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Internal Medicine Shelf Exam > Nephrology > Flashcards

Nephrology Flashcards

1
Q

Nephrotic vs. Nephritis

A

NephrOtic:
- proteinuria ( > 3.5)
- edema
- hypoalbuminemia
- Oval fatty bodies ( maltase Cross) in urinalysis
- biopsy shows hypo-cellular specimen
- related to obesity—> hyperlipidemia+ edema + fatty casts/oval fatty body

NephrItic:
- proteinuria (< 3.5)
- hematuria
- HTN

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2
Q

Nephrotic syndrome primary etiology

A
  1. minimal change disease
    - most common in children
    - loss of negative charge in basement membrane promoting proteinuria (lack of charge at basement membrane)
  2. Membranous nephropathy:
    - Men > 40
    - Malaria
    - Medication (penicillinase)
  3. Focal Segmental Glomerulosclerosis:
    - seen with: HIV, heroin users, HTN
    - most common in African American
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3
Q

Nephritic syndrome/ glomerulonephritis

A

1.IgA Nephropathy
- most common cause of acute glomerulonephritis
- most common affect young males
- occurs 24-48 hours after URI or GI infection

  1. Post infectious/ Post streptococcal Glomerulonephritis:
    - most common after group A strep (GAS) infection
    - Coca-Cola color urine
    - seen in adolescent boy 2-14 years
    - facial edema is common
  2. GoodPasture’s Disease:
    - Glumeronephritis + Hemoptysis
    - anti-GBM antibody against the type 4 collagen of the glomerular basement membrane
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4
Q

Acute kidney injury —> Prerenal

A
  • kidney is fine
  • but decrease renal perfusion
  • due to hypovolemia (volume depleted)—> ( diuretics, diarrhea, vomiting, dehydrated)
  • other causes:
    1. NSAIDS: Afferent arterial constriction
    2. ACE-inhibitors: Efferent arterial dilation

Diagnosis:
- BUN/Cr ratio > 20:1
- Fractional excretion of sodium < 1%
- concentrated urine
- decrease urinary sodium < 20 (kidney are working fine, and able to retain sodium)

Treatment:
- IV fluid ( respond well !!)

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5
Q

Acute kidney injury —> Post-renal Azotemia

A
  • due to obstruction (stop urine flow from kidney to bladder)—> (kidney stone, tumors, BPH, prostate, cancer)

Diagnosis:
- ultrasound —> look for sign of obstruction

Treatment:
- remove obstruction —> lithotripsy, urinary stent

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6
Q

Intra-renal or Intrinsic Renal Failure ( acute interstitial Nephritis, acute tubular necrosis)

A
  1. Acute Interstitial Nephritis:

caused by:
1. Medication (70%) —> NSAIDS, penicillin, Sulfa-, rifampin
2. infection, autoimmune process

clinical:
- fever, esosinophellia, rash

diagnosis:
- WBC casts ( neutrophils) seen in urinalysis

Treatment:
- remove offending agent

  1. Acute Tubular Necrosis:
    - most common type of Intrinsic kidney injury

Caused by:
- ischemia —> prolonged prerenal azotemia
- nephrotoxic agents —> contrast dye, aminoglycosides

Diagnosis:
- Granular or muddy brown casts in urinalysis
- increase urinary sodium > 40 (kidney not working properly, unable to retain sodium)
- BUN/Cr ratio 10-15:1

Treatment:
- remove offending agent & IV fluid

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7
Q

Microscopic finding on Urinalysis

A
  1. Acute Glomerulonephritis or vasculitis:
    - RBC Casts
  2. Acute interstitial Nephritis or pyelonephritis:
    - WBC casts
  3. Nephrotic syndrome: ( or pre-renal azotemia)
    - fatty casts or oval fat bodies
  4. End stage renal disease:
    - waxy casts
    - or broad cast ( in CKD)
  5. Interstitial nephritis
    - Eosinophils
  6. Acute Tubular necrosis (ATN)
    - Muddy Brown Cast
    - following a hypovolemic shock (prolonged hypotension)
    - BUN/Cr ratio ( 10-15: 1)
    - urine osmolality of 300-350 ( never < 300)
    - urine Na > 20
    - fraction excretion of Na > 2 %
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8
Q

Horseshoe kidney

A
  • fusion at lower lobe of each kidney
  • associated with:
    1. Uritopelvic junction obstruction
    2. Turner syndrome
  • increase risk for:
    1. Pyelonephritis ( due to urinary stasis)
    2. Kidney stone
    3. Renal malignancy
    4. Renal cell carcinoma

Clinical:
-most patients asymptomatic

Diagnosis:
- CT urography

Treatment:
- most cases require no treatment

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9
Q

Polycystic kidney disease

A
  • autosomal dominant
  • cyst is seen in the kidney or liver

Clinical:
- abdominal & flank pain
- increase risk for cerebral (berry) aneurysm & Mitral valve prolapse

PE:
- palpable flank mass
- HTN

Diagnosis:
- renal US

Treatment:
- increase fluid intake
- ACE-I/ARB

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10
Q

Chronic kidney disease (CKD)

A

-progressive functional decline for 3 months or more, accompanied by: proteinuria, abnormal urine, sediment, abnormal imaging

Stages of CKD:
1. Stage 1:
- GFR (>90) & proteinuria & abnormal urinalysis

  1. Stage 2:
    - GFR (60-89) & proteinuria & abnormal urinalysis
  2. Stage 3
    - GFR (30-59) & proteinuria & abnormal urinalysis
  3. Stage4
    - GFR (15-29) & proteinuria & abnormal urinalysis
  4. Stage 5:
    - GFR (<15) indicates END stage Renal disease —> REQUIRE Dialysis

Causes:
1. Diabetic mellitus (1st)
2. HTN (2nd)

Diagnosis:
- proteinuria (24 hr urine, or albumin/Cr ratio)
- waxy cast (in urinalysis)
- renal US ( shows small kidney)

Treatment:
- treat HTN —> maintain BP < 140/90
- ACE-I or ARB in most patients
- A1C < 7
- dialysis at stage 5

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11
Q

Wilms tumor (Nephroblastoma)

A
  • most commonly seen with children less than 5

Clinical:
- iris malformation ( aniridia = absence of iris)
- locked In position tumor (doesn’t cross midline of abdomen, unlike neuroblastoma of adrenal which does)
- mental retardation
- sexual malformation (hypospadias, cryptorchidism)
- palpable abdominal mass
- hematuria
- constipation

Diagnosis:
- abdominal US

Treatment:
- total nephrectomy with chemo 80-90% cure rate

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12
Q

Renal cell carcinoma (RCC)

A
  • Tumor of the proximal convoluted renal tubule cells
  • 95% of tumor in kidney

Risk:
- smoking, HTN, obesity, dialysis, Men

Clinical:
- Triad: hematuria + flank/abdominal pain + palpable abdominal mass
- left sided varicocele (due to the tumor blocking the left testicular vein)
- most common area of matastesis is the lung

Diagnosis:
- hypercalcemia ( tumor secrets PTHrP, which mimics primary hyperparathyroidism
- CT

Treatment:
- radical nephrectomy

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13
Q

Acid based disorder

A
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14
Q

Hepatorenal syndrome (HRS)

A

Seen in:
- seen with patients with liver cirrhosis secondary to systemic or renal hypoperfusion
- creatinine > 1.5
- urine sodium < 10
- absent of blood, protein, casts in urine
- renal function does not improve with IV fluid resuscitation

Caused by:
- splanchnic arterial dilation
Factors:
- reduce renal perfusion
- GI bleed, vomiting, sepsis, excessive diuretic use, SBP
- reduce glomerular pressure & GFR ( NSAIDs use—> constrict afferent arterioles)

Diagnosis:
- Fraction excretion of sodium < 1 % ( urine Na < 10)
- absence of tubular injury
- No RBC, protein, or granular casts in urine
- no improvement in renal function with fluid

Treatment:
- splanchnic vasoconstrictors ( midodrine, octreotide, norepinephrine)
- liver transplantation

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15
Q

Hyponatremia ( Na < 135 )

A

Caused by:
1. Increase ADH
2. Polydipsia, starvation

Clinical:
- confusion, lethargy, muscle cramps, N

Diagnosis:
- measure serum osmolality ( if the measured Sosm, is higher than calculated —> by more than 10-15 mOsm —> indicates an oxygenous osmole diluting the serum sodium.

  • correct sodium in hyperglycemia ( sodium correction —> sodium decrease by 1.6 for every 100 elevation in glucose)
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16
Q

Dirty medicine videos nephrotic vs. nephritic

A
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17
Q

Indication of dialysis:

A
  1. Symptoms ( confusion, lethargy, N/V — severe uremic symptoms !!
  2. Elect. ( potassium = HYPERKALMEIA and acidosis NOT RESPONDING TO MEDICAL MANAGEMENT)
  3. Volume over load not responding to dieuritic
  4. Minimal/ No urine output
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18
Q

Renal biopsy is confirmative of CKD

A

Ratinopathy, for how long
HTN ( for how long)
1. Urine amount + frequency
2. Dysuria + hematuria
3. Have you been seen by nephrology
4. History of NSAIDS —>
5. HAVE YOU BEEN IN HOSPITAL … did they provide you with Intermascular medication
6. History of renal stone ?
7. Did you ever need dialysis before?

Contrast

  • SPEP
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19
Q
A

Anemia
Leukopenia
Hyponatremia
Hypokalemia
BUN/Cr ratio > 30
- urine output decreased —> after holding diuretics
- urine sodium = 5

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20
Q

Microscopic finding on Urinalysis

A
  1. broad cast
  2. Muddy brown cast
    - renal tubular necrosis (RTN)
  3. RBC cast
    - renal interstitial
  4. WBC cast
  5. Fatty casts
  6. Eosinophils
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21
Q

Muddy brown cast in patient with ampho, AG, cisplatin or prolonged ischemia

A
  • acute tubular necrosis
  • treat with fluid
  • avoid nephrotoxic agent ( contrast dye, ARBs, NSAID)
  • DIALYSIS if needed
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22
Q

Protein, blood, eosinophils in urine + fever + rash + who took TM-SMX for past 1-2 weeks

A
  • Acute interstitial nephritis
  • stop offending agent
  • steroid if no improvement
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23
Q

Army recruit or crush victim with CPK of 50 K + blood on dip, but no RBCs

A
  • Rhabdomyolysis
  • test: check K concentration on ECG
  • Treat with: Bicarb ( to alkanize urine to prevent precipitation)
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24
Q

Enveloped shaped crystal on Urinalysis

A
  • ethylene glycol intoxication
  • Anionic gap metabolic acidosis ( AGMA)
  • treat with dialysis or sodium-bicarb, if PH < 7.2
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25
Q

If creatinine level jumped in the 48-72 hours after Cardiac cath or CT

A
  • contrast nephropathy.
  • prevent by hydration before or giving bicarb or NAC
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26
Q

Indication for emergent dialysis

A
  1. Acidosis
  2. Electrolyte imbalance —> especially K > 6.5
  3. Intoxication —> anti-freeze (ethylene glycol) or lithium
  4. Overload of volume —> symptoms of CHF or pulmonary edema
  5. Symptoms of uremia —> pericarditis, confusion, itching, blood loss
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27
Q

Chronic kidney disease (CKD)

A
  • Caused by —> 1st DM, 2nd HTN
  • death due to cardiovascular disease —> maintain LDL < 100

Complication:
1. HTN, fluid retention ( CHF)
2. Normochromic normocystic anemia —> loss of EPO
3. High K, High PO4, low Ca ( lead to secondary hyperparathyroidism)
4. High PO4 lead to precipitate Ca in tissue —> skin necrosis
5. Uremia —> confusion, pericarditis, itching, blood loss ( due to platelet dysfunction)

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28
Q

Causes of hyponatremia ( too much water)

A
  1. Hypervolemic hyponatremia ( gain too much water)
    - CHF
    - nephrotic syndrome
    - cirrhosis
  2. Hypovolemic hyponatremia: (loose too much water)
    - diuretics
    - vomiting
    - free water
  3. Euvolemic hyponatremia:
    - SIADH ( check chest xray if smoker)
    - addison disease
    - hypothyroidism

Treatment:
- IV normal saline (fluid restrict them)

  • only use hypertonic saline (3%) if patient have sign/symptoms of seizure or Na concentration of < 120
  • avoid treating them fast (ONLY 12-24 mEq/Day)—> to prevent central pontine myelinolysis (CPM)
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29
Q

Causes of hypernatremia

A
  • caused by loss of water
  • treat with:
    1. Replace water with D5W or other hypotonic fluid
    2. Don’t correct fast of else —> patient develop cerebral edema
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30
Q

Hypocalcemia

A
  • numbness
  • prolonged QT
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31
Q

Hypercalcemia

A
  • painful bone + renal stones + abdominal groan + psychiatric moans
  • shortened QT
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32
Q

Hypokalemia

A
  • paralysis (severe muscle weakness) + ilues + decrease DTR + palpitation + arrhythmia
  • ST depression + T-wave flattening followed by U-wave development
  • treat with:
    1. Oral K ( make sure patient can pee), IV in severe cases
    2. Maximum 40 mEQ/ hr

Causes:
1. GI loss ( diarrhea, vomiting, diuretics; thiazide, loop)
2. Medication that causes intracellular K shift —> (beta 2 agonist, insulin)
3. Hypomagnesemia —> ( low mg opens the mg-dependent K Channel spilling K into urine)

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33
Q

Hyperkalemia

A
  • prolonged PR + prolonged QRS + tall peaked T wave + sine wave
  • muscle weakness, flaccid paralysis, cardiac arrhythmia, abdominal distention, diarrhea
  • Treat with: ( C BIG K Drop)
    1. Calcium gluconate ( prevent arrhythmia )
    2. Beta 2 agonist (albuterol) or ( sodium bicarb)
    3. Insulin ( drive K into cells)
    4. Glucose
    5. Kayxalate ( poop out K; takes days; outpatients)
    6. Last resort —> dialysis, in refractory patient

Caused by: CARED

  1. Cellular lysis: rhabdomyolysis, burns, tumor lysis
  2. Decrease Aldosterone: hypoaldosteronism, adrenal insufficiency
  3. Renal failure
  4. Excessive K intake ( eating too much banana in dialysis patient)
  5. Drugs: ACE I/ ARBS, Spironolactone
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34
Q

Acute renal allograft

A
  • T-cell mediated
  • occurs within first 6 months following transplant
  • asymptomatic rise in serum creatinine
  • renal biopsy confirms diagnosis—> lymphocytic infiltration of the intima
  • treatment: high dose IV glucocorticoid
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35
Q

Pyelonephritis

A
  • affect transplanted patient
  • symptoms: fever + dysuria + pelvic pain
  • finding: nitrate or leukocyte esterase on UA
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36
Q

Acute toxicity to calcineurin inhibitor ( tacrolimus & cyclosporine)

A
  • vasoconstriction of renal afferent & efferent arteriole
  • lead to prerenal acute kidney injury + HTN
  • BUN/Cr ratio= > 20
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37
Q

Acute renal failure present with hypocalcemia, however if hypercalcemia present this suggest multiple myeloma

A

multiple myeloma/malignancy:
- anemia + hypercalcemia + bone pain + acute renal failure

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38
Q

Determine which type of acute kidney injury

A

Prerenal:
- low urine sodium ( < 20)
- elevated BUN/Cr ratio (> 20)
- urine osmolality (> 500 mOsm)
- microscopy (Bland; without WBC, Protein or casts )

Intrinsic
- Acute tubular necrosis (ATN)
- High urine sodium ( > 40)
- normal BUN/Cr (10-15: 1)
- urine osmolality ( almost 300)
Microscopy: muddy brown casts

Post renal:
- hydronephrosis on Ultrasound

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39
Q

Effect of hypovolemia of renin-angiotensin system (RAS)

A
  • Hypovolemia stimulated RAS system
  • improve intravascular system & GFR & BP via vasoconstriction & kidney- mediated Na & water resorption
  • increased renin + increased efferent arteriolar resistance + increase tubular sodium reabsorption
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40
Q

Acute gallstone pancreatitis

A
  • colicky abdominal pain after eating
  • severe epigastric pain + vomiting + elevated lipase
  • pancreatitis lead to hypovolemia:
    1. Activates RAS system
    2. Increase renin secretion
    3. Lead to:
  • vasoconstriction: increase efferent arteriole resistance= improve GFR & BP
  • sodium retention: increase sodium reabsorption at the proximal convoluted tubules
  • aldosterone production: reabsorption of sodium & water at the distal convoluted tubules
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41
Q

Metformin

A
  • used in diabetes type 2
  • can cause: lactic acidosis, diarrhea, vitamin B12 deficiency
  • metformin should be withhold in the sitting of AKI ( Dehydration, decrease mucous membrane, increase Bun/Cr > 20)
  • metformin is avoided in Chronic kidney disease ( GFR < 30)
  • Sepsis ( fever + hypotension + tachycardia) & dehydration = increase lactic acid levels
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42
Q

Pre-renal AKI

A
  • result from total body-volume depletion
  • it can occur in volume-overloaded states that involves ( reduced effective arterial blood volume) —> due to acute heart failure exacerbation & AKI is most likely due to cardiorenal syndrome
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43
Q

Cardio-renal syndrome

A

LV & RV failure

  1. Decrease CO
    • decrease renal perfusion
    • decrease GFR
    • activates RAS system
    • vasoconstriction + aldosterone production + increase sodium/water reabsorption
      - LV & RV failure
  2. Increase central venous & renal venous pressure
    - decrease glomerular capillary filtration gradient
    - decrease GFR
    - activates RAS system
    • vasoconstriction + aldosterone production + increase sodium/water reabsorption
      - LV & RV failure
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44
Q

Renal venous congestion & AKI in cardio-renal syndrome

A
  1. Increase renal venous pressure
  2. Increase vasa recta fluid leakage

3.Tubulo-interstitial edema —> increase intratubular pressure

  1. Increase Bowman capsule hydrostatic pressure —> decrease filtration gradient —> decrease GFR
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45
Q

Diuretics are the most effective therapy for AKI due to cardiorenal syndrome

A
  • furosemide (lasix)
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46
Q

Crystal- induced AKI (renal tubular obstruction)

A
  1. EXAMPLES:
    - Acyclovir
    - Sulfa
    - uric acid
    - methotrexate
  2. increase risk with volume depletion & CKD
  3. Diagnosis:
    - on UA: hematuria ( RBC in urine) + pyuria ( WBC in urine) + crystals
  4. Management:
    - discontinue drug
    - volume repletion
    - loop diuretics ( furosemide)
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47
Q

Work-up of high anion- gap metabolic acidosis

A
  • High anion gap metabolic acidosis (MUDPILES)
  • associated clues
  1. Drug ingested
    - salicylate ( early respiratory alkalosis)
    - Isoniazid
    - Iron
  2. Hypoperfusion
    - increase lactic acid —> lactic acidosis ( example Metformin in DM2 avoid in CKD)
  3. Renal failure:
    - increase BUN —> uremia ( confusion, pericarditis, itching, blood loss)
  4. Hyperglycemia:
    - urine & serum ketones —> diabetic ketoacidosis
  5. Osmolal gap:
    - ethylene glycol ( urinary calcium oxalate crystal; renal failure)
    - methanol ( blindness)
    - propylene glycol

Note: (MUDPILES)
Methanol, uremia, DKA, propylene glycol, isoniazid/Iron, lactic acid, ethylene glycol, salicylate

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48
Q

Analgesic nephropathy

A

Patho:
- prolonged use of combination analgesics
1. Acetaminophen
2. Aspirin/NSAIDs

  • manifest as “chronic interstitial nephritis ± papillary necrosis”

Clinical:
- chronic pain ( headache, lower back pain)
- malaise, fatigue, flank pain
- UA: WBC + WBC cast ± mild proteinuria
- hematuria & urine RBC, if papillary necrosis present
- imaging: small kidney ± papillary calcification & irregular contour

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49
Q

Rhabdomyolysis

A

Etiology:
Skeletal muscle lysis/necrosis due to:
1. Crush injury or prolonged immobilization
2. Intense muscle activity ( seizure, excretion)
3. Drug/medication in-toxicity ( statin)
4. Alcohol abuse + cocaine abuse

Clinical:
1. Muscle pain/weakness
2. Dark urine ( myoglubinuria/ pigmenturia)
3. Presence of blood in UA, absence of RBC on microscopy
4. Increase serum K & PO4, decrease Ca
5. Increase AST > ALT
6. AKI

Diagnosis:
- serum Creatinine Kinase (CK > 1000)

Management:
- aggressive IV fluid
- sodium Bicarbonate

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50
Q

Patient with COPD develops pulmonary HTN & cor Pulmonary

A
  1. COPD ( dyspnea + cough + wheezing + hypoxia) + chronic respiratory acidosis ( high CO2; from CO2 retention) + compensatory metabolic alkalosis ( high bicarb + near normal pH)
  2. Pulmonary HTN & cor pulmonary ( JVD, hepatomegaly, peripheral edema in the presence of clear lung)
  3. In Cor pulmonary —> loop diuretics (furosemide) is used to lower right ventricular filling volume & reduce peripheral edema
  4. Loop diuretic can lead to hypovolemia, low CO, renal hypo-perfusion —> prerenal azotemia/ AKI can develop
    - elevated creatinine ( double of baseline)
    - BUN/Cr ratio > 20
    - elevated Anion Gap Metabolic Acidosis ( > 14)
  5. Diuretics can cause hypokalemia, but AKI negates that effect explaining the stable potassium level ???
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51
Q

Sepsis lead to prerenal AKI

A
  1. Sepsis ( hypotension, tachycardia, altered mental status, leukocytosis, lung consolidation) due to community acquired pneumonia
  2. Sepsis lead to peripheral vasodilation ( hypotension) & volume depletion ( decrease appetite, decrease oral intake, dry mucous, hypernatremia)
  3. Sepsis + volume depletion = prerenal AKI ( due to decrease renal perfusion)

Note:

  1. Renal hypoperfusion —> decrease GFR —> Increase creatinine —> activates RAS —> increase sodium reabsorption —> urine sodium < 20 & low fractional excretion of sodium (<1) —> urea passively follow sodium & water reabsorption —> increase BUN/Cr (> 20) —> urine sediment is bland ( no WBC, no protein, no casts)
  2. Treatment: IV fluid ( crystalloids)
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52
Q

Contrast- associated AKI

A
  • Creatinine elevation 24-48 hours after arterial contrast, followed by gradual return to baseline (in 3-7 days)
  • patient with CKD are at increased risk
  • preventative measures include: IV (0.9% saline), avoid NSAIDS, use of smallest possible volume of contrast
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53
Q

Chronic kidney disease (CKD)

A
  1. Lead to unintentional weight loss in elderly
    • Watchful waiting + nutritional supplement
  2. Platelet dysfunction is the most common cause of abnormal hemostasis ( easy bruises, non-palpable purpura). PT & PTT are normal. Platelet count is normal or mildly low.
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54
Q

What is the most common cause of nephrotic syndrome in children

A
  • minimal change disease
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55
Q

IGA nephropathy is precedded by what type of infection ?

A
  • upper respiratory infection (± GI infection)
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56
Q

Describe the finding on biopsy in a patient with rapidly progressive Glumerulonephritis ?

A
  • crescent formation

( like a moon)

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57
Q

Young patient ( 7 year old) + Dark urine + puffy face + Sick a couple of days ago + positive ASO titer ?

What type of infection happened in the past 10-14 days ?

A
  • Group A strep infection
  • lead to post-strep glomerulonephritis
  1. Coca-cola urine
  2. Periorbital edema
  3. Common in 5-12 years old males
  4. Positive ASO titer
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58
Q

What is the most common etiology of Acute interstitial nephritis ?

A

Drug hypersensitivity ( antibiotics, NSAIDS)

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59
Q

What is the most common cause of ESRD

A
  • DIABETIC MELLITUS
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60
Q

Fatty casts or oval fat bodies are commonly associated with what renal disorder ?

A
  1. Nephrotic syndrome
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61
Q

Middle age man ( 45 years) + history of HIV + history of heroine use + bubbly urine + swelling in the leg + HTN + fatty casts on microscopy.

What is the likely etiology of the symptoms seen ?

A
  • nephrotic syndrome —> Focal segmental Glomerulosclerosis (FSG)

Signs:
- middle age man
- frothy urine (from proteinuria)
- generalized edema
- seen with: HIV + Heroin use + HTN

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62
Q

Kidney stones & BPH are both common causes of which type of acute kidney injury

A
  • post-renal AKI
  1. obstructive uropathy ( from Bladder neck obstruction from BPH)
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63
Q

What is the first line treatment for patient with acute tubular necrosis ?

A
  • supportive ( IV fluid + discontinue of any offending agent)
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64
Q

What 2 types of HTN medication classes reduce proteinuria seen in renal disease?

A
  1. ACE inhibitors (-pril)
  2. ARBs (-sartan)
  • used in DM patients —> have a vasodilation effect on efferent arterioles
65
Q

What type of acute glomerulonephritis has positive anti-GBM antibodies that attack the type 4 collagen in the glomerular basement membrane ?

A
  • Goodpasture syndrome ( Anti- GBM disease)

Signs:
- hematuria + hemoptysis

66
Q

What type of nephrotic syndrome has glomerular basement membrane thickening seen on renal biopsy ?

A
  • membranous nephropathy
67
Q

What type of AKI is seen in volume depleted patients, such as patients with a history of diarrhea, vomiting & blood loss?

A
  • pre-renal AKI
68
Q

Elderly + hematuria + smoking + left sided varicocele is palpable .

What diagnosis ?

A

Renal cell carcinoma (RCC)

  • left kidney mass = obstruct proximal left gonadal vein = lead to distal left varicocele
69
Q

Elderly man + with AKI after CT with contrast + urinalysis shows muddy brown casts

What type of AKI ?

A
  • Acute tubular necrosis (ATN)
  • also seen with: vancomycin or aminoglycosides
70
Q

Middle age patient + persistent flank pain + BP running high for sometimes + bilateral palpable flank mass.

Likely diagnosis?

A
  • polycystic kidney disease

Symptoms:
- bilateral abdominal mass + flank pain

71
Q

A BUN/Cr ratio > 20: 1 should make you suspect which type of AKI?

A
  • pre-renal AKI

( due to dehydration, hypovolemia)

72
Q

Elderly women + elevated K of 6.3 + no ECG abnormality + patient is asymptomatic + history of phlebotomy struggling before drawing blood + multiple needle sticks + the tourniquet was placed for so long her finger turned blue

Causes of elevated K level?

A
  • psuedo-hyperkalemia

—> lead to RBC hemolysis during blood withdraw

73
Q

At what stage & GFR level is ERSD defined ( AKA kidney failure)?

A

At stage 5 ( GFR < 15) (Dialysis is required)

74
Q

A patient with history of turner syndrome & nephrolithiasis (kidney stone) presents with third UTI in the last 6 months.

What abnormality will be likely seen on CT urography ?

A

Horseshoe kidney ( fusion of the poles of the kidney) ( U-shaped kidney)

Symptoms:
- recurrent UTI
- recurrent kidney stones
- seen in turner syndromes

75
Q

Elderly male ( 68 yr) + history of hyperlipidemia, HTN, 2 coronary stents + on 3 different HTN medication ( amlodipine, lisinopril, hydrochlorothiazide) + BP today is elevated (174/96) + abdominal bruits heard

What is likely found on CT angiography of the abdomen/pelvis ?

A

Renal artery stenosis

Sign:
- persistent HTN ( unresponsive to 3 different HTN medication)

76
Q

What is the first line medication for patient with minimal change disease?

A

Glucocorticoid

77
Q

Middle age man ( 49) + fever + rash on abdomen+ recent history of lower back sprain + prescribed naprosyn for pain + increase Cr level + increase eosinophilia + urinalysis shows WBC casts

Initial treatment for patient?

A
  • acute interstitial nephritis (AIN)

Treatment:
1. Discontinue offending agent ( Naprosyn = NSAID) —> lead to drug hypersensitivity

78
Q

What type of renal disorder can lead to extra-renal manifistation such as cerebral aneurysm & mitral valve prolapse ?

A
  • polycystic kidney disease

Symptoms:
- Autosomal dominant
- abdominal pain + flank pain
- increase risk for cerebral aneurysm (subarachnoid hemorrhage) & MVP

79
Q

What classic finding will be seen on ECG in a patient with hyperkalemia early on ?

A

Early:
- tall peaked T wave ( with shortened QT interval)

Progress:
- prolonged PR interval + prolonged QRS

Severely ill:
- Sine wave

80
Q

What is the first line outpatient empiric treatment option for Acute pyelonephritis, as long as there is no resistance or contraindication to this class ?

A
  • fluoroquinolone (ciprofloxacin, levofloxacin)
  • for outpatient empiric treatment —> once culture result is received —> change treatment to suit the culture !!
81
Q

What is classic triad can be seen in patient with Renal Cell Carcinoma in advanced disease ?

A

Triad:
- palpable abdominal mass + flank pain + hematuria

82
Q

A patient with pH of 7.27, PCO2 of 56 & HCO3 of 24 has what type of acid base disorder ?

A
  • primary respiratory acidosis uncompensated
83
Q

What electrolyte abnormality should be suspected in a patient with T wave flattening & prominent U wave development on ECG ?

A

Hypokalemia

84
Q

what medication is used in patients with hyperkalemia to stabilize the myocardium & decrease incidence of cardiac arrhythmia

A
  • IV calcium gluconate
85
Q

A patient that rapidly responds to IV fluid administration, with normalization of serum creatinine in 24 to 72 hours is considered to likely have which type of acute kidney injury ?

A
  • prerenal AKI
86
Q

What is the most common site of metastasis in the renal cell carcinoma

A
  • Lung
  • followed by bone, lymph nodes
87
Q

Diffused effacement or loss of the epithelial cell ( podocytes) foot process is a classic finding on electrone microscopy in what type of nephrotic syndrome ?

A

Minimal change disease

88
Q

What is the most common type of renal cell carcinoma ?

A
  • clear cell
89
Q

What is the most common bacterial organism found in acute pyelonephritis ?

A
  • E.coli (80%)
90
Q

Beside the kidney, what area of the body does Goodpasture syndrome commonly affect ?

A

Lungs

91
Q

Before initiating treatment in patient with hypokalemia, what other electrolyte should you check to ensure there will not be resistance to the potassium replenishment ?

A
  • Magnesium
92
Q

Central pontine myelinolysis ( AKA: osmotic demyelinating syndrome) can be a serious consequence of rapidly correcting which type of electrolyte abnormality?

A
  • hyponatremia
93
Q

What compensatory mechanism do the lungs employ to counteract metabolic acidosis

A
  • increasing the respiratory rate (hyperventilate) —> - respiratory alkalosis
94
Q

What finding on microscopy are indicative of acute glomerulonephritis ?

A
  • RBC casts
95
Q

Elderly male (76 yrs) + with ESRD (stage 5 of CKD) + symptoms of vomiting, weight loss, muscle cramps, fatigue, altered mental status

What is the most common cause ?

A
  • Uremia
  • elevated concentration of Urea in the blood
96
Q

A 71 yr old female present with severe muscle weakness, and N/V + Loss of DTR + ECG shows decreased T wave amplitude + currently taking furosemide ( loop diuretic) for CHF.

Replenishing of what electrolyte is needed ?

A
  • potassium replacement ( she has hypokalemia)
97
Q

A nepphroblastoma (wilm’s tumor) can be differentiated from neuroblastoma by what physical exam finding ?

A
  • The mass in a nephroblastoma (wilm’s tumor) rarely cross the midline of the abdomen
  • unlike a neuroblastoma which commonly crosses the midline
98
Q

Elderly woman (62 yrs) + weakness & palpitation + ECG shows tall peaked T wave & shortened QT interval + history of Diabetes, HTN, Hyperlipidemia + medication ( metformin + rovastatin + lisinopril)

Which medication is the most probable offending agent leading to her symptoms?

A
  • patient have hyperkalemia
  • lisinopril ( ACE-inhibitor) is the cause
99
Q

Urinary outflow obstruction that leads to dilation & distention of the renal collecting system of one or both kidney is known as ?

A

Hydronephrosis

100
Q

What is the gold standard/ definitive test to diagnose renal artery stenosis ?

A
  • renal arteriography ( diagnostic & therapeutic)
  • can diagnose it and stent the artery at same time
101
Q

CKD is defined as the presence of kidney damage or decreased kidney function ( eGFR < 60) for at least how many months ?

A

Three or more months

  • to differentiate CKD from AKI
102
Q

Methanol, uremia,DKA, propynele glycol, isoniazid/iron, lactic acid, ethenyle glycol, salicylates

causes what type of acid base disorder ?

A
  • anion gap metabolic acidosis
103
Q

What is the most common renal malignancy in children ?

A

Nephroblastoma ( Wilm’s tumor)

104
Q

Bleeding types

A
  • CKD —> easy bruising + non-palpable purpura + due to platelet dysfunction. normal PT, PTT. Normal or mildly low platelet count
  • hemophilia A ( factor 8 deficiency) —> easy bruising + prolonged PTT
  • DIC —> bleeding + risk of sepsis or trauma + prolonged PT & PTT
  • vasculitis —> palpable purpura

Note:
- non-palpable purpura seen with platelet or coagulation disorders

105
Q

Calciphylaxis ( calcific uremic arteriolopathy)

A
  • systemic arteriolar calcification & soft-tissue calcium deposition with local ischemia & necrosis
  • commonly seen in patient with longstanding ESRD
  • risk factors include: hyperparathyroidism, hyperphosphatemia, hypercalcemia ( often serum Ca is normal)
106
Q

Rheumatic arthritis ( chronic inflammation) —> lead to AA amyloidosis —> lead to nephrotic syndrome

A
  1. Nephrotic patient ( proteinuria, pitting edema, hypoalbuminemia)
  2. Present with rheumatoid arthritis ( swan neck deformity, ulnar deviation, nodules)
  3. Complicated with AA amyloidosis

Note:
- AA amyloidosis can develop in the setting of chronic inflammation ( long standing Rheumatic arthritis)

  • the most common manifestation of AA Amyloidosis is:
    1. Renal disease ( proteinuria or nephrotic syndrome)
  • laboratory shows: elevated ESR + normocytic anemia
  • histology reveals:
    1. Amorphous hyalin material that is stained in Congo-red
    2. Green birefringence is noted under polarized light
107
Q

Common cause of nephrotic syndrome in adults

A
  1. membranous nephropathy (glomerulopathy)
  2. Focal segmental Glomerulosclerosis
  3. Amyloidosis
108
Q

Two types of amyloidosis

A

AA Amyloidosis
- associated with inflammatory conditions ( Rheumatoid arthritis & Inflammatory bowel disease; PU)
- associated with chronic infection: TB, osteomyelitis

AL Amyloidosis
- associated with Multiple myeloma
- associated with W. Microglobulinemia

109
Q

First line therapy for renal artery stenosis ?

A
  1. ACE- Inhibitors (-pril)
    Or
  2. ARBs ( -sartan)
  • patient with renal artery stenosis & on ACE-inhibitors are less likely to develop MI, stroke, ESRD.
    BUT, have high risk for AKI. Thus, renal function must be monitored closely
110
Q

Unilateral vs. bilateral renal artery stenosis

A

Unilateral renal artery stenosis:
1. Affected kidney has reduced renal blood flow & GFR
2. The healthy kidney compensate. Thus, lead to low acute changes in GFR

Bilateral renal artery stenosis:
1. Affected kidneys have reduced renal flow & significant low GFR. Patient can only tolerate ACE or ARBs only if creatinine rise < 30%

111
Q

Second line of treatment to patient with renal artery stenosis

A
  1. Renal artery stent
    Or
  2. Surgical Revascularization

Only use when:
1. Reserved for patient with resistant HTN
2. recurrent flash pulmonary edema
3. refractory heart failure due to severe HTN.

112
Q

Hypertensive nephrosclerosis

A
  • develop in patient with uncontrolled HTN
  • characterized by hyaline arteriolosclerosis & ischemic glomerulosclerosis
  • feature:
    1. Elevated CR ( due to decrease GFR)
    2. Ultrasound shows small, atrophic kidney
    3. Bland ( no WBC, no RBC) urinalysis with mild proteinuria
113
Q

Dialysis-related amyloidosis

A
  • inadequate removal/clearance of beta-2 microglobulin despite dialysis
  • present with shoulder pain/hypertrophy + Carpal tunnel syndrome + bone cysts
114
Q

Peritoneal dialysis-related peritonitis

A
  • caused by:
    1. touch contamination of the dialysis catheter lumen with skin bacteria
    Or
    2. Extension of a localized skin infection at the catheter site

Common organisms:
1. Staph. Epidermidis
2. Staph. Aureus

Diagnosis:
- abdominal pain + cloudy fluid
- neutrophil on fluid analysis
- positive fluid gram stain or culture

Treatment:
- combination of (vancomycin & gentamicin)
—> empiric treatment covers both (+) & (-) gram bacteria

115
Q

Relationship of diabetic nephropathy to ESRD

A

Measured via:
1. Urine Albumin to Creatinine ratio
- normal: <30
- microalbuminuria: 30-300
- macroalbuminuria: >300

Diagnosis of DN:
1. Persistent (more than 3 month) or elevated albuminuria (>30)

  1. Patient with diabetes can have diabetic nephropthy as micro vascular complication that can lead to ESRD.
  2. UACR should be measured at initial diagnosis of DM type 2 or at 5 years after diagnosis of DM type 2
  3. Hyperglycemia signs ( polydipsia and polyuria)
116
Q

Lupus nephritis

A

Caused by:
-SLE ( fatigue, inflammatory arthritis, anemia, thrombocytopenia)

Clinical:
Shows both:
1. Glomerulonephritis ( hematuria, proteinuria, renal failure, HTN, peripheral edema)
2. Nephrotic syndrome ( proteinuria, hypoalbuminemia, edema)

  1. Significant protein loss —> low serum albumin —> lower extremity edema + pleural effusion ( dullness on percussion + decreased breath sound)

Diagnosis:

  1. Positive anti-double standard DNA ( deposits on glomerulus)
117
Q

Membranoproliferative glumerulinephritis

A
  • Is type of nephrotic-range with hematuria and proteinuria
  • persistence activation of alternative complement system and causes kidney damage

-absence of immunoglobulin

118
Q

Renal venous thrombosis

A

Present with:
Abdominal pain, fever, hematuria

Associated with: membranous glomerulopathy

119
Q

SLE

A
  • anemia, thrombocytopenia, leukopenia
  • anti-ANCA, anti-dsDNA, anti-smith
  • low complement level and high immune complex
120
Q

Renal vein thrombosis (RVT)

A

Clinical:
- hematuria + flank pain + scrotal edema ( in men)

NOTE:
- patients with nephrotic syndrome have increase risk for DVT, PE, RVT
- patient with hypoalbuminuemia

121
Q

Type of stones

A
  1. Calcium ( oxalate or phosphate) ( > 75%):
    - high sodium or oxalate diet or malabsorption —> oxalate
    - renal tubular acidosis ( phosphate)
    - small, radiopaque stone
    - envelop ( oxalate), wedge (phosphate)
  2. Magnesium ammonium phosphate ( struvite) ( 15%) :
    - UTI with urease producing organism ( proteus)
    - large, radiopaque stone
    - rectangular
  3. Uric acid ( 8%):
    - Gout, diabetic/metabolic syndrome, myeloproliferative disorders
    - small, radiopaque
    - yellow/brown

Risk factor for kidney stone ( calcium oxalate stone):
- dehydration, increase sodium or oxalate in the diet, obesity, hyperparathyroidism, malabsorptive disorders

122
Q

Rhabdomyolysis

A

Signs:
- muscle weakness
- dark urine
- decrease urine output
- elevated creatinine
- elevated blood in UA, but no blood in microscopy
- AKI

  • associated with:
    1. drug myotoxicity ( statin, fibrates, colchicine, cocaine
    2. vasoconstriction: cocaine
    3. prolonged immobilization compression ischemia : alcohol, opioid, BDZ
123
Q

Patient with sickle cell trait

A
  • patient don’t have the symptoms of sickle cell disease
  • sickling of RBC occurs under phycological stress —> hypoxia, dehydration, acidosis
  • lead to renal papillary necrosis with hematuria & possible flank pain

Note:
Complication of sickle cell trait:
1. Hematuria/ papillary necrosis
2. Splenic infarct ( at high altitude)
3. Exertional rhabdomyolysis ( positive myoglubinuria + positive blood in urine + No RBC in urine/microscopy)
4. Renal tubular acidosis ( when urine pH = 5.8) —> tubular damage with impaired H+ secretion

124
Q

Nephrolithiasis

A
  • acute flank pain + hematuria
  • pain radiates to the groin

Management:
-dietary:
1. Increase fluid
2. Reduce sodium
3. Reduce protein
4. Normal Ca intake
5. Increase citrates ( fruits/veg)

-drugs: ( to lower urinary calcium excretion)
1. Thiazide diuretics
2. Urine alkalinization ( potassium citrate/ bicarbonate salts)
3. Allopurinol ( for hyperuricuria-related stones)

Note:
1. Hypercalciuria = when urine calcium excretion > 4 mg/kg

125
Q

Pyelonephritis

A

Flank pain + hematuria + urine WBC/Bacteria/nitrites/leukocyte esterase

126
Q

Glomerulonephritis

A

Hematuria + Proteinuria + HTN + dysmorphic RBC + RBC casts

  • NO acute flank pain
127
Q

Low urine PH seen with:

A
  • chronic diarrhea
  • diabetes/ metabolic disorders
128
Q

Increase urine concentration seen with:

A
  • dehydration
  • hot climate
129
Q

Increase uric acid secretion in urine seen with:

A
  • gout
  • myeloproliferative disorders
130
Q

If urine pH in low ( less than 5)

A
  • use potassium citrate ( to alkalinize urine)
131
Q

Bladder cancer

A
  • painless hematuria
  • associated with smoking, elderly, carcinogenic chemicals
  • malignant transformation of bladder epithelial cells

Diagnosis:
- flexible cystoscopy + biopsy

Treatment:
- no muscle invasion —> TURBT ( transurethral resection of bladder tumor) + intravesical immunotherapy

  • muscle invasion—> radical cystectomy & systemic chemo
  • metastatic —> systemic chemo & immunotherapy
132
Q

Bladder infection

A
  • hematuria + suprapubic pain + dysuria + sign of infection ( urine WBC/bacteria/leukocyte esterase/nitrite)
133
Q

Ureterolithiasis

A
  • epithelial injury due to scrapping of surface by stone
  • hematuria + flank pain that radiates to groin + crystal on urinalysis
134
Q

Glomerulonephritis

A
  • increase permeability of the glomerulus
  • allow RBCs to pass into urinary tract from circulation
  • symptoms: hematuria + proteinuria + RBC casts ….

Types:
- strep A
- IgA
- RPG
-MPGN

135
Q

Most common cause of painless hematuria in older people who used to smoke

A
  • bladder cancer
136
Q

Renal infarction —> caused by endocarditis

A

Symptoms:
- flank pain + N/V
- hematuria + proteinuria + without casts
- wedge-shaped cortical infarction seen on CT

  • Can occur after:
    1. Endocarditis ( fever, leukocytosis, cardiac murmur)
137
Q

Sodium nitroprusside ( for HTN emergency) can lead to cyanide toxicity in patient with renal insufficiency ( high creatinine)

A
  1. Metabolic acidosis + neurologic changes ( headache, confusion )
138
Q

CKD patient taken ACE-Inhibitor or ARBS

A
  1. Can develop hyperkalemia
  2. Treat with Ka-removal from stool ( patiromer)
139
Q

Hypercalcemia in sarcoidosis

A
  • finding: skin nodules & erythema nodusom
  • occurs from extra-renal calcitrioil production in the lung & lymph node & is independent from PTH production
  • usually high (calcitriol), low (PTH), high (urinary calcium)
140
Q

Hypokalemia result from

A
  1. Increase intracellular entry via:
    - insulin
    - beta-adrenergic agonist (albuterol)
    - hematopoiesis
  2. GI loss
  3. renal- Ka wasting:
    - hyperaldosteronism
    - diuretics
141
Q

Non-anion metabolic acidosis (Normal anion gap)

( loss of bicarbonate) (between 10-14)

—> (low pH< 7.35) & ( low bicarbonate < 22) & ( compensatory low PCO2)

A
  1. Severe diarrhea
  2. Renal tubular acidosis
  3. Excess saline infusion
  4. Intestinal or pancreatic fistula
  5. Diuretics ( CAI or MRA)
142
Q

Renal tubular acidosis —> non-anion gap metabolic acidosis (has a normal anion gap )

(Loss of bicarbonate )

A

Caused by: Impaired urinary acid excretion

Type 1 RTA:
1. Impaired H+ excretion ( being retained) in the distal tubule & can be recognized by inappropriate high urine pH (> 5.5) in the setting of acidosis
2. Hypokalemia
3.Treat with: oral sodium bicarbonate

Type 2 RTA:
1. Impaired bicarbonate reabsorption in the proximal tubule
2. Hypokalemia
3. Treat with: high dose oral/Iv sodium bicarbonate

Type 4 RTA
1. Hyperkalemia + moderate renal insufficiency
2. Occurs in uncontrolled diabetes

143
Q

Methanol or ethanol ingestion lead to

A
  1. High anion gab metabolic acidosis & high osmolal gap
144
Q

Diabetic ketoacidosis

A

Lead to metabolic acidosis ( low pH, low bicarbonate) & compensatory respiratory alkalosis ( hyperventilation, low PCO2)

145
Q

Management of hypercalcemia

( 1. normal saline + calcitonin; 2. bisphosphonate)

A
  1. Normal saline + calcitonin
    • Avoid loop diuretics (unless
      volume overload/heart failure exist)
  2. Long term —> bisphosphonate
146
Q

Hyperkalemia caused by

(ACE-I, ARB, NSAID, TMX, K-sparing, heparin…)

A
  1. ACE-i & ARBs
  2. Cyclosporine
  3. Digitalis
  4. Heparin
  5. Non-selective beta adrenergic blocker
  6. NSAIDs
  7. Potassium- sparing diuretics (triametrene) & (amiloride)
  8. Succinylcholine
  9. Trimethoprim
147
Q

Familial hypocalciuric hypercalcemia (FHH)

( High Ca, high PTH, low urinary Ca)

A
  1. Asymptomatic hypercalcemia
  2. Normal/elevated PTH
  3. Low urinary calcium excretion

—> differentiated from primary hyperparathyroidism ( shows high urinary calcium excretion)

—> differentiate from Multiple myeloma & malignancy ( has low PTH)

148
Q

Pneumonia lead to

A
  • primary respiratory alkalosis (hyperventilation) (High pH, low PCO2)

—> few days after antibiotic treatment, patient can have foul-smelling diarrhea, related to C.difficile —> more severe diarrhea can lead to non-anionic gap metabolic acidosis (loss of bicarbonate)

149
Q

Hypovolemic hyponatremia management

(Increase renin, increase aldosterone, increase ADH)

A

Hypovolemia: diarrhea, poor skin turger, hypotension, low renal perfusion

Low renal perfusion —> stimulated RAAS system —> increase renin, increase aldosterone —> this, stimulates ADH to reabsorb sodium & water at distal tubule

150
Q

Hypercalcemia treatment

A

Normally,
1. IV hydration + calcitonin
2. Bisphosphonate

Renal insufficiency & heart failure:
1. Hemodialysis

Hypercalcemia due to excessive vitamin intake, granulomatous disease (sarcoidosis), lymphoma
1. Glucocorticoid

151
Q

Mixed primary acid base disorders

(Sepsis, salicylate toxicity)

( hyperemesis/pregnancy + HF/COPD)

A
  1. Metabolic acidosis + respiratory acidosis: sepsis
    —> pH is low
  2. Metabolic acidosis + respiratory alkalosis: salicylate toxicity
    —> pH is near normal
    —> tinnitus + fever + tachypnea

——————

  1. Metabolic alkalosis + respiratory alkalosis: hyperemesis gradidarum & hyperventilation of pregnancy
    —> pH is high
  2. Metabolic alkalosis + respiratory acidosis: overdiureses heart failure & underlying COPD
    —> pH is near normal

——

Metabolic acidosis + metabolic alkalosis: DKA with severe vomiting
—> pH is near normal

152
Q

Hypokalemic, hypochloremic metabolic alkalosis

A

—> seen with:
1. Gastric suction or severe vomiting
2. Diuretic (loop or thiazide) overuse

—> management:
1. Normal saline

153
Q

Differential diagnosis of metabolic alkalosis

( high pH > 7.45) & ( high bicarbonate > 24)

A
  1. Low urine chloride < 20:
  • nasogastric feeding & vomiting
  • diuretics
  • responsive to normal saline
  1. High urine chloride > 20:
  • with hypovolemia —> bartter & Gitelman syndrome
  • with hypervolemia —> excessive mineralocorticoid treatment ( primary hyperaldosteronism, cushing syndrome, ectopic ACTH production)

** unresponsive to normal saline

154
Q

SIADH vs. diabetic insipidus

A

SIADH:
1. Hyponatremia + hyperkalemia + hypoglycemia + hypotension + hypovulemia
2. Low serum osmolarity + high urine osmolarity
3. Correct with hypertonic solution

DI:
1. Hypernatremia + hypokalemia
2. High serum osmolality + low urine osmolality
3. Correct with DDAVP (ADH)

155
Q

Site of action of various diuretics

A
  1. Proximal tubule —> CAI —> acetazolamide
  2. Descending loop of Henle —> osmotic diuretic —> mannitol
  3. Ascending loop of henle —> loop diuretic —> furosemide
  4. Distal tubules —> thiazide —> hydrochlorothiazide
  5. Collecting duct —> potassium-sparing —> Sodium channel blocker ( amiloride) & aldosterone receptor antagonist ( spironolactone)
156
Q

Evaluation of hyponatremia

A
  1. Serum osmolality > 290:
    - hyperglycemia
    - marked renal failure
  2. Urine osmolality < 100:
    - primary polydipsia
    - malnutrition (beer drinker’s potomania)
  3. Urine sodium < 25:
    - volume depletion
    - CHF
    - cirrhosis
  4. Urine sodium > 25
    - SIADH
    - adrenal insufficiency
    - hypothyroidism
157
Q

Hypomagnesemia can be seen with hypokalemia and hypocalcemia (in alcoholic use disorder)

A
  • lead to refractory hypokalemia ( seen in patient with hypokalemia that is difficult to correct with potassium replacement)
  • lead to hypocalcemia due to suppression of PTH
158
Q

PH & CO2 from ABG

A
  • are best measurement for acid-base status
  • HCO3 can be calculated from H-H equation
159
Q

Respiratory alkalosis

( pH is high) ( PCO2 is low ) ( HCO3 is low)

A

—> kidney compensate for respiratory alkalosis by excreting bicarbonate in urine —> this alkalize urine —> gives high urine pH

Internal Medicine Shelf Exam (12 decks)

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