutaneous Syndrome

A
  • Key Features: Brain and skin abnormalities, indicating a neurocutaneous syndrome.
  • MRI Findings: Subependymal masses suggestive of subependymal astrocytomas.
  • Skin Findings: Hypopigmented patches (Ash-leaf spots) and thickened skin in the lumbosacral region (Shagreen patch).
291
Q

Tuberous Sclerosis and Renal Angiomyolipomas

A
  • Renal Risk: Patients with tuberous sclerosis are at risk for renal angiomyolipomas.
  • Tumor Characteristics: Benign proliferations of endothelial cells, immature smooth muscle, and fat; the most common benign kidney tumor.
  • Clinical Note: Lesions are often asymptomatic but can cause hemorrhage due to high vascularity. Bilateral tumors are common in tuberous sclerosis.
292
Q
A

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