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M.T.B > Internal Med- Nephrology > Flashcards

Internal Med- Nephrology Flashcards

1
Q

What are the 3 best initial tests in Nephrology?

A
  • Urinalysis
  • Blood Urea Nitrogen (BUN)
  • Creatinine
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2
Q

What are the main components of a Urinalysis (UA)?

A

1) Gross Assessment (Color, Turbidity)
2) Urine dipstick
3) Microscopic Analysis

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3
Q

What is measured by the urine dipstick?

A
  • Protein
  • Blood (RBC, WBC)
  • Ketones
  • Glucose
  • Nitrates
  • pH
  • Specific gravity
  • Leukocyte Esterase
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4
Q

What are the components of the Microscopic Analysis in a Urine Analysis?

A

3-C’s
1- Cells (WBC,RBC)
2-Casts (WBC casts, RBC casts, Granula casts, Fatty casts)
3-Crystals (crystals of; Uric acid, CaPO4, Calcium Oxalate)

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5
Q

What is the normal range of protein excretion?

What is Tamm-Horsfall proteinuria?

A

<300mg /24r

It is proteinuria <30-50mg /24hr

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6
Q

What does severe proteinuria denote?

A

Glomerular Disease

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7
Q

Which situation would indicate a kidney biopsy in terms of proteinuria?

A

Persistant proteinuria which unrelated to prolonged standing (orthostatic proteinuria) or physical activity

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8
Q

What is the major limitation of UA in terms of measuring protein urea

A
  • The dipstick only measures albumin
  • It measures only the amount of protein excreted at a particular moment not the average or total amount excreted over 24hrs
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9
Q

What are the 2 ways used to assess the total amount of protein in a day?

A

1) Protein-to-Creatinine ratio

2) 24hr urine collection

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10
Q

To asses proteinuria;

1) What is the best initial test?
1) What is the most accurate test in determining the amount?

A

1) UA

2) Protein-to-Creatinine ratio or 24hr urine collection (but is rarely done)

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11
Q

How can the cause of proteinuria be determined?

A

Biopsy

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12
Q

What is the relationship between the Protein-to-Creatinine ratio and the actual amount of proteinuria

A

A P/Cr of 1 = 1g/24hr

A P/Cr of 2,5 = 2,5g/24hr

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13
Q

What is microalbuminuria?

A

Proteinuria too small to detect on UA (30-300mg/24hr)

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14
Q

What is the best initial therapy for a Pt with proteinuria and diabetes?

A

ACEi and ARBs, they delay development of renal insufficiency

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15
Q

What can the presence WBC’s on a UA indicate?

A

Inflammation
Infection
Allergic Interstitial Nephritis.

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16
Q

1) What are the limitations of a UA interims of interpreting WBC’s?
2) How can the limitations be overcome?

A

1) The UA cannot distinguish between Neutrophils and Eosinophils.

Neutrophils=> Infection
Eosinophils=> allergic or acute interstitial nephritis

2) Using the Wright and Hansel stains can detect eosinophils

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17
Q

What is considered to be a normal number of RBC on UA?

A

<5 RBC’s per high power field.

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18
Q

What are some of the possible etiologies of Hematuria?

A 
Stones (bladder ureter, kidney)
Infection (cystitis, pyelonephritis)
Cancer 
Drugs (cyclophosphamide=> hemorrhagic cystitis)
Trauma
Coagulopathy
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19
Q

What can cause a false positive of hematuria on dipstick?

A

Hemoglobin or Myoglobin

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20
Q

What is the best initial step to confirm the etiology of bleeding after a positive dipstick?

A

Microscopic examination of the urine. Hemoglobin or Myoglobin will cause a positive dipstick but no RBC’s will be found on microscopy

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21
Q

What is pathognomonic for glomerulonephritis on UA?

A

“Dysmorphic RBC’s”

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22
Q

What scenario would make Cystoscopy the next best step?

A

Hematuria without infection or prior trauma + :

  • Renal imaging show no etiology
  • Bladder sonography show a mass for possible biopsy
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23
Q 
What is the most likely diagnosis if  the following types of casts are found:
RBC casts
WBC casts 
Eosinophil casts
Hyaline casts
Broad, waxy casts
Grannular "muddy-brown" casts
A

RBC casts- Glomerulonephritis

WBC casts- Pyelonephritis

Eosinophil casts- Acute(allergic) Interstitial Nephritis

Hyaline casts- Dehydration (it concentrates the urine and the normal Tamm-Horsfall protein precipitates into casts)

Broad, waxy casts- Chronic renal diseases

Grannular “muddy-brown” casts- Acute Tubular Necrosis

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24
Q

What is Acute Kidney Injury (AKI) or Acute Renal Failure (ARF)?

A

decreased Creatinine clearance resulting in an increased BUN and Creatinine

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25
Q

What are the 3 types of Acute Kidney Injury (AKI)?

A

1) Prerenal azotemia- Decreased perfusion
2) Postrenal azotemia- Obstruction
3) Intrinsic renal disease- Ischemia and Toxins

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26
Q

What are some of the causes of Prerenal azotemia?

A

Inadequate perfusion:
Renal artery Stenosis
Hypotension and Hypovolemia- sepsis, anaphylaxis, bleeding, dehydration, diuretics, burns, CHF, Tamponade, hypoalbuminemia, cirrhosis

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27
Q

What are some of the causes of Postrenal azotemia?

A

obstruction of drainage/flow of urine:
Prostate hypertrophy or cancer
Neurogenic (atonic) bladder
bilateral obstruction (stones, tumors or strictures)
Cervical cancer
Urethral strictures
Retroperitoneal fibrosis (due to bleomycin, methylsergide or radiation)

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28
Q

What are the 3 main groups of pathologies in Intrinsic renal disease?

A

1) Glomerulonephritis (GN)- Glumerular disease
2) Acute Tubular Nephritis (ATN)- Tubular disease **Most common
3) Interstitial Nephritis (IN)

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29
Q

What are some of the causes of Glomerulonephritis (GN)?

A 
Membranous GN
Focal Segmental GN
Post Strep GN
Minimal Change Disease
IgA Nephropathy
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30
Q

What are some of the causes of Acute Tubular Nephritis (ATN)?

A 
Ischemia- Prolonged hypoperfusion 
Toxins:
Myoglobin 
Hemoglobin (Malaria)
Bence-Jones proteins from myeloma
Drugs and Contrasts
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31
Q

What are some of the causes of nterstitial Nephritis (IN)?

A

Acute:
Antibiotics=> Penicilins (acute (allergic) IN)
NSAIDs
Diuretics

Chronic:
NSAIDs

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32
Q

What is the best initial test in AKI?

A

BUN and Creatinine (ratio)

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33
Q

What does a BUN:Creatinine ratio above 20:1 indicate in terms of etiology?

A

Prerenal or Postrenal kidney damage

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34
Q

What would be the BUN:Creatinine ratio in Intrinsic renal disease?

A

closer to 10:1

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35
Q

What clinical features and BUN:Creatinine ratio would make Prerenal azotemia the most likely diagnosis?

A

BUN:Creatinine ratio above 20:1

and

A clear history of hypoperfusion or hypotension

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36
Q

What clinical features and BUN:Creatinine ratio would make Postrenal azotemia the most likely diagnosis?

A

BUN:Creatinine ratio above 20:1

and

a distended bladder or massive release of urine with catheter placement.
Bilateral or unilateral hydronephrosis on ultrasound

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37
Q

If UA is not available what other tests can be done

A

1) Urine sodium (UNa <20)
2) Fractional excretion of sodium (F E Na <1%)
3) Urine osmolality

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38
Q

What is the physiology behind Urine sodium and Fractional excretion of sodium?

A

Decrease BP or intravascular volume normally will increase aldosterone from the RAAS system and increases sodium reabsorption.. It is normal for urine sodium to decrease when there is decreased renal perfusion because aldosterone levels rise.

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39
Q

What is the principle behind Urine Osmolality?

A

Increased water reabsorption leads to an increase in urine osmolality: more concentrated urine.
Urine specific gravity correlates to urine osmolality.

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40
Q

What is the pathophysiology in ATN?

A

Tubule cells are damaged so cannot reabsorb water and concentrate urine. The osmolality of the urine and blood becomes similar (isosthenuria).

  • Loss of sodium (UNa> 20)
  • Loss of water into urine- Urine Osmolarity<300 mOsm/L
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41
Q

A 20-year-old African American man comes for a screening test for sickle cell. he is found to be heterozygous (trait or AS) for sickle cell.
What is the best advice for him?

a. Nothing needed until he has a painful crisis
b. Avoid dehydration
c. Hydroxyurea
d. Folic acid supplementation
e. Pneumococcal vaccination

A

*B
The only significant manifestation of sickle cell trait is a defect in renal concentrating ability or isosthenuria. These Pt will continue to produce inappropriately dilute, high-volume urine despite dehydration.

Hydroxyurea is used to prevent painful crises when they occur more than 4 times a year.
*Painful crises rarely occur in sickle cell trait.
They do not have hemolysis, so there is no need for additional Folic Acid supplementation.
Splenic function is abnormal only in those who are homozygous, so pneumococcal vaccine is not routinely indicated.

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42
Q

A patient comes with fever and acute, left lower quadrant abdominal pain. Blood cultures on admission grow E. coli and Candida albicans. She is started on vancomycin, metronidazole and gentamicin and amphotericin. she has a CT scan that identifies diverticulitis. After 36 hours, her creatinine rises dramatically.
Which of the following is the cause of her renal insufficiency?

a. Vancomycin
b. Gentamicin
c. Contrast media
d. Metronidazole
e. Amphotericin

A

*C
Radiographic contrast has a very rapid onset of injury. creatinine rises the next day. Vancomycin, gentamicin and amphotericin are all potentially nephrotoxic, but they would not cause renal failure with just 2 or 3 doses. They need 5 to 10 days to result in nephrotoxic. Metroindazole is hepatically excreted and does not cause renal failure.

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43
Q

A 74-year-old blind man is admitted with obstructive uropathy and chest pain. He has a history of hypertension and diabetes. His creatinine drops from 10mg/dL to 1.2mg/dL 3 days after catheter placement. The stress test shows reversible ischemia.
What is the most appropriate management?

a. Coronary artery calcium score on CT scan
b. One to two litres of normal saline hydration prior and during angiography
c. N-acetylcysteine
d. Mannitol during angiography
e. Furosemide during angiography
f. Intravenous sodium bicarbonate before and during angiography

A

*B
Saline hydration has the most proven benefit at preventing contrast-induced nephrotoxicity. Mannitol and furosemide may or may not prevent nephrotoxicity. There is minimal data to support their use. N-acetylcysteine and sodium bicarbonate have some benefit, but the evidence is not as clear as that with saline. Calcium scoring on CT scan is still considered experimental. It does not provide sufficient information to eliminate angiography.

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44
Q

A Pt with mild renal insufficiency undergoes angiography and develops a 2mg/dL rise in creatinine from ATN despite the use of saline hydration before and after the procedure.
What do you Expect to find on laboratory testing?

a. Urine sodium 8 (low), F E Na>1%, urine specific gravity 1.035 (high)
b. Urine sodium 58 (low), F E Na>1%, urine specific gravity 1.005 (low)
c. Urine sodium 5 (low), F E Na<1%, urine specific gravity 1.040 (very high)
d. Urine sodium 45 (low), F E Na>1%, urine specific gravity 1.005 (low)

A

*C
Although contrast-induced renal failure is a form of ATN, the urinary lab values are an exception from the other forms of ATN.
Contrast causes spasm of the afferent arteriole that lead to renal tubular dysfunction. There is tremendous reabsorption of sodium and water, leading the specific gravity of the urine to become very high. This results in profoundly low urine sodium.
The usual finding in ATN from nephrotoxins would be UNa above 20, F E Na >1%, but a low specific gravity. Specific gravity correlates with urine osmolarity.

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45
Q

A Pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises.
What is the most likely cause?

a. Cisplastin
b. Hyperuricemia
c. Bence-Jones proteinuria
d. Hypercalcemia
e. Hyperoxaluria

A

*B
2 days after chemotherapy, the creatinine rises in a person with hematologic malignancy. This is most likely from tumor lysis syndrome leading to hyperuricemia.
Cisplatin, as with most drug toxicities, would not produce a rise in creatinine until 5 to 10 days.
Bence-Jone protein and hypercalcemia both cause renal insufficiency, but it would not be rapid and it would not happen as a result of treatment. Treatment for myeloma would end up decreasing both the calcium and Bence-Jones protein levels because they are produced from the leukaemia cells. Cancer cells do not release oxalate.

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46
Q

A Pt with extremely severe myeloma with a plasmacytoma is admitted for combination chemotherapy. Two days later, the creatinine rises.
What may have caused this and how would you prevent it?

A

Tumor lysis syndrome leading to hyperuricemia from Chemo.

Mgx
Allopurinol, hydration and rasburicase should be given prior to chemotherapy to prevent renal failure from tumor lysis syndrome.

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47
Q

What are some of the etiologies of Rhabdomyolysis?

A

Trauma, prolonged immobility, snake bites, seizures and crush injuries.

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48
Q

What is the best initial test to confirm Rhabdomyolysis?

What will the test show?

A

UA with a positive Dipstick for large amounts of “blood”, because the dipstick cannot tell the difference between; Hemoglobin, Myoglobin and RBCs

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49
Q

What are the lab findings in Rhabdomyolysis?

A
  • Markedly elevated Creatine Phosphokinase (CPK)
  • Hyperkalemia (released from damaged cells)
  • Hyperuricemia (when cells breakdown, nucleic acids are released and metabolised into uric acid {same in tumor lysis syndrome})
  • elevated Phosphate (from cells)
  • Hypocalcemia (coz calcium binds to damaged muscle)
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50
Q

Why doesn’t Hemolysis cause hyperuricemia?

A

RBCs have no nuclei

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51
Q

How would you manage Rhabdomyolysis?

A

Saline hydration and Manitol to increase urine flow rates and decrease contact time between the tables and myoglobin which is a severe oxidative stressor.
Bicarbonate is used to drive potassium back into cells and also prevents myoglobin from precipitating on the tubules
**Dont treat hypocalcemia in rhabdomyolysis if asymptomatic coz in recovery, the calcium disassociate with the muscle and normal levels will be restored

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52
Q

A man comes to the emergency department after a triathlon, followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and the urine is dark. Intravenous fluids are started.
What is the next best step in the management of this patient?

a. CPK level
b. EKG
c. Potassium replacement
d. Urine dipstick
e. Urine myoglobin

A

*B
EKG is done to detect life-threatening hyperkalemia.
CPK level, urine dipstick for blood and myoglobin should all be done, but the EKG will see if he is about to die of a fatal arrhythmia from hyperkalemia. *Potassium replacement in a person with rhabdomyolysis would be fatal.

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53
Q

What are some of the indications for dialysis?

A 
Fluid overload
Encephalopathy
Pericarditis
Metabolic acidosis
Hyperkalemia
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54
Q

What are some of the features of Hypocalcemia?

How would you manage it?

A

Seizures, prolonged QT interval leading to arrhythmia

Mgx
Vitamin D and calcium

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55
Q

A patient develops ATN from gentamicin. She is vigorously hydrated and treated with high doses of diuretic, low-dose dopamine, and calcium acetate as a phosphate binder. Urine output increases but she still progresses to end-stage renal failure. She also becomes deaf.
What caused her hearing loss?

a. Hydrochlorothiazide.
b. Dopamine.
c. Furosemide.
d. Chlorthalidone.
e. Calcium acetate.

A

*C
Furosemide causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss. This is related not only to the total dose, but how fast it is injected. It essentially “burns” the inner ear. Aminoglycoside antibiotics also cause hearing loss. Furosemide in ATN adds no proven overall benefit. It does add ototoxicity to the gentamicin.

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56
Q

What clinical features are consistent with Hepatorenal Syndrome?

A
  • Severe liver disease (cirrhosis)
  • New-onset renal failure with no other explanation

Lab values consistent with prerenal azotemia:

  • Very low urine sodium (less than 10–15 mEq/dL)
  • FENa below 1%
  • Elevated BUN:creatinine ratio (greater than 20:1)
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57
Q

How would you Mgx Hepatorenal Syndrome?

A

Midodrine
Octreotide
Albumin (albumin is less clear)

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58
Q

What is the etiology of Atheroembolc disease?

A

Cholesterol plaques in the aorta or near the coronary arteries are sometimes large and fragile enough that they can be “broken off” when these vessels are manipulated during catheter procedures. Cholesterol emboli lodge in the kidney, leading to AKI.

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59
Q

What is the clinical presentation on physical exam and labs of Atheroembolc disease?

A

Blue/purplish skin lesions in fingers and toes, livedo reticularis (lacy-purplish discolouration), and ocular lesions.

Labs:

  • Eosinophilia
  • Low complement levels
  • Eosinophiluria
  • Elevated ESR
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60
Q

What are Peripheral pulses are normal in Atheroembolc disease?

A

Emboli are too small to occlude vessels such as the radial or brachial artery.

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61
Q

What set of clinical features would make Acute (Allergic) Interstitial Nephritis the most likely diagnosis?

A

Acute renal failure (rising BUN and creatinine) with:

  • Fever (80%)
  • Rash (50%)
  • Arthralgias
  • Eosinophilia and *Eosinophiluria (80%)
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62
Q

What is the most accurate test for Acute (Allergic) Interstitial Nephritis?

A

Hansel or Wright stain.
The UA is able to detect only WBCs, RBCs, and protein; it is not sufficiently accurate to determine that they are eosinophils.

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63
Q

How would you Mgx Acute (Allergic) Interstitial Nephritis?

A

AIN usually resolves spontaneously with stopping the drug or controlling the infection. Severe disease is managed with dialysis

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64
Q

How would you Mgx a situation where creatinine continues to rise after stopping the offending drug in Acute (Allergic) Interstitial Nephritis?

A

Giving glucocorticoids (prednisone, hydrocortisone, methylprednisolone)

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65
Q

What kind of nephropathies can Analgesic nephropathy present with?

A

-ATN from direct toxicity to the tubules
-AIN
-Membranous glomerulonephritis
-Papillary necrosis
-Vascular insufficiency of the kidney from inhibiting prostaglandins.
Prostaglandins dilate the afferent arteriole. NSAIDs constrict the afferent arteriole and decrease renal perfusion. This is asymptomatic in healthy
patients. When patients are older and have underlying renal insufficiency from diabetes and/or hypertension, then NSAIDs can tip them over into clinically apparent renal insufficiency.

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66
Q

What is Papillary Necrosis?

A

Coagulative necrosis of the renal medullary pyramids and papillae

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67
Q

What is the etiology of Papillary Necrosis?

A

POSTCARDS Pyelonephritis, obstruction, sickle cell disease/trait, tuberculosis, cirrhosis, **analgesics (abuse), renal transplant rejection, diabetes mellitus, systemic vasculitis

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68
Q

What percentage of damage to the kidneys must be done in order to elicit a rise in BUN and
Creatinine levels?

A

A patient must lose at least 60% to

70% of renal function before the creatinine even begins to rise.

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69
Q

What is the clinical picture of Papillary Necrosis?

which disease would present with a similar clinical picture?

A

Sudden onset of flank pain, fever, and hematuria in a patient with any POSTCARDS (diseases)
-Grossly visible necrotic material passed in
the urine.
-Pyelonephritis

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70
Q

1) What is the best initial test for Papillary Necrosis?

2) What is the most accurate test for Papillary Necrosis?

A

1) UA that shows red and white cells and may show necrotic kidney tissue. The urine culture will be normal (no growth).
2) CT scan that shows the abnormal internal structures of the kidney from the loss of the papillae.

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71
Q

In general what is the relationship between Nephrotic syndrome and Tubular Disease?

A

None of them (Tubular Diseases) ever cause nephrotic syndrome or give massive
proteinuria.

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72
Q

In general are Tubular Diseases, Acute or Chronic?

A

Acute

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73
Q

In general are Glomerular Diseases, Acute or Chronic?

A

Chronic

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74
Q

In general what is the relationship between Nephrotic syndrome and Glomerular Disease?

A

All of them can cause nephrotic syndrome.

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75
Q

What is the most accurate test to establish a diagnosis for Glomerular Diseases?

A

Biopsy

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76
Q

In general which drugs are used in the Mgx of Glomerular Disease?

A

-Steroids, though several resolve spontaneously
-Additional immunosuppressive medications like cyclophosphamide,
mycophenolate are frequently used.

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77
Q

What are some of the typical Diagnostic features present in all forms of glomerulonephritis?

A 
-UA with hematuria
“Dysmorphic” red cells (deformed as they “squeeze” through an abnormal glomerulus)
-Red cell casts
-Urine sodium and FENa are low
-Proteinuria
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78
Q

What is the main difference between glomerulonephritis and nephrotic syndrome?

A

The degree or amount of proteinuria is the main difference

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79
Q

What are the main clinical features in all forms of Glomerular Diseases?

A

Every type of glomerulonephritis causes proteinuria, red cells, red cell casts in
urine, hypertension, and edema.

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80
Q

What is the pathophysiology in Goodpasture Syndrome and what are its main clinical features?

What is pathognomonic for Goodpasture Syndrome

A

Auto-antibodies against collagen type IV in the renal and pulmonary capillary basement membrane

Hemoptysis, cough, dyspnea.
Anemia is often present from chronic blood loss from hemoptysis

Its the only kidney disease which will present with lung involvement

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81
Q

1) What is the best initial test to Dx Goodpasture Syndrome?

2) What is the most accurate test to Dx Goodpasture Syndrome?

A

1) Antiglomerular basement membrane antibodies. Anti-GBM antibodies
2) Lung or kidney biopsy=> shows “linear deposits.”

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82
Q

What is the Mgx for Goodpasture Syndrome?

A

Plasmapheresis + Steroids/Immunosuppression (Cyclophosphamide)

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83
Q

What would make you suspect IgA Nephropathy (Berger Disease)?

A

Asian patient with recurrent episodes of gross hematuria 1 to 2 days after an upper respiratory tract infection.
**Poststreptococcal glomerulonephritis follows pharyngitis by 1 to 3 weeks.

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84
Q

What is the Mgx for IgA Nephropathy (Berger Disease)?

A

There is no treatment proven to reverse the disease. 30% will completely resolve. Between 40% and 50% will slowly progress to end-stage renal disease.

Severe proteinuria is treated with ACE inhibitors and steroids. Fish oil is of uncertain benefit.

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85
Q

What is the relationship between proteinuria and severity of kidney disease?

A

More proteinuria = worse progression

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86
Q

What is the relationship between Postinfectious Glomerulonephritis and Poststreptococcal
glomerulonephritis?

A

The most common organism leading to postinfectious glomerulonephritis
(PIGN) is Streptococcus, but almost any infection can lead to abnormal
activation of the immune system and PIGN. Poststreptococcal
glomerulonephritis (PSGN) follows throat infection or skin infection (impetigo) by 1 to 3 weeks.

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87
Q

What is the clinical presentation in postinfectious glomerulonephritis
(PIGN)?

A
  • Dark (cola-colored) urine
  • Edema that is often periorbital
  • Hypertension
  • Oliguria
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88
Q

How would you go about Dx Postinfectious Glomerulonephritis?

A

UA with proteinuria, red cells, and red cell casts tells you that glomerulonephritis is present.

PSGN from group A beta hemolytic streptococci (pyogenes) is confirmed first by antistreptolysin O (ASO) titers and anti-DNase antibody titers

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89
Q

What is the Mgx of Postinfectious glomerulonephritis

(PIGN)?

A

Antibiotics

Diuretics to control fluid overload

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90
Q

What is Alport Syndrome?

A

Alport syndrome is a congenital defect of type IV collagen that results in glomerular disease combined with:

  • Sensorineural hearing loss
  • Visual disturbance from loss of the collagen fibers that hold the lens of the eye in place
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91
Q

What is Polyarteritis Nodosa?

A

Polyarteritis nodosa (PAN) is a systemic vasculitis of small and medium-sized
arteries which leads to tissue ischemia and most commonly affects the kidney. Virtually every organ in the
body can be affected, but it tends to spare the lung. Although it is of unknown
etiology, it can be associated with hepatitis B or C and all patients with PAN
should be tested.

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92
Q

What are some of the clinical features of Polyarteritis nodosa (PAN)?

A

Neurologic: Damage to small blood vessels around nerves starves them into neuropathy: polyneuropathy (mononeuritis multiplex)

Skin: Vasculitis of any cause leads to purpura (large) and petechiae (small).
PAN also gives ulcers, digital gangrene, and livedo reticularis.

Cardiovascular: Stroke or MI in a young person suggests PAN.

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93
Q

1) What is the best initial test to Dx Polyarteritis nodosa (PAN)?
2) What is the most accurate test to Dx Polyarteritis nodosa (PAN)?

A

1) Angiography of the renal, mesenteric, hepatic artery or vessels of involved organ showing aneurysms and stenosis

2) Biopsy of a symptomatic site such as
skin, nerves, or muscles.

**ANCA-negative

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94
Q

How would you Mgx Polyarteritis nodosa (PAN)?

A

Immunosuppression: corticosteroids, cyclophosphamide

Antiviral therapy against HBV and HCV may be required.

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95
Q

Why is a Biopsy performed in Lupus Nephritis?

A

Although a biopsy is the most accurate test, it is not performed to diagnose lupus, but rather to guide intensity of therapy.

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96
Q

How would you Mgx Lupus Nephritis?

A

Mild inflammatory changes => glucocorticoids

Severe proliferative disease => glucocorticoids + cyclophosphamide or mycophenolate.

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97
Q

List a few diseases that will show large kidneys on sonogram and CT scan/

A

Amyloidosis, HIV nephropathy, polycystic kidneys, and diabetes

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98
Q

What does a biopsy when suspecting Amyloidosis show?

A

Green birefringence with

Congo red staining.

99
Q

How would you Mgx Amyloidosis?

A

Treat amyloidosis by trying to control the underlying disease. When this is unsuccessful or there is no primary disease to control, the treatment of
amyloidosis is with melphalan and prednisone.

100
Q

Give a brief description of Nephrotic Syndrome

A

Nephrotic syndrome is a measure of the severity of proteinuria (>3,5 g/day) [rather than etiology] in association with any form of glomerular disease.

Massive proteinuria leads to:

  • Edema
  • Hyperlipidemia and fatty casts on urinalysis (Maltese crosses)
  • Thrombosis (clots)
101
Q

Which glomerular disease is associated with Nephrotic Syndrome in Children?

A

Minimal Change Disease

102
Q

Which glomerular disease is associated with Injection drug use and AIDS?

A

Focal-Segmental GN

103
Q

What is the clinical presentation of Nephrotic Syndrome?

A

Massive proteinuria leads to:
-Edema
-Hyperlipidemia and fatty casts on urinalysis (Maltese crosses)
-Thrombosis (clots): from urinary loss of the natural anticoagulants protein C,
protein S, and antithrombin
-Infections are more
frequent because of increased urinary loss of immunoglobulins and
complement

104
Q

What is the difference between edema in CHF and in Pt with Nephrotic Syndrome?

A

CHF leads to edema of dependent areas like the legs. Nephrotic patients are edematous everywhere.
*Periorbital edema is characteristic of nephrotic syndrome.

105
Q

Since the UA only gives protein levels at a particular time and they may vary because of different factors like time of day and posture, what can be done to better estimate protein urea equivalent to a 24-hour urine?

A

The urine albumin/creatinine ratio gives a measure of the average protein produced over 24 hours. A ratio of 2:1 means 2 grams of protein excreted over
24 hours. A ratio of 5.4 to 1 means 5.4 grams excreted over 24 hours.

106
Q

How would you Mgx Nephrotic Syndrome?

A

The best initial therapy for nephrotic syndrome is glucocorticoids. If there is
no response after several weeks of therapy, other immunosuppressive medications such as cyclophosphamide are used.
ACE inhibitors or ARBs are used to try to control proteinuria.
Edema is managed with salt restriction and diuretics.
Hyperlipidemia is managed with statins as you would any form of hyperlipidemia.

107
Q

What is End-stage renal disease (ESRD)?

A

End-stage renal disease (ESRD), or chronic renal failure, is defined as the loss of renal function leading to uremia.

108
Q

Which type of dialysis, Peritoneal dialysis or hemodialysis is more effective at removing
wastes from the body?

A

Both are equally effective at removing

wastes from the body.

109
Q

What is constitutional in the clinical presentation of Uremia?

A
  • Metabolic acidosis
  • Fluid overload
  • Encephalopathy
  • Hyperkalemia
  • Pericarditis
110
Q

What are the manifestations of Renal Failure / End-stage renal disease (ESRD)?

A

Anemia: Loss of erythropoietin leads to normochromic, normocytic anemia.

Hypocalcemia: The kidney transforms the less active 25-hydroxy-vitamin D into the much more active 1,25-dihydroxy-vitamin D. Without the 1,25-dihydroxy form of vitamin D, the body will not absorb enough calcium from the gut.

Osteodystrophy: Low calcium leads to secondary hyperparathyroidism.
High parathyroid hormone levels remove calcium from bones, making them soft and weak.

Bleeding: Platelets do not work normally in a uremic environment. They do not degranulate. If a platelet does not release the contents of its granules, it will not work.

Infection: The same defect occurs with neutrophils. Without degranulation, neutrophils will not effectively combat infection.

Pruritus: Urea accumulating in skin causes itching.

Hyperphosphatemia: Phosphate is normally excreted through kidneys. High parathyroid hormone levels release phosphate from bones, but the body is unable to excrete it.

Hypermagnesemia: from loss of excretory ability.

Accelerated atherosclerosis and hypertension: The immune system (lymphocytes) helps keep arteries clear of lipid accumulation. White cells
don’t work normally in a uremic environment.

Endocrinopathy: Women are anovulatory. Men have low testosterone. Erectile dysfunction is common. Insulin levels tend to go up because insulin
is excreted renally. However, insulin resistance also increases. Glucose levels therefore can be up or down.

111
Q

How would you manage the following in End-stage renal disease (ESRD);

1) Anemia
2) Hypocalcemia and
osteomalacia
3) Bleeding
4) Pruritus

A

1) Erythropoietin replacement and iron supplementation
2) Replace vitamin D and calcium
3) DDAVP increases platelet function; use only when bleeding
4) Dialysis and ultraviolet light

112
Q

How would you manage the following in End-stage renal disease (ESRD);

1) Hyperphosphatemia
2) Hypermagnesemia
3) Atherosclerosis
4) Endocrinopathy

A

1) Oral binders: Calcium acetate, Calcium carbonate
2) Restriction of high-magnesium foods, laxatives, and antacids
3) Dialysis
4) Dialysis, estrogen and testosterone replacement

113
Q

Why is not recommended to us aluminum-containing phosphate binders for Hyperphosphatemia?

A

Aluminum causes

dementia

114
Q

How long do HLA-identical, related donor kidneys last?

A

24 years on average

115
Q

How would you manage the following in End-stage renal disease (ESRD);

1) Anemia
2) Hypocalcemia and
osteomalacia
3) Bleeding
4) Pruritus

A

1) Erythropoietin replacement and iron supplementation
2) Replace vitamin D and calcium
3) DDAVP increases platelet function; use only when bleeding
4) Dialysis and ultraviolet light

116
Q

How would you manage the following in End-stage renal disease (ESRD);

1) Hyperphosphatemia
2) Hypermagnesemia
3) Atherosclerosis
4) Endocrinopathy

A

1) Oral binders: Calcium acetate, Calcium carbonate
2) Restriction of high-magnesium foods, laxatives, and antacids
3) Dialysis
4) Dialysis, estrogen and testosterone replacement

117
Q

Why is not recommended to us aluminum-containing phosphate binders for Hyperphosphatemia?

A

Aluminum causes

dementia

118
Q

How long do HLA-identical, related donor kidneys last?

A

24 years on average

119
Q

What is the relationship between Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS)?

A

They are both thrombotic microangiopathies, where microthrombi, consisting primarily of platelets, form and occlude the microvasculature (i.e. the arterioles and capillaries)

TTP=> primarily in Adults
HUS=> primarily in Children

120
Q

What are some of the associations of Thrombotic thrombocytopenic purpura (TTP)?

A

HIV, cancer, and drugs such as cyclosporine, ticlopidine, and clopidogrel.

121
Q

What are some of the associations of Hemolytic uremic syndrome
(HUS)?

A

E. coli 0157:H7 and Shigella

122
Q

Which clinical features are associated with both TTP and HUS?

A
  • Intravascular hemolysis
  • Renal insufficiency
  • Thrombocytopenia
123
Q

Whats the best way to establish hemolysis?

A

Peripheral blood smear=> schistocytes, helmet cells, and fragmented red cells

124
Q

What is the pentad of clinical features associated with TTP?

A
  • Intravascular hemolysis
  • Renal insufficiency
  • Thrombocytopenia
  • Neurological symptoms
  • Fever
125
Q

What is the level of PT and aPTT in HUS/TTP.?

A

PT and aPTT are normal or slightly elevated in HUS/TTP

126
Q

What blood test can help support the Dx of TTP?

A

A low ADAMTS 13 level

127
Q

What is the best way to Mgx TTP

A

Plasmapheresis

128
Q

What is your opinion on giving Platelets for TTP or HUS?

A

Platelet transfusion is never the correct choice for TTP or HUS

129
Q

What is the most important thing upon recognising that a Pt has a Cyst?

A

Recognising a cyst

that is potentially malignant and needs to be aspirated.

130
Q

What is the etiology of Hypernatremia?

A

Hypernatremia occurs when there is loss of free water.

  • Sweating
  • Burns
  • Fever
  • Pneumonia: from insensible losses from hyperventilation
  • Diarrhea
  • Diuretics
  • Diabetes insipidus (DI)
131
Q

What is the difference between a Simple cyst and a Complex according to the following parameters:

  • Echogenicity
  • Walls
  • Demarcation
  • Transmission
A

Echogenicity:
Simple Cyst- Echo free
Complex Cyst- Mixed echogenicity

Walls:
Simple Cyst- Smooth, thin
Complex Cyst- Irregular, thick

Demarcation:
Simple Cyst- Sharp
Complex Cyst- Lower density on back wall

Transmission:
Simple Cyst- Good through to back
Complex Cyst- Debris in cyst

132
Q

What is the clinical presentation of Polycystic kidney disease (PCKD)?

A 
Pain
Hematuria
Stones
Infection
Hypertension
133
Q

What is the most common cause of death from PCKD?

a. Intracerebral haemorrhage
b. Stones
c. Infection
d. Malignancy
e. Renal failure

A

*E
Renal failure occurs in PCKD from recurrent episodes of pyelonephritis and nephrolithiasis causing progressive scarring and loss of renal function.
PCKD does not have malignant potential. Only 10% to 15% of affected people have cerebral aneurysms, most of which do not
rupture.
Connective tissue is weak throughout the body.
These patients may have:
-Liver cysts (most common site outside the kidney)
-Ovarian cysts
-Mitral valve prolapse
-Diverticulosis

134
Q

What is the etiology of Hypernatremia?

A 
Hypernatremia occurs when there is loss of free water.
Sweating
-Burns
-Fever
-Pneumonia: from insensible losses from hyperventilation
-Diarrhea
-Diuretics
-Diabetes insipidus (DI)
135
Q

Give a short account of Diabetes insipidus (DI) and its types.

A 
Diabetes insipidus (DI) leads to high-volume water loss from insufficient or ineffective antidiuretic hormone (ADH)
1) Central DI, the most common form of diabetes insipidus, is caused by insufficient levels of circulating antidiuretic hormone (ADH) [due to damage of the hypothalamus or storage in the posterior pituitary]

2) Nephrogenic DI, however, is characterized by defective renal ADH receptors in the kidneys. [caused by lithium or
demeclocycline, chronic kidney disease]

136
Q

What is the relationship in the presentation of DI and hypernatremia of any cause?

A

They will both present with neurological symptoms such as confusion, disorientation, lethargy, and seizures. If uncorrected, severe
hypernatremia causes coma and irreversible brain damage.

137
Q

What is pathognomonic for Diabetes insipidus (DI)?

A

High-volume nocturia

138
Q

What is the difference between Polyuria and Frequency?

A

Polyuria is high urine volume.
Frequency just means increased attempts at
voiding. The volume in urinary frequency might be very small (such as in urethritis or cystitis).

139
Q

What is the best initial test for Diabetes insipidus (DI)?

A

Water Deprivation Test

140
Q

What are the possible outcomes after doing the Water Deprivation Test?

A

1) Urine volume stays high and urine osmolality stays low=> Diabetes insipidus
2) Urine volume becomes low and urine osmolality becomes high=> Pyschogenic polydipsia

141
Q

What is the next best test and the most accurate test after doing the Water Deprivation Test?

A

ADH administration test

142
Q

What are the possible outcomes after doing the ADH administration test?

A

1) Urine volume becomes low and urine osmolality becomes high=> Central DI
2) Urine volume stays high and urine osmolality stays low=> Nephrogenic DI

143
Q

How do CDI and NDI compare in terms of;

  • Polyuria and nocturia
  • Urine osmolality and sodium
  • Positive water deprivation test
  • Response to ADH
  • ADH level
A 
Polyuria and nocturia- Present in both
Urine osmolality and sodium- both low
Positive water deprivation test- +ve in both
Response to ADH- only central responds
ADH level- low in CDI and high in NDI
144
Q

What is the Tx for DI

A

1) CDI=> Desmopressin, a synthetic ADH(Vasopressin) analog
2) NDI:
a. Hereditary forms=> Thiazide diuretics or NSAIDs
b. Acquired forms=> Treating the underlying disease

145
Q

What is a possible complication of treating DI or hypernatremia?

A

If sodium levels are brought down too rapidly, cerebral edema will occur. This is from the shift of fluids from the vascular space into the cells of the brain. Cerebral edema presents with worsening confusion and seizures.

146
Q

How can Hyponatremia be characterized according to the overall volume status of the body?

A

1) Hypervolemia
2) Hypovolemia
3) Euvolemia

147
Q

What is the etiology of Hyponatremia in accordance with a Hypervolemic fluid status?

A

CHF
Nephrotic syndrome
Cirrhosis

These are cases in which intravascular volume depletion leads to increased ADH levels. Pressure receptors in the atria and carotids sense the decrease in volume and stimulate ADH production and release.

148
Q

What is the etiology of Hyponatremia in accordance with a Hypovolemic fluid status?

A
  • Sweating
  • Burns
  • Fever
  • Pneumonia: from insensible losses from hyperventilation
  • Diarrhea
  • Diuretics
  • Diabetes insipidus (DI)

All of these are also causes of hypernatremia; however, they cause hyponatremia if there is chronic replacement with free water. A little sodium and a lot of water are lost in urine, which is then replaced with free water that has no sodium. Over time, this process depletes the body of sodium and the serum sodium level drops.
Addison disease or loss of adrenal function also causes hyponatremia because of loss of aldosterone. Aldosterone causes sodium reabsorption.

149
Q

How would you manage Hyponatremia?

A

No symptoms=> Mild hyponatremia=> Restrict fluids

Minimal confusion=> Moderate hyponatremia=> Saline and loop diuretic

Lethargy, seizures,
coma=> Severe hyponatremia=> Hypertonic saline, ADH antagonists; conivaptan,
tolvapta

150
Q

What disease/disorder is in a Pts Hx is suggestive of Psychogenic polydipsia?

A

A history of bipolar disorder

151
Q

What is the clinical presentation of Hyponatremia?

A 
Its the same as Hypernatremia.
CNS symptoms:
-Confusion
-Lethargy
-Disorientation
-Seizures
-Coma
If the sodium levels drop very fast, the patient can immediately seize. Slow drops may be entirely asymptomatic even if the level is very low.
152
Q

What are the diagnostic findings in Syndrome of inappropriate ADH release (SIADH)?

A

The urine is inappropriately concentrated (high urine osmolality).
The urine sodium is inappropriately high while uric acid level and
BUN are low.

153
Q

What level of serum Potassium is considered high?

A

K> 5mEq/L

154
Q

What are the 3 main etiological groups of Hyperkalemia?

A

1) Pseudohyperkalemia
2) Decreased excretion
3) Release from tissues

155
Q

Name a few examples of Hyperkalemia etiologies under Pseudohyperkalemia?

A

Hemolysis
Thrombocytosis
Leukocytosis

156
Q

How slow should correction of sodium must be?

A

“Slow” is defined as under 0.5 to 1 mEq per hour or 12 to 24 mEq per day.

157
Q

What level of serum Potassium is considered high?

A

K> 5mEq/L

158
Q

What is the clinical presentation of Hyperkalemia?

A

Weakness
Paralysis when severe
Ileus (paralyzes gut muscles)
Cardiac rhythm disorders

*Hyperkalemia does not cause seizures.

159
Q

Name a few examples of Hyperkalemia etiologies under Pseudohyperkalemia?

A

Hemolysis
Thrombocytosis
Leukocytosis

160
Q

What is the next best step after getting a potassium level when suspecting Hyperkalemia? and what do you expect to see?

A

The EKG in severe hyperkalemia shows:
Peaked T waves
Wide QRS
PR interval prolongation

161
Q

What are some of the ways you can use to Mgx Hyperkalemia?

A
  1. Calcium chloride or calcium gluconate
  2. Insulin and glucose to drive potassium back into cells
  3. Bicarbonate: drives potassium into cells
  4. Sodium polystyrene sulfonate (Kayexalate) removes potassium from the body through the bowel
162
Q

What is the clinical presentation of Hyperkalemia?

A

Weakness
Paralysis when severe
Ileus (paralyzes gut muscles)
Cardiac rhythm disorders

*Hyperkalemia does not cause seizures.

163
Q

What are the general differences between Hyperkalemia and Sodium disturbances?

A 
Sodium = CNS symptoms
Hyperkalemia = muscular and cardiac symptoms
164
Q

What is the next best step after getting a potassium level? and what do you expect to see?

A

The EKG in severe hyperkalemia shows:
Peaked T waves
Wide QRS
PR interval prolongation

165
Q

What are some of the ways you can use to Mgx Hyperkalemia?

A
  1. Calcium chloride or calcium gluconate
  2. Insulin and glucose to drive potassium back into cells
  3. Bicarbonate: drives potassium into cells
  4. Sodium polystyrene sulfonate (Kayexalate) removes potassium from the body through the bowel
166
Q

What is the difference between using Calcium or Insulin and bicarbonate in Hyperkalemia?

A

Calcium is only used if the EKG is abnormal to protect the heart. It does not lower the potassium level.

Insulin and bicarbonate lower the potassium level through redistribution into the cells.

167
Q

What other methods can be used to lower potassium, besides, using Calcium, Insulin, bicarbonate or Sodium polystyrene sulfonate?

A
  • Inhaled beta agonists (albuterol)
  • Loop diuretics
  • Dialysis
168
Q

What level of serum Potassium is considered low?

A

K< 3,5mEq/L

169
Q

What are the 4 main etiological groups of Hypokalaemia?

A
  1. Decreased intake
  2. Shift into cells
  3. Renal losses
  4. GI losses
170
Q

Why is a decreased amount of intake of K+ a very rare etiology for Hypokalaemia?

A

Because the kidney can decrease potassium excretion to extremely small amounts.

171
Q

Name a few examples of Hypokalaemia etiologies causing K+ to shift into cells

A

Alkalosis
Insulin
B-agonists (stimulate Na/K pump)

172
Q

Name a few examples of Hypokalaemia etiologies due to Renal losses

A

Increased aldosterone:

  • Primary hyperaldosteronism (Conn syndrome)
  • Blood volume depletion
  • Cushing syndrome
  • Bartter syndrome (genetic disease causing salt loss in loop of Henle)
  • Licorices
173
Q

Name a few examples of Hypokalaemia etiologies due to GI losses

A

Vomiting
Diarrhea
Laxative abuse

174
Q

What is the clinical presentation of Hypokalemia?

A 
*similar to Hyperkalemia;
Weakness
Paralysis when severe
Ileus (paralyzes gut muscles)
Loss of reflexes 
Cardiac rhythm disorders

*Hypokalemia does not cause seizures.

175
Q

What is an anion gap?

A

It is defined as sodium minus chloride plus bicarbonate.
(Na+) minus (Cl− and HCO3−)
A normal anion gap is between 6 and 12.

176
Q

How would you manage hypokalemia?

A

Intravenous potassium replacement must be very slow.
There is no maximum rate of oral potassium replacement because the kidneys excrete K+ faster than it can be absorbed by the GI system.

177
Q

Why is the anion gap normal in Renal Tubular Acidosis (RTA) and Diarrhea?

A

Because the chloride level rises.

Hence, they are also referred to as hyperchloremic metabolic acidosis.

178
Q

A woman with ESRD and glucose 6-phosphate dehydrogenase deficiency skips dialysis for a few weeks and then is crushed in a motor vehicle accident. She is taking dapsone and has recently eaten fava beans. What is the most urgent step?

a. Initiate dialysis.
b. EKG.
c. Bicarbonate administration.
d. Insulin administration.
e. Kayexalate.
f. Urine dipstick.
g. CPK levels.
h. Urine myoglobin.

A

B.
All of these interventions may be helpful in a person with life-threatening hyperkalemia. The most important step is to determine if there are EKG changes from hyperkalemia.
If the EKG is abnormal, she needs calcium chloride or gluconate in order to protect her heart while the other interventions are performed. Kayexalate and dialysis take hours to remove potassium from the body.
Bicarbonate and insulin work in 15 to 20 minutes, but they are not as instantaneous in effect as giving calcium.

179
Q

Define RTA (Type I) and RTA (Type II)

A 
Distal RTA (Type I)
It is a transporter and or channel defect resulting in the inability to secrete/excrete fixed acid, while the tubular apical membranes become more permeable to allow H+ into the blood stream=> Academia + Increased urine pH
Proximal RTA (Type II)
It is a transporter and or channel defect resulting in a decreased ability of the proximal tubule to reabsorb (HCO3−)=> Academia + low urine pH
**The urine pH is variable. First it is basic (above 5.5) until most bicarbonate is lost from the body, then it is low (below 5.5).
180
Q

Which type(s) of Renal Tubular Acidosis (RTA) will result in Nephrolithiasis? Explain why

A

Both Type I & II will lead to Chronic metabolic acidosis and leaching of calcium out of the bones (osteomalacia) but with Type I the urine is alkaline and increases the chance for formation of kidney stones (nephrocalcinosis).

Distal RTA (Type I):
Since the normal buffers for acid (HCO3−) are excreted the body releases Ca2+ from bone to serve as a plasma buffer=> Nephrolithiasis
181
Q

Why is the anion gap normal in Renal Tubular Acidosis (RTA) and Diarrhea?

A

Because the chloride level rises.

Hence, they are also referred to as hyperchloremic metabolic acidosis.

182
Q

What are the types of Renal Tubular Acidosis (RTA)?

A

1) Distal RTA (Type I)
2) Proximal RTA (Type II)
3) Type III is a comination of I & II
4) Hyporeninemia, Hypoaldosteronism (Type IV RTA)

183
Q

Define RTA (Type I) and RTA (Type II)

A 
Distal RTA (Type I)
It is a transporter and or channel defect resulting in the inability to secrete/excrete fixed acid, while the tubular apical membranes become more permeable to allow H+ into the blood stream=> Academia + Increased urine pH
Proximal RTA (Type II)
It is a transporter and or channel defect resulting in a decreased ability to of the proximal tubule to reabsorb (HCO3−)=> Academia + low urine pH
184
Q

Which type(s) of Renal Tubular Acidosis (RTA) will result in Nephrolithiasis? Explain why

A

Both Type I & II will lead to Chronic metabolic acidosis and leaching of calcium out of the bones (osteomalacia) but with Type I the urine is alkaline and increases the chance for formation of kidney stones.

Distal RTA (Type I):
Since the normal buffers for acid (HCO3−) are excreted the body releases Ca2+ from bone to serve as a plasma buffer=> Nephrolithiasis
185
Q

How would you Tx RTA (Type II)?

A

It is difficult to treat it with bicarbonate replacement, because bicarbonate is not absorbed well in proximal RTA.

Thiazide diuretics cause volume depletion which enhance bicarbonate reabsorption.

186
Q

What is the best initial test to diagnose RTA (Type I)?

What is the most accurate test

A

The best initial test is a UA looking for an abnormally high pH above 5.5.
The most accurate test is to infuse acid into the blood with ammonium chloride.
**in Pt with RTA (Type I), pH will remain basic (over 5.5) despite an increasingly acidic serum.
*Urine pH should decrease in a healthy person

187
Q

How would you Tx RTA (Type I)?

A

Replace bicarbonate

188
Q

What is the best initial test to diagnose RTA (Type II)?

What is the most accurate test

A

The best initial test is a UA but the urine pH is variable in proximal RTA. First it is basic (above 5.5) until most bicarbonate is lost from the body, then it is low (below 5.5).

The most accurate test giving bicarbonate and testing the urine pH
*Because the kidney cannot absorb
bicarbonate, the urine pH will rise.

189
Q

How would you Tx RTA (Type II)?

A

It is difficult to treat it with bicarbonate replacement, because bicarbonate is not absorbed well in proximal RTA.

Thiazide diuretics cause volume depletion which enhance bicarbonate reabsorption.

190
Q

What is the best initial test to diagnose RTA (Type IV)?

A

Sodium-restriction diet that results in a persistently high urine sodium

191
Q

How would you Tx RTA (Type IV)?

A

Fludrocortisone

* Fludrocortisone is the steroid with the highest mineralocorticoid or “aldosteronelike” effect.

192
Q

What is the common factor between diarrhea and RTA?

How can we distinguish between diarrhea and RTA?

A

Both present with normal anion gap metabolic acidosis

urine anion gap (UAG)
UAG= (Na+) - (Cl-)

193
Q

What is the physiology behind the urine anion gap (UAG)?

A

UAG= (Na+) - (Cl-)
Acid excreted by the kidney is buffered off as NH4Cl. The more acid excreted, the greater the amount of chloride found in the urine.
In RTA there is a defect in acid excretion into the urine, so the amount of chloride in the urine is diminished. This gives a positive number when
calculating Na+ minus Cl–.
In diarrhea, the ability to excrete acid through the kidney remains intact. Because diarrhea is associated with metabolic acidosis, the kidney tries to compensate by increasing acid excretion. So, in diarrhea, more acid in
the urine means more chloride in the urine. Na+ minus Cl– will become a negative number in diarrhea.

194
Q

What are some of the main causes of Metabolic Acidosis with an Increased Anion Gap?

A

[LKO-For-US]

[LaKe Ox For Ur Salicylates]

Lactate, Ketoacids, Oxalic acid, Formic acid, Uremia, Salicylates

195
Q

What can cause increased levels of Lactate, leading to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

Hypotension or hypoperfusion

Blood lactate level

Correct hypoperfusion

196
Q

What can cause increased levels of Ketoacids, leading to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

DKA, starvation

Acetone level

Insulin and fluids

197
Q

Name an example of an Oxalic acid that can lead to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

Ethylene glycol overdose

Crystals on UA

Fomepizole, dialysis

198
Q

Name an example of a Formic acid that can lead to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

Methanol overdose

Inflamed retina

Fomepizole, dialysis

199
Q

Name an example of Uremia that can lead to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

Renal failure

BUN, creatinine

Dialysis

200
Q

Name an example of Salicylates that can lead to Metabolic Acidosis with an Increased Anion Gap?

What is the best initial test?

What is the best initial Tx?

A

Aspirin overdose

Aspirin level

Alkalinize urine

201
Q

What is the mechanism of compensation for all forms of metabolic acidosis?

A

Respiratory alkalosis from hyperventilation

202
Q

What are the findings on an arterial blood gas (ABG) in metabolic acidosis?

A
  • Decreased pH <7.40
  • Decreased bicarbonate
  • Decreased pCO2 indicating respiratory alkalosis as compensation
203
Q

What unique finding in terms of compensation sets Metabolic problems apart from respiratory problems?

A

Metabolic problems always show compensation

204
Q

What are the findings on an arterial blood gas (ABG) in metabolic alkalosis?

A

Increased pH >7.40
Increased bicarbonate
Increased pCO2 indicating respiratory acidosis as compensation

205
Q

What are some of the causes of Respiratory alkalosis?

A 
Anemia
Anxiety
Pain
Fever
Interstitial lung disease
Pulmonary emboli
206
Q

What are some of the causes of Respiratory acidosis?

A 
COPD/emphysema
Drowning
Opiate overdose
Alpha 1-antitrypsin deficiency
Kyphoscoliosis
Sleep apnea/morbid obesity
207
Q

Is the minute ventilation in Respiratory alkalosis increased or decreased?

A

Increased

208
Q

Is the minute ventilation in Respiratory acidosis increased or decreased?

A

Decreased

209
Q

A 46-year-old man comes to the emergency department with excruciating pain in his left flank radiating to the groin. He has some blood in his urine.

What is the most appropriate next step in the management of this patient?

a. Ketorolac.
b. X-ray.
c. Sonography.
d. Urinalysis.
e. Serum calcium level.

A

*A.
Ketorolac is an NSAID that is available orally and intravenously. It provides a level of analgesia similar to opiate medications. When the presentation of nephrolithiasis is clear, it is more important to provide relief for this excruciating form of pain than to obtain specific diagnostic tests.

210
Q

What is the most accurate diagnostic test for nephrolithiasis?

a. CT scan.
b. X-ray.
c. Sonography.
d. Urinalysis.
e. Intravenous pyelogram.

A

*A.
The CT scan for nephrolithiasis does not need contrast and is more accurate (sensitive) than an x-ray or sonogram. Intravenous pyelogram (IVP) needs intravenous contrast and takes several hours to perform. Urinalysis and straining the urine may show blood or the passage of a stone, but will not help manage acute renal colic. X-ray has a false negative rate between 10% and 20%.
IVP is always a wrong answer for nephrolithiasis.

211
Q

What is the most common type of kidney stone?

Which type of stones are not detectable on X-ray?

A

Calcium oxalate

Uric acid

212
Q

What is the best initial therapy for acute renal colic or nephrolithiasis?

A

Analgesics (Ketorolac) and hydration

213
Q

What is the nest best step after giving analgesics and hydration in nephrolithiasis?

A

CT and sonography to detect and determine size of obstruction.

214
Q

How is nephrolithiasis managed according to the size of the stone?

A
  • Stones <5 mm pass spontaneously
  • Stones 5–7 mm get nifedipine and tamsulosin to help them pass
  • Stones 0,5 to 2cm should be managed with Lithotripsy
  • Stones >2cm - Surgery
215
Q

A woman with her first episode of renal colic is found to have a 1.8 cm stone in the left renal pelvis. She has no obstruction and her renal function is normal (normal BUN and creatinine).

What is the most appropriate next step in the management of this patient?

a. Wait for it to pass; hydrate and observe.
b. Lithotripsy.
c. Surgical removal.
d. Hydrochlorothiazide.
e. Stent placement.

A

B. Lithotripsy is used to manage stones between 0.5 and 2 to 3 centimeters. Small stones (less than 5 mm) will spontaneously pass. Stones larger than 2 centimeters are not well-managed with lithotripsy because the fragments will get caught in the ureters. These large stones are best managed surgically. Stent placement relieves hydronephrosis from stones caught in the distal ureters.
Stones halfway up the ureters are treated with lithotripsy. Those halfway down the ureter are removed from below with a basket.

216
Q

Describe the types and characteristics of Urinary Incontinence

A

1) Stress incontinence
Painless urinary leakage with coughing, laughing, or lifting heavy object

2) Urge incontinence
Sudden pain in the bladder followed immediately by the overwhelming urge to urinate

217
Q

How would you test for Stress incontinence?

A

Have patient stand and cough;

observe for leakage

218
Q

How would you test for Urge incontinence?

A

bladder; manometry

219
Q

What is the relationship between Metabolic Acidosis and Stone Formation?

A

Metabolic acidosis removes calcium from bones and increases stone formation. In addition, metabolic acidosis decreases citrate levels. In normal cases, Citrate binds calcium, making it unavailable for stone formation.

220
Q

Describe the types and characteristics of Urinary Incontinence

A

1) Stress incontinence
Painless urinary leakage with coughing, laughing, or lifting heavy object

2) Urge incontinence
Sudden pain in the bladder followed immediately by the overwhelming urge to urinate

221
Q

How would you test for Stress incontinence?

A

Have patient stand and cough;

observe for leakage

222
Q

How would you test for Stress incontinence?

A

bladder; manometry

223
Q

What are the options for managing Stress incontinence?

A
  1. Kegel exercises
  2. Local estrogen cream
  3. Surgical tightening of urethra
224
Q

What are the options for managing Urge incontinence?

A
  1. Bladder training exercises
  2. Local anticholinergic
    therapy:
    Oxybutynin
    Tolterodine
  3. Surgical tightening of urethra
225
Q

Is there a difference in what is considered as hypertension according to age?

A

In general high BP is 140/90 BP but 150/90 mmHg in Pt >60years

226
Q

What are some of the causes of Secondary HTN?

A 
Coarctation of the aorta
Closer of renal artery (Renal artery stenosis)
Congenital adrenal hyperplasia
Cushing syndrome or any cause of hypercortisolism including therapeutic use of glucocorticoids
Obstructive sleep apnea
Pheochromocytoma
Hyperaldosteronism
Glomerulonephritis
227
Q

What other tests are conducted upon Dx a Pt with HTN?

A
  • EKG
  • Urinalysis
  • Glucose measurements to exclude concomitant diabetes
  • Cholesterol screening
228
Q

What is the best initial therapy for HTN?

A

lifestyle management such as:

  • Weight loss (most effective)
  • Sodium restriction
  • Dietary modification (less fat and red meat, more fish and vegetables)
  • Exercise
  • Tobacco cessation does not stop hypertension, but becomes especially important to prevent cardiovascular disease.
229
Q

How long do we try Lifestyle modifications in a Pt with HTN?

A

Lifestyle modifications are tried for 3 to 6 months before medications are started.

230
Q

Which medications should be considered in the initial Mgx of HTN?

A

The best initial therapy is a thiazide diuretic, calcium blocker, ACE inhibitor, or angiotensin receptor blocker.

Diuretics are not considered specifically better as the initial therapy.

231
Q

Which situation would warrant the use of 2 medications to control HTN?

A

If blood pressure is very high on presentation (above 160/100), 2 medications should be used

232
Q

If diuretics do not control blood pressure, what is the most appropriate next step in management?

A
  • ACE inhibitor
  • Angiotensin receptor blocker (ARB)
  • Beta blocker (BB)
  • Calcium channel blocker (CCB)
233
Q

Which drugs are the pregnancy safe hypertension drugs?

A

BB—use first
CCB
Hydralazine
Alpha methyldopa

234
Q

If the Pt has a history of Coronary artery disease, what is the best initial therapy?

A

BB, ACE, ARB

235
Q

If the Pt has a history of Diabetes mellitus, what is the best initial therapy?

A

ACE, ARB (goal <140/90)

236
Q

If the Pt has a history of Benign prostatic hypertrophy, what is the best initial therapy?

A

Alpha blockers

237
Q

If the Pt has a history of Depression and asthma, what is the best initial therapy?

A

Avoid BBs

238
Q

If the Pt has a history of Hyperthyroidism, what is the best initial therapy?

A

BB first

239
Q

If the Pt has a history of Osteoporosis, what is the best initial therapy?

A

Thiazides

240
Q

What is the best initial therapy for hypertensive crisis?

A

Labatolol or Nitroprusside

241
Q

What gives Nitroprusside a disadvantage in comparison to Labatolol?

A

Nitroprusside needs monitoring with an arterial line

242
Q

Besides Labatolol and Nitroprusside, which other drugs can be used in acute hypertensive crises?

A 
Enalapril
CCBs: diltiazem, verapamil
Esmolol
Hydralazine
Peripheral dopamine receptor antagonist: fenoldopam
243
Q

What precaution needs to be taken into consideration when Tx hypertensive crises?

A

Don’t lower the BP by more than 25% on the first day. You may provoke a stroke if you do so.

M.T.B (9 decks)

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