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Nephrology - MTB Flashcards

1
Q

Best initial test in nephrology

A
  • Urinalysis

- BUN/ Cr

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2
Q

Urinalysis measurements

A
  • Protein
  • WBC
  • Red cells
  • Specific gravity and pH
  • Nitrites
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3
Q

Severe proteinuria

A
  • means glomerular damage
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4
Q

Tamm-Horsfall protein

A
  • tubules secrete slight amounts of protein

- less than 30 - 50 mg per 24 hrs

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5
Q

If there is persistent proteinuria

A
  • not related to prolonged standing (orthostatic proteinuria), a kidney biopsy should be performed
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6
Q

Activities that increase urinary protein excretion

A
  • Standing

- Physical activity

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7
Q

Normal protein per 24 hrs

A

< 300 mg

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8
Q

Assess proteinuria

A
  • UA is the intial test

- Protein to creatinine ration is more accurate at determining the amount

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9
Q

Protein to creatinine ratio

A

1 is equivalent to one gram of protein on a 24 hr

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10
Q

Protein: creatinine ratio vs 24 hr urine

A

Protein: creatinine ratio can be superior in accuracy

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11
Q

Microalbunemia

A
  • tiny amount of protein that is too small to detect on UA

- long term microalbinuria leads to worsening renal function in a diabetic patient should be treatment

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12
Q

Microalbunemia

A
  • 30 - 300 mg/24 hrs
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13
Q

Diabetic patient is evaluated with a UA that shows no protein. Microalbuminuria is detected (level btwn 30 and 300 mg per 24 hrs). Next best step?

A

ACE inhibitors or angiotension receptor blocker

- best initial therapy for any degree of proteinuria in a diabetic patient

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14
Q

Is Bence-Jones protein in myeloma detectable on dipstick?

A

No. Use Immunoelectrophoresis

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15
Q

White blood cells on UA

A
  • detect inflamation, infection, and allergic interstitial nephritis
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16
Q

Eosinophils

A
  • indicate allergic or acute intersitial nephritiris
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17
Q

Detecting eosinophils in the urine

A

Wright and Hansel stains
- allergic intersitial nephritis
-

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18
Q

Hematuria

A

= / > 5 RBCs per high power field

  • stones in bladder, ureter, or kidney
  • hematologic disorders that cause bleeding (coagulopathy)
  • infection (cystitis, pyelonephritis)
  • cancer of bladder, ureters, or kidney
  • tx ( cyclophosphamide gives hemorrhagic cysts)
  • trauma
  • glomerulonephritis
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19
Q

Ig A nephropathy

A

common for mild recurrent hematuria

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20
Q

Reason for false positive tests for hematuria

A
  • Hemoglobin OR

- myoglobin

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21
Q

Woman is admitted to the hospital with trauma and dark urine. The dipstick is markedly positive for blood. Best initial test to conform the etiology?

A

Microscopic exam of the urine

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22
Q

Why is intravenous pyelogram is always wrong on boards?

A
  • Slower and the contrast is renal toxic
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23
Q

When is dysmorphic red cells?

A

Glomerulonephritis

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24
Q

If the patient has hematuria without infection or prior trauma but

  • Renal U/S or CT doesn’t show etiology
  • Bladder shows mass for possible biopsy

Next step?

A

Cystoscopy

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25
Q

Most accurate test of the bladder

A

Cystoscopy

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26
Q

Red cell casts in UA

A

Glomerulonephritis

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27
Q

White cell casts in UA

A

Pyelonephritis

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28
Q

Eosinophils casts in UA

A

Acute (allergic) interstitial nephritis

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29
Q

Hyaline casts in UA

A

Dehydration concentrates the urine and the normal Tamm-Horsfall protein precipitaes or concentrates into a cast

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30
Q

Waxy casts in UA

A

Chronic renal disease

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31
Q

Granular “muddy-brown” casts on UA

A

Acute tubular necrosis

- they are collections of dead tubular cells

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32
Q

Acute Kidney Injury

A
  • formerly called acute renal failure

- decrease in creatinine clearance resulting in a sudden rise in BUN and creatinine

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33
Q

Three different types of AKI

A
  • Prerenal azotemia (decreased perfusion)
  • Postrenal azotemia (obstruction)
  • Intrinsic renal disease (ischemia and toxins)
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34
Q

Prerenal azotemia

A
  • due to inadequate perfusion of the kidney when kidney is normal
  • hypotension
  • hypovolemia
  • renal artery stenosis
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35
Q

NSAIDS on afferent arteriole

A
  • constrict the afferent arteriole
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36
Q

ACE inhibitors on efferent arteriole

A
  • cause efferent arteriole vasodilation
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37
Q

Postrenal azotemia

A
  • obstruction of any cause damages the kidney by blocking filtration at the glomerulus
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38
Q

Causes of postrenal azotemia

A
  • PROSTATE HYPERTROPHY or cancer
  • STONE in the ureter
  • Cervical CANCER
  • Urethral CANCER
  • Neurogenic (atonic) bladder
  • Retroperitoneal FIBROSIS
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39
Q

Causes of retroperitoneal fibrosis

A
  • Bleomycin
  • Methylsergide
  • Radiation
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40
Q

Most common cause of intrinsic renal disease

A

Acute tubular necrosis

- from toxins and prolonged ischemia of the kidney

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41
Q

Other causes of intrinsic renal disease

A
  • Acute (allergic) interstitial nephritis
  • Rhabdomyolysis and hemoglobinuria
  • Contrast agents, aminoglycosides, cisplatin,
  • Crystals such as hyperuricemia, hypercalcemia
  • Bence-Jones protein from myeloma
  • Poststreptococcal infection
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42
Q

Clinical presentation of intrinsic renal disease

A
  • Nausea and vomiting
  • Tired/malaise
  • Weak
  • Short of breath and edema from fluid overload
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43
Q

Clinical presentation of severe intrinsic renal disease

A
  • Arrhythmia from hyperkalemia and acidosis

- Sharp, pleuritic chest pain from PERICARDITIS

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44
Q

Clinical presentation of postrenal azotemia

A
  • Enlargement (distention) of the bladder

- Massive diuresis after urinary catheter

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45
Q

Best initial test for acute kidney injury

A
  • BUN : Cr
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46
Q

Prerenal azotemia

A
  • BUN:CR > 20:1

- Clear hx of hypoperfusion and hypotension

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47
Q

Postrenal azotemia

A
  • BUN:Cr > 20:1
  • Distended bladder or massive release of urine with catheter placement AND bilateral or unilateral HYDRONEPHROSIS on U/S
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48
Q

Intrinsic renal disease

A
  • BUN: Cr < 10:1
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49
Q

When is kidney biopsy the answer for AKI?

A

Never

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50
Q

Tests for AKI of unclear etiology

A
  1. Urinanalysis
  2. Urine sodium
  3. Fractional excretion of sodium
  4. Urine osmolality
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51
Q

Best test for AKI of unclear etiology

A

Urinalysis

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52
Q

Increased urine osmolality

A
  • when intravascular volume is low, normally ADH levels should rise
  • healthy kidney will reabsorb more water to fill vascularture
  • increased water reabsorption leads to an increase in urine osmlolality – more concentrated urine
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53
Q

Isosothenuria (same osmolality to the blood ~ 300 mOsm/L) or Low urine osmolality

A
  • During ATN, the urine cannot be concentrated because the tubules cells are damaged
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54
Q

Urine osmolality: Healthy person with fluid overload

A

Low urine osmolality or dilute urine

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55
Q

Urine osmolality: Health person with dehydration

A

High urine osmolality or concentrated urine

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56
Q

20 y/o African American man comes for a screening test for sickle cell. He is found to be heterozygous (trait or AS) for sickle. Best advice for him?

A

Avoid dehydration

- sickle cell trait in renal concentrating ability or isosthenuria

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57
Q

Prerenal azotemia

A
  • BUN:Cr > 20:1
  • Urine Na < 20mEq/L
  • Fractional excretion of sodium: < 1%
  • Urine osmolality: > 500 mOsm/kg
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58
Q

Acute tubular necrosis

A
  • BUN: Cr < 20: 1
  • Urine Na > 20mEq/L
  • Fractional excretion of sodium: >1%
  • Urine osmolality: < 300mOsm/kg
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59
Q

Acute Tubular Necrosis

A
  • an injury to the kidneys from ischemia and/or toxins resulting sloughing off of tubular cells into the urine
  • Sodium and water reabsorptive mechanisms are lost with the tubular cells
  • Proteinuria is not significant since protein, not tubule, spills into the urine
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60
Q

Urine specific gravity correlates to urine osmolality

A
  • High UOsm = high specific gravity
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61
Q

Pt has acute renal failure and a toxin. What is the most likely diagnosis?

A

Acute Tubular Necrosis

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62
Q

Pt comes with fever and acute, left lower quadrant abdominal pain. Blood cx 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 hrs, her creatinine rises dramatically. Most likely cause of her renal insufficiency?

A

Contrast media

- rapid onset of injury

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63
Q

Timeline for nephrotoxic drugs

A

Drugs (e.g. vancomycin, gentamicin, and amphotericin)
are nephrotoxic
- usually takes 5 to 10 days to result in nephrotoxicity

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64
Q

74 y/o blind man is admited with obstructive uropathy and chest pain. He has a hx of hypertension and diabetes. His creatinine drops from 10mg/dL to 1.2 mg/dL 3 days ater catheter placement. The stress test show reversible ischemia. Most appropriate management?

A

Saline hydration is has the most proven benefit at prevent contrast-induced nephrotoxicity

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65
Q

Pt with mild renal insufficiency undergoes angiograpy and develops 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 lab testing?

A

Urine sodium 5 (very low), FENA

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66
Q

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

A

Hyperuricemia

  • most likely from tumor lysis syndrome
  • cisplatin (drug toxicities) would not produce RISE in CREATININE In 5-10 days
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67
Q

Prevention of tumor lysis syndrome

A
  • Allopurinol, hydration, and rasburicase should be given prior to chemotherapy to prevent renal failure from tumor lysis sndrome
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68
Q

Pt who is suicidal ingests an unknown substance and develops renal failure 3 days later. Her calcium level is also low and the urinalysis shows an abnormality. What did she take?

A

Ethylene glycol

  • AKI based on oxalic avid and oxalate precipitating within the kidney tubules cause ATN
  • envelope shaped crystals
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69
Q

Drug-induced ATN

A
  • nonoliguric renal injury caused by aminoglycosides, amphotericin, cisplatin, vancomycin, acyclovir, and cyclosporine
  • slower onset: FIVE to TEN days
  • dose dependent
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70
Q

What electrolyte deficiency predisposes someone to drug-induced aminoglycosides?

A

Low magnesium levels

- may increase risk of aminoglycosides or cisplatin toxicity

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71
Q

Contrast media nephrotoxicity

A
  • can cause immediate renal toxicity
  • prevented with saline hydration
  • n-acetylcysteine and sodiu bincarbonate proven beneficial
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72
Q

Rhabdomyolysis

A
  • caused by TRAUMA, prolonged IMMOBILITY, snake bites, seizures, and CRUSH INJURIES
  • best initial test to confirm UA
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73
Q

Hyperuricemia

A
  • ATN
  • usually from tumor lysis syndrome
  • long standing hyperuricemia from gout can cause chronic renal failure
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74
Q

Best initial to confirm the diagnosis of rhabdomyolysis

A

UA

- positive only on dipstick for large amounts of blood, but no cells will be seen on microscopic examination

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75
Q

Reasons for false positive urine dipstick

A

Urine dipstick can’t tell the difference between:

  • Hemoglobin
  • Myoglobin
  • Red blood cells
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76
Q

Bence Jones protein

A
  • directly toxic to renal tubules
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77
Q

Rhabdomyolysis: lab findings

A
  • ELEVATED CPK - lets you know “hematuria” is myoglobin
  • HYPERKALEMIA due to release of K from damaged cells
  • HYPERURICEMIA due to degradation of nucleic acid from damaged cells
  • HYPOCALCEMIA due to increased calcium binding to damaged muscle
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78
Q

Rhabdomyolysis: treatment

A
  • SALINE HYDRATION
  • MANNITOL as an osmotic diuretic
  • BICARBONATE which drives K back into cells and prevent precipitation of myoglobin
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79
Q

Do you treat hypocalcemia in rhabdomyolysis?

A

No, if patient is asymptomatic.

- in recovery, the calcium will come back out of muscles

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80
Q

A man comes to ED after a triathlon, followed by status epilepticus. He takes simvastatin at triple the recommended dose. His muscles are tender and the urine is dark. IV fluids are started . What is the next step?

A

EKG

  • to detect life threatening hyperkalemia
    • potassium replacement in a person with rhabdomyolysis would be fatal**
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81
Q

Rhabdomyolysis proven to benefit ATN

A
  • No therapy proven to benefit ATN

- diuretics increase urine output, but do not change overall outcome

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82
Q

Wrong answers for treatment of ATN

A
  • Low-dose dopamine
  • Diuretics
  • Mannitol
  • Steroids
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83
Q

Indications for dialysis

A
  • Fluid overload
  • Encephalopathy
  • Pericarditis
  • Metabolic acidosis
  • Hyperkalemia
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84
Q

BUN:Cr indications for dilaysis

A
  • No specific level of BUN:Cr

- based on development of life threatening conditions

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85
Q

Hypocalcemia symtpoms

A
  • Seizures

- prolonged QT interval leading to arrhythmia

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86
Q

Patient develops from 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 causes her hearing loss?

A

Furosemide

- causes ototoxicity by damaging the hair cells of the cochlea, resulting in sensorineural hearing loss

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87
Q

Hepatorenal syndrome

A

renal failure developing secondary to liver disease

- kidneys are intrinsically neural

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88
Q

Hepatorenal syndrome: Hx and PE

A
  • severe liver disease (CIRRHOSIS)
  • new-onset renal failure w/ no other explanation
  • VERY LOW URINE NA (less than 10 - 15 mEq/L)
  • FENA < 1%
  • ELEVATED BUN:Cr > 20:1
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89
Q

Hepatorenal syndrome: Treatment

A
  • Midodrine
  • Octreotide
  • Albumin (albumin is less clear)
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90
Q

Atheroemboli: Etiology

A
  • CHOLESTEROL PLAQUES found in aorta and/or coronary arteries can be “broken off” manipulated during catheter procedures
  • CHOLESTEROL EMBOLI lodged in kidney causes AKI
  • BLUE/PURPLISH SKIN LESIONS in fingers and toes, LIVEDO RETICULARIS and ocular lesions
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91
Q

Peripheral pulses in atheroemboli

A
  • cholesterol plaques are too small to occlude vessels such as the radial or brachial artery
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92
Q

Atheroemboli: diagnostic tests

A
  • Eosinophilia
  • Low complement levels
  • Eosinophiluria
  • Elevated ESR
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93
Q

Most accurate diagnostic test for atheroemboli?

A
  • Biopsy of one purplish skin lesions
  • cholesterol crystals, but this result does not change management b/c there is no specific therapy to reverse atheroembolci disease
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94
Q

Acute (Allergic ) Interstitial Nephritis

A
  • is a form acute renal failure that damages the tubules occurring on idiopathic issues
  • antibodies and EOSINOPHILS ATTACK THE CELLS LINING THE TUBULES as a rxn to the drugs (70%), infxn, and autoimmune disorders
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95
Q

Most common cause of acute (allergic) interstitial nephritis

A
  • PENICILLINS and cephalosporin
  • SULFA DRUGS
  • Phenytoin
  • Rifampin
  • Quinolones
  • Allopurinol
  • Proton Pump Inhibitors
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96
Q

Medications that cause AIN are that same as those cause:

A
  • Drug allergy and rash
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Hemolysis
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97
Q

Acute (Allergic) Interstitial Nephritis: Clinical Presentation

A
  • FEVER (80%)
  • RASH (50%)
  • Arthralgias
  • Eosinophilia and EOSINOPHILURIA (80%)
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98
Q

Aside from drugs, other causes of AIN

A

Autoimmune diseases (e.g. SLE, Sjorgen, and sarcoidosis)

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99
Q

AIN Diagnostic Tests

A
  • Elevated BUN: CR < 20:1

- White and red cells in the urine

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100
Q

Most accurate test for acute (allergic) interstitial nephritis

A
  • Hansel or Wright stain determines whether eosinophils are present
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101
Q

Acute interstitial nephritis: treatment

A

AIN usually resolves spontaneously w/ stopping the drug or controlling the infection

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102
Q

Analgesic Nephropathy

A
  • ATN from direct toxicity to the tubules
  • AIN
  • MEMBRANOUS GLOMERULONEPHRITIS
  • VASCULAR INSUFFICIENCY
  • PAPILLARY NECROSIS
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103
Q

Vascular insufficiency induced analgesic nephropathy

A
  • INHIBIT PROSTAGLANDINS

- NSAIDS inhibit prostaglandins to constrict afferent arteriole and decrease renal perfusion

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104
Q

Papillary necrosis

A
  • sloughing off of the renal papillae

- caused by toxins such as NSAIDS, or sudden vascular insufficiency leadingot death of cells in the pappillaw

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105
Q

Papillary necrosis: Hx and PE

A
  • patient loses 60 - 70% renal function before the creatinine even begins to rise
  • Look for extra NSAID use with a hx of:
    • SICKLE CELL DISEASE
    • Diabetes
    • Urinary obstruction
    • Chronic pyelonephritis
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106
Q

Papillary necrosis: Clinical presentation

A
  • sudden onset of flank pain, fever, and hematuria in a patient with one of the diseae perviously list
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107
Q

Best initial test for suspected papillary necrosis

A

Urinanalysis

- grossly visible NECROTIC MATERIAL passed IN THE URINE

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108
Q

Most accurate test for papillary necrosis

A

CT scan

- shows the abnormal internal structures of the kidney from the loss of the papillae

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109
Q

Papillary Necrosis: Treatment

A

No specific therapy

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110
Q

Pyelonephritis

A
  • onset in a few days
  • Sx: dysuria
  • Urine cx: positive
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111
Q

CT findings of pyelonephritis

A

Diffusely swollen kidney

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112
Q

Pyelonephritis: Treatment

A

Antibiotics

- such as ampicillin/gentamicin or fluoroquinolones

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113
Q

Papillary necrosis

A
  • onset in a few hours
  • necrotic material in urine
  • negative urine culture
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114
Q

Papillary necrosis: treatment

A

No treatment

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115
Q

Tubular Disease: Overview

A
  • Acute
  • Toxins
  • None nephrotic
  • No biopsy usually
  • No steroids
  • Never additional immunosuppressive agents
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116
Q

Tubular Disease: Treatment

A
  • Correcting HYPOPERFUSION and REMOVING TOXIN
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117
Q

Glomerular Diseases

A
  • generally chronic
  • not caused by toxins or hypoperfusion
  • all of them can cause nephrotic syndrome
  • biopsy indicated
  • treated with steroids
  • additional immunosuppresive medications
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118
Q

Most accurate diagnostic test for glomerular disease

A
  • Steroids
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119
Q

Main difference between glomerulonephritis and nephrotic syndrome

A

Degree or AMOUNT of proteinuria

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120
Q

Diagnostic tests for glomerulonephritis

A
  • UA with HEMATURIA
  • “DYSMORPHIC” red cells
  • RED CELL CASTS
  • Urine sodium and FENA are low
  • PROTEINURIA
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121
Q

Goodpasture Syndrome

A
  • presents with LUNG AND KIDNEY involvement
  • no UPPER RESPIRATORY TRACT INVOLVEMENT
  • no skin, joint, GI, eye, or neurological involvement
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122
Q

Best initial test for Goodpasture Syndrome

A
  • Antiglomerular basement membrane antibodies
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123
Q

Most ACCURATE test for Goodpasture Syndrome

A
  • Lung or kidney biopsy with “LINEAR DEPOSITS”

- anemia is often present from chronic blood loss from hemoptysis

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124
Q

Goodpasture Syndrome: Treatment

A
  • Plasmapheresis and steroids
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125
Q

IgA Nephropathy

A
  • most common cause of acute glomerulonephritis in US
  • look for Asian patient w/ recurrent epsiodes of gross hematuria 1 - 2 days after upper respiratory tract infxn
  • poststreptococcal glomerulonephritis follows pharyngitis by 1 -2 weeks
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126
Q

Most accurate test for IgA nephropathy

A

Kidney biopsy

** IgA levels are increased in 50%**

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127
Q

Proteinuria and progression of disease

A

More proteinuria = worse progression

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128
Q

IgA Nephropathy

A
  • no treatment proven to reverse the disease

- severe proteinuria is treated with ACE inhibitors and steroids

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129
Q

Postinfectious Glomerulonephritis

A
  • most common organism leading to infectious glomerulonephritis is Streptococcus
  • follows throat infectiou or skin infection (impetigo) by 1 to 3 weeks
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130
Q

Postinfectious Glomerulonephritis: Clinical Presentation

A

Patients present with:

  • dark (cola-colored) urine
  • periorbital edema
  • hypertension
  • oliguria
131
Q

Postinfectious Glomerulonephritis: Diagnostic Tests

A

UA with proteinuria, red cells, red cell casts

- low complement

132
Q

Pt had infection 2 weeks ago and is c/o dark urine, facial edema, and oliguria. Next step?

A

ASO titers and anti-DNAse antibod

133
Q

Most accurate test for postinfectious glomerulonephritis

A

Kidney biopsy

134
Q

Postinfectious glomerulonephritis: Treatment

A

Supportive treatment such as:

  • antibiotics
  • diuretics to control fluid overload
135
Q

Alport Syndrome

A

congenital defect of type I collagen that results in glomerular disease combined with:

  • sensorineural hearing loss
  • visual disturbance from loss of the collagen fibers that hold lens of eye in place
136
Q

Alport Syndrome: Treatment

A

No specific therapy to reverse defect

137
Q

Polyarteritis Nodosa

A

systemic vasculitis of small and medium sized arteries that commonly affect kiney

  • SPARES THE LUNG
  • ASSOCIATED WITH HEPATITIS B
138
Q

Why do patients with PAN have neuropathy?

A

Damage to small blood vessels around nerves starve them into neuropathy

139
Q

Polyarteritis Nodosa: Clinical Presentation

A

Nonspecific symptoms of: fever, malaise, weight loss, mya;gias, and arthralgia

GI: abdominal pain, pain worsened by eating due to mesenteric ischemia

Neurologic: “mononeuritis multiplex” when damage occurs around large peripheral nerve (brachial, radial, ulnar)

Skin: purpura (large), petechiae (small), digital gangrene, livedo reticularis

140
Q

Young patient has a stroke or MI.

A

Think vasculitis

- PAN

141
Q

Polyarteritis Nodosa: Diagnostic Tests

A

Blood tests will show:

  • anemia and leukocytosis
  • elevated ESR and C-protein
  • ANCA NEGATIVE
  • ANA and rheumatoid

Angiography

142
Q

Best diagnostic for polyarteritis nodosa

A

ANGIOGRAPHY of the renal, mesenteric, or hepatic artery showing aneurysmal dilation in association with new-onset w/ HTN

143
Q

Most accurate test for polyarteritis nodosa

144
Q

POlyarteritis Nodosa: Treatment

A

Prednisone
Cyclophosphamide
- treat Hep B when found

145
Q

Lupus Nephritis

A
  • SLE can give any degree of renal involvement
    can present with normal or mild proteinuria
  • severe disease presents with membranous glomerulonephritis
146
Q

Most accurate test for lupus nephritis

A

Biopsy

  • will show glomerulosclerosis which has no active inflammatory component
  • helps determine therapy based on stage
147
Q

Lupus Nephritis: Treatment

A

Glucocorticoids combined with either cyclophosphamide or mycophenolate

148
Q

Which conditions give LARGE kidneys on sonogram or CT scan?

A
  • Amyloid
  • HIV
  • Nephropathy
  • Polycystic kidneys
149
Q

Amyloidosis

A

Abnormal protein produced in association with:

  • myeloma
  • chronic inflammatory diseases
  • rheumatoid arthritis
  • inflammatory bowel disease
  • chronic infections
150
Q

Most accurate test for amyloidosis

A

Biopsy

- show green birefringerence with Congo red staining

151
Q

Amyloidosis: Treatment

A

Melphalan and prednisone

152
Q

Nephrotic Syndrome

A
  • measure of the severity of proteinuria in association with glomerular disease
  • Massive proteinuria leads to:
    • edema
    • hyperlipidemia
    • thrombosis: urinary anticoagulants protein C, protein S, and antithrombin
153
Q

Nephrotic Syndrome: Etiology

A

Diabetes and HTN are most common causes of nephrotic syndrome

154
Q

Nephrotic Syndrome associated with cancer (solid organ)

A

Membranous

155
Q

Nephrotic syndrome associated with children

A

Minimal change disease

156
Q

Nephrotic syndrome associated with drug use and AIDS

A

Focal segmental

157
Q

Nephrotic syndrome associated with SLE

A

All types of nephrotic syndrome

158
Q

Major difference between nephritic syndrome and nephrotic syndrome

A

Amount of proteinuria

159
Q

Nephrotic syndrome: clinical presentation

A

Generalized edema

160
Q

Why are infections more common with nephrotic syndrome?

A

Increased urinary loss of immunoglobulins and complement

161
Q

Why are patients more clot prone with nephrotic syndrome?

A

Loss of antithrombin, protein C, and protein S

162
Q

Best initial test for suspected nephrotic syndrome?

A

Urinalysis

- wil show Maltese crosses, which are lipid deposits from sloughed off tubular cells

163
Q

Urine albumin/creatinine ration

A
  • measure of the average protein produced over 24 hrs

- ratio of 2:1 means 2 grams of protein excreted over 24 hrs

164
Q

Most accurate test to detect nephrotic syndrome

A

Renal biopsy

165
Q

Nephrotic Syndrome: definition

A

Hyperproteinuria (> 3.5 g per 24 hrs)
Hypoproteinemia
Hyperlipidemia
Edema

166
Q

Best initial therapy for nephrotic syndrome

A

Glucocorticoids

- if no response after several weeks, immunosuppresive meds such as cyclophosphamide

167
Q

How are ACE inhibitors and ARBs used in nephrotic syndrome?

A

Try to control proteinuria

168
Q

How is edema managed in nephrotic syndrome

A

Salt restriction and diuretics

169
Q

How is hyperlipidema managed in nephrotic syndrome

170
Q

End Stage Renal Disease

A
  • kidney failure so sever as to need dialysis

- no defined as a particular BUN or creatiinine

171
Q

Most common cause of end stage renal disease

A

Diabetes

Hypertension

172
Q

ESRD: Clinical Presentation

A

Uremia in the presence of:

  • metabolic acidosis
  • fluid overload
  • encephalopathy
  • hyperkalemia
  • pericarditis
173
Q

Manifestations of Renal Failure

A
  • Anemia
  • Hypocalcemia and osteomalacia
  • Bleeding
  • Pruritis
  • Hypoerphosphatemi
  • Hypermagnemias
  • Atherosclerosis
  • Endocrinopathy
174
Q

Renal Failure: Anemia

A
  • loss of erythropoietin leads to monochromic anemia

- treat with erythropoietin and Fe supplements

175
Q

Renal Failure: hypocalcemia

A
  • less active 25- hydroxy-vitamin D into the much more active 1,25 dihydroxy vitamin D
  • without 1,25 dihydroxy form of vitamin D, body will not absorb enough Ca from gut
  • treat with vitamin D and calcium
176
Q

Renal Failure: osteodystrophy

A

Low calcium leads to secondary hyperparathyroidism

- high parathyroid levels remove Ca from bones, making them soft and week

177
Q

Bleeding 2/2 bleeding

A

Platelets do not work normally in uremic enviroment

- treat with DDVAP increases platelet function; use only when bleeding

178
Q

Infection 2/2 renal failure

A

Neutrophils do not work because they cannot degranulate

179
Q

Pruritis 2/2 renal failure

A

Urea accumulating in skin causes itching

- treat with dialysis and UV light

180
Q

Hyperphosphatemia 2/2 renal failure

A

Phosphate normally excreted throgh kidneys. High parathyroid levels release phosophate from bones, but body is unable to excrete
- treat with oral binders

181
Q

Hypermagnesmemia 2/2 renal failure

A
  • loss of excretory ability

- treat with high Mg foods, laxatives, and antacids

182
Q

Accelerated atherosclerosis and hypertension 2/2 renal failure

A

Immune system keeps artery clear of lipid acculiaton
WBCs dont work in uriemic environment - common cause of death in dialysis patients
- treat with dialysis

183
Q

Endocrinopathy 2/2 renal failure

A

Women are anovulatory and men have low testosterone

- treat with dialysis, estrogen (women ) and testosterone (men ) replacement

184
Q

Erectile dysfunction 2/2 renal failure

A

Insulin level tend to go up because insulin is excreted renally Insulin resistance also increases. Glucose leels are therefore up and down

185
Q

Treatment of hyperphosphatemia

A

Oral phosphate binders

  • prevent reabsorption of phosphate from bowe
  • treat hypocalemia eill b/c it is hyperparathyroidsm that causes increase phosphate release from bone
186
Q

When treating hypocalcemia why should you give oral phosphate binders?

A

If you use Vitamin D alone without oral phosphate binder then bowel will absorb increase GI absorption of phosphate

187
Q

Why do you never use aluminum phosphate binders?

A

Aluminum causes dementia

188
Q

Thrombotic Thrombocytic Purpura

A

platelet disorder in which microthrombi block small vessels leading to end organ ischemia .
RBCs are fragmented by microthrombi leading to microangiopathic hemolytic anemia

189
Q

TTP associated conditions

A

HIV
Cancer
Drugs (cyclosporine, ticlopidine and clopidogrel)

190
Q

TTP presentation

A

Clinical syndrome with 5 symptoms (3 of 5)

  • low platelet
  • microangiopathic hemolytic anemia
  • neuro changes (seizures, stroke, delirium)
  • impaired renal function
  • fever
191
Q

How is TTP hemolysis visible on smear?

A

Schistocytes

Helmet cells

192
Q

Hemolytic Uremic Syndrome

A
  • common in children
  • associated with E.coli 0157:H7 and Shigella
  • intravascular hemolysis (schistocytes)
  • renal failure
  • thrombocytopenia
193
Q

TTP Treatment

A

Plasmaphoresis

    • if not a choice, choose fresh frozen plasma
    • NEVER CHOOSE PLASMA INFUSION
194
Q

HUS: Treatment

A

Often resolves spontaneously

195
Q

Simple renal cysts

A
  • echo free
  • smooth thin walls
  • sharp demarcation
  • good transmission to the back
196
Q

Complex renal cysts

A
  • mixed echogenecity
  • thick, irregular walls
  • lower density on back wall with demarcation
  • transmission shows debris in cyst
197
Q

Polycystic Kidney Disease

A

presents with:

  • pain
  • hematuria
  • stones
  • infection
  • hypertension
198
Q

What is the most common cause of death from PCKD?

A

Renal failure

- from recurrent episodes of pyelonephritis and nephrolithiasis

199
Q

Conditions associated with PCKD

A
  • liver cysts (most common site outside of kidney)
  • ovarian cysts
  • mitral valve prolapse
  • diverticulosis
  • berry aneurysms
200
Q

Hypernatremia

A

due to loss of free water

  • sweating, burns, fever
  • pneumonia: insensible losses from hyperventilation
  • diarrhea
  • diuretic
201
Q

Diabetes insipidus

A
  • leads to high volume water losss from insufficient or ineffective ADH
202
Q

Central diabetes insipidus

A
  • can be caused by CNS disorders (stroke, tumor, trauma, hypoxia, infection) can damage ADH production in hypothalamus or storage in posterior pituitary
  • low ADH
203
Q

Nephrogenic diabetes insipidus

A
  • loss of ADH effect on collecting duct of the kidney
  • can be caused by lithium or demecycline, CKD, hypokalemia, or hypercalcemia
  • elevated ADH
204
Q

Pt has high volume nocturia

A

Think about presence of diabetes insipidus

205
Q

Diabetes insipidus: presentation

A

DI w/ hypernatremia presents with neurological symptoms such as:

  • confusion
  • disorientation
  • lethargy
  • seizures
206
Q

Complications of diabetes insipidus

A

If uncorrected, severe hypernatremia causes coma and irreversible brain damage

207
Q

Polyuria

A
  • high urine volume
208
Q

Hypernatremia: diagnostic test

A 
hyperosmolality
fluid losses from skin, kidney, or stool lead to:
  - decreased urine volume  
  - increased urine osmolality
   - decreased urine sodium
209
Q

Diabetes Insipidus: Diagnostic Test

A
  • high urine volume in DI

- decreased urine osmolality in DI

210
Q

Best initial test for diabetes insipidus

A

Water deprivation then observation of urine output and urine osmolality
- In DI, high volume urine and low urine osmolality

211
Q

Central diabetes insipidus response to ADH

A

Sharp decrease in urine volume, increase in osmolality

212
Q

Nephrogenic diabetes insipidus response to ADH

A

No change in urine volume or osmolality with ADH administration

213
Q

Positive water deprivation

A

means urine volume stays high despite withholding water

214
Q

Diabetes inspidus: Treatment

A
  1. Fluid loss: correct underlying water loss
  2. CDI: replace ADH
  3. NDI
    • correct potassium and calcium
    • stop lithium and demeclocycline
    • give thiazide or NSAIDs despite these interventions
215
Q

Complications of hypernatremia

A

Cerebral edema – if sodium levels brought down too rapidly from shift of fluids from vascular space into cells of brain
- presents with worsening confusion and seizures

216
Q

Hyponatremia

A
  • characterized according to overall VOLUME STATUS of the body
217
Q

Hypervolumia hyponatremia: causes

A
  • CHF
  • Nephrotic syndrome
  • Cirrhosis
218
Q

Intravascular volume depletion in regards to ADH levels

A

Increased ADH levels

- pressure receptors in atria and carotid sense decrease in volume and stimulate ADH production and release

219
Q

Hypovolemia hypernatremia: causes

A
  • Sweating

- Pneumonia: due to secondary losses from hyperventilation

220
Q

Addison disease

A
  • loss of adrenal function also causes hyponatremia b/c of loss of aldosterone
  • less aldosterone, less sodium
221
Q

Euvolemia hyponatremia: causes

A
  • Pseudohyponatremia (hyperglycemia)
  • Psychogenic polydipsia
  • Hypothyroidism
  • Syndrome of inappropriate ADH
222
Q

Hyperglycemia induced hyponatremia

A
  • very high glucose levels lead to a decrease in soidum levels
  • hyperglycemia acts an osmotic draw on fluid inside the cells
223
Q

Na correction with hyperglycemia

A

For every 100 mg/dL of glucose above normal, there is a 1.6 mEq/L decrease in Na

224
Q

Psychogenic polydipsia

A

massive ingestion of free water above 12 to 24 liters/day will overwhelm kidney’s ability to excrete water

  • minimum urine 50 mOsm/kg
  • can produce 12 - 24 liters of urine a day, depending whether or not you can get urine osmolality down to 50 or 100 mOsm/kg
225
Q

Pt is hyponatremic with a hx of bipolar disorder. Likely diagnosis?

A

Psychogenic polydipsia

226
Q

Hypothyroidism induced hyponatremia

A
  • thyroid hormone is needed to excrete water. If thyroid hormone level is low, free water excretion is decreased
227
Q

SIADH induced hyponatremia

A

Any LUNG or BRAIN DISEASE can cause SIADH for unclear reasons
- certain drugs: SSRIs, sulfonyureia, vincristine, cyclophosphamide

228
Q

Cancers associated with SIADH

A

Small cell cancer of the lung produce ectopic ADH

229
Q

Hyponatremia presentation

A

Presents entirely with CNS symptoms

  • confusion
  • lethargy
  • disorientation
  • seizures
  • coma
230
Q

Hyponatremia: Diagnostic Test

A

SIADH - urine is appropriately concentrated (high urine osmolality)

  • urine sodium is high in SIADH
  • uric acid level and BUN are low in SIADH
231
Q

Most accurate test for SIADH

A

high ADH level

232
Q

Mild hyponatremia: treatment

A

restrict fluids

233
Q

Moderate hyponatremia: treatment

A

Saline and loop diuretic

* pt may present with minimal confusion

234
Q

Severe hyponatremia: treatment

A
  • patient presents with lethargy, seizures, coma

- treat with hypertonic saline, conivaptan, tolvaptan

235
Q

ADH antagonists

A

Tolvaptan and conivaptan

- treated for severe, symptomatic SIADH

236
Q

Chronic SIADH

A
  • can be from underlying disorder that cannot be corrected (e.g. metastatic cancer)
237
Q

Chronic SIADH: treatment

A

Demeclocycline

- blocks the action of ADH at the collecting of the kidney tubule

238
Q

Hyponatremia complications

A

Central pontine myelinolysis

- must be corrected “slowly” as under 0.5 - 1.0 mEq/hr or 12 to 24 mEq per day

239
Q

Pseudohyperkalemia

A

Falsely elevated potassium levels due to:

  • hemolysis
  • repeated fist clenching with tourniquet
  • thrombocytosis or leukocutosis will leak out of cells in the lab specimen
240
Q

Hyperkalemia due to decreased excretion

A
  • Renal failure
  • Aldosterone decrease
    • ACE inhibitors/ ARBS
    • type IV renal tubular acidosis
    • spironolactone and eplerenone (aldosterone inhibitors)
    • triamterene and amiloride (K sparing diuretics)
    • Addison disease
241
Q

Hyperkalemia due to K release from ittuse

A
  • Tissue destruction (hemolysis, rhabdomyolysis, tumor lysis syndrome)
  • Decreased insulin (insulin drive K into cells)
  • Acidosis: cells take in H+ and release K in exchange
  • Beta blockers and digoxin: drugs inhibit Na/K ATPase
  • Heparin increases K levels, presumable through increased tissue release
242
Q

Hyperkalemia: presentation

A

K disorders interfere with muscle contraction and cariac conductance

  • weakness
  • paralysis when severe
  • ileus (paralyzes gut muscles)
  • cardiac rhythm disorders
243
Q

Best initial test for hyperkalemia

244
Q

Hyperkalemia: EKG findings

A

Peaked T waves
Wide QRS
PR interval prolongation

245
Q

Treatment for life threatening hyperkalemia

A
  1. Calcium chloride or calcum gluconate
  2. Insulin and glucose to drive potassium back into cells
  3. Bicarbonate: drive potassium into cells but should be used most when acidosis causes hyper
246
Q

Removing potassium fro body

247
Q

Other methods to lower potassium

A
  • Inhaled beta agonists
  • Loop diuretics
  • Dialysis
248
Q

When there is hyperkaelmia and an abnormal EKG, what is the most appropriate next step?

A

Calcium chloride or calcium gluconate

249
Q

Hypokalemia

A
  • due to decreased intake
  • shift in to cells
  • renal loss
  • hypomagnesmia
  • renal tubular acidosis
250
Q

Hypokalemia 2/2 shift into cells

A
  • Alkalosis (H+ ions come out cell in exchange for K)
  • Increased insulin
  • Beta adrenergic stimulation (accelerates Na/K ATPase)
251
Q

Hypokalemia 2/2 renal loss

A
  • Loop diuretics
  • Increased aldosterone
  • Primary hyperaldosteronism (Conn syndrome)
  • Volume depletion raises aldosterone
  • Cushing syndrome
  • Bartter syndrome (genetic disease causing salt loss in Loop of Henle)
  • Licorice
252
Q

Hypokalemia 2/2 hypomagnesmia

A

There are Mg-dependent K channels. When magnesium is low, they open and spill potassium in the urine

253
Q

Hypokalemia 2/2 GI loss

A
  • seen in vomiting, diarrhea, and laxative abuse
254
Q

Hypokalemia presentation

A

Leads to issue with muscular contraction and cardiac conduction

  • Weakness
  • Paralysis
  • Loss of reflexes
255
Q

Hypokalemia EKG findings

A

U waves are the most characteristics

  • ventricular ectopy (PVCs)
  • flattened T waves
  • ST depression
256
Q

Hypokalemia: treatment

A

No maximum rate of oral K replacement

- however with rapid IV potassium replacement, it can cause arrhythmia

257
Q

PT is admitted with vomiting and diarrhea from gastroenteritis. His volume status is corrected with IV fluids and the diarrhea resolves. His pH is 7.40 and his serum bicarbonate has normalized. Despite oral and IV replacement, his potassium level fails to rise. What should you do?

A

Check magnesium level

- hypomagnesmia can be lead to increased urinary loss of K

258
Q

A woman with ESRD and G6PD deficiency skips dialysis for a few weeks and then is crushed in a MVA. She taking dapsone and has recently eating a few fava beans. What is the most urgent step?

A

EKG

if abnormal, give patent Ca chloride

259
Q

Renal Tubular Acidosis

A

metabolic acidosis with a normal anion cap (6 - 12)

260
Q

Two most important causes of metabolic acidosis with normal anion gap

A
  • RTA

- Diarrhea

261
Q

Why is the anion gap normal in RTA and diarrhea

A

Chloride level rises 2/2 they are also refer to hyperchloremic metabolic acidosis

262
Q

Anion gap metabolic acidosis

A

due to ingested substances:

  • ethylene glycol or methanol
  • organic acids (e.g. lactate) that are anion and drive down chloride level
263
Q

Distal RTA (Type I)

A
  • distal tubule is responsible for generating new bicarbonate under the influence of aldosterone
  • increased formation of kidney stones from calcium oxalate 2/2 alkaline urine
  • calcifies the kidney parenchyma
264
Q

Drugs that cause distal RTA (Type I)

A
  • Amphotericin

- Autoimmune disease (e.g. SLE or Sjorgen syndrome can damage distal tubule)

265
Q

Best initial test for Distal RTA

A

Urinalysis

- looking for an abnormally high pH > 5.5

266
Q

Most accurate test for Distal RTA

A
  • infuse acid into the blood with ammonium chloride
267
Q

Treatment of Distal RTA

A

Replace bicarbonate which will be absorbed at the proximal tubule

268
Q

Proximal RTA (Type II)

A
  • decreased ability for kidney to reabsorb most of filtered bicarbonate
  • eventually bicarbonate is lost in urine until the body is so depleted of bicarbonate that the distal tubule can absorb the rest
  • the urine pH will become low (at or below 5.5)
  • chronic metabolic acidosis can leach calcium to cause osteomalacia
269
Q

Proximal RTA (Type II): Causes

A
  • Amyloidosis
  • Myeloma
  • Fancomi syndrome
  • Acetazolamide
  • Heavy metal
270
Q

Most accurate test for proximal RTA (Type II)

A

Testing urine pH after giving bicarbonate

271
Q

Urine pH during proximal RTA (Type II)

A

First it is basic (above 5.5) until most bicarbonate is lost from body, then is low (below 5.5)

272
Q

Status of potassium in both proximal and distal RTA

A

Hypokalemia

- potassium is lost in the urine

273
Q

Proximal RTA (Type II)

A

Thiazide diuretics cause volume depletion. Volume depletion will enhance bicarbonate reabsorption.

274
Q

Hyporeninemia, hypoaldosteronism (Type IV RTA)

A
  • occurs most often in diabetes
  • decreased amount or effect of aldosterone at the kidney tubule
  • leads to loss of Na and retention and K and H_
275
Q

Best testing for Type IV RTA

A

Finding a persistently high urine sodium despite a sodium depleted diet

276
Q

Treatment for Type IV RTA

A

Fludrocortisone

- steroid with the highest mineralcorticoid or “aldosteronelike” effect

277
Q

Urine anion gap (UAG)

A

way to distinguish between diarrhea and RTA

Na - Cl

278
Q

Why is chloride high in acidotic conditions

A

Acid excreted by kidney is buffered by NH4Cl

- more acid excreted, the greater amount of chloride found in urine

279
Q

Why is the UAG (Na - Cl) positive in RTA

A

RTA is defect in acid excretion into urine, so the amount of chloride in urine is diminished

280
Q

Why is UAG (Na - Cl) negative in RTA

A

diarrhea associated w/ metabolic acidosis thus kidney tries to compensate by increasing acid excretion

  • acid is excreted with chloride
  • more acid in urine means more chloride in urine
281
Q

Causes of metabolic acidosis

A 
MUDPILES
Methanol
Uremia
Diabetes ketoacidosis
Paraaldehyde
Isoniazid or Iron
Lactate
Ethylene glycol
Salicylates
282
Q

Metabolic acidosis 2/2 lactate

A
  • caused by hypotension or hypoperfusion
  • tested with blood lactate levels
  • treat by correcting hypoperfusion
283
Q

Metabolic acidosis 2/2 ketoacidosis

A
  • caused by DKA and starvation
  • tested by measuring acetone levels
  • treat with insulin and fluids
284
Q

Metabolic acidosis 2/2 oxalic acid

A
  • caused by ethylene glycol overdose
  • tested by seeing crystals in UA
  • treat with fomepizole and dialysis
285
Q

Metabolic acidosis 2/2 formic acid

A
  • caused by methanol overdose
  • tested by seeing inflamed retina
  • treated with fomepizole and dialysis
286
Q

Metabolic acidosis 2/2 uremia

A
  • caused by renal failure
  • test by evaluating BUN and Cr
  • treated with dialysis
287
Q

Metabolic acidosis 2/2 salicylates

A
  • caused by aspirin overdose
  • test for aspirin levels
  • treat by alkanizing urine
288
Q

ABG in metabolic acidosis

A
  • decreased pH below 7.4
  • decreased pCO2 indicating respiratory alkalosis as compensation
  • decreased bicarbonate
289
Q

Metabolic alkalosis

A
  • elevated serum bicarbonate level
  • compensated with respiratory acidosis
  • relative HYPOventilation that will increased pCO2 to compensate for metabolic alkalosis
290
Q

Metabolic alkalosis: etiology

A
  • GI loss: vomiting or nasogastric suction
  • Increased aldosterone: primary hyperaldosteronism, Cushing syndrome
  • Diuretics
  • Milk-alkali syndrome: high volume liquid antacids
  • Hypokalemia: H+ move into cells so K can be released
291
Q

Metabolic alkalosis on ABG

A
  • increased pH > 7.4
  • increased pCO2 indicating respiratory acidosis as compensation
  • increased biarbonte
292
Q

Minute ventilation

A

respiratory rate x tidal volume

293
Q

Respiratory alkalosis

A
  • decreased pCO2
  • increased minute ventilation
  • metabolic acidosis as compensation
294
Q

Causes of respiratory alkalosis

A
  • Anemia
  • Anxiety
  • Pain
  • Fever
  • Interstitial lung disease
  • Pulmonary emboli
295
Q

Respiratory acidosis

A
  • increased pCo2
  • decreased minute ventilation
  • metabolic alkalosis as compensation
296
Q

Respiratory acidosis: causes

A
  • COPD / emphysema
  • Drowning
  • Opiate overdose
  • Alpha 1 antitryspin deficiency
  • Kyphoscoliosis
  • Sleep apnea / morbid obesity
297
Q

Most common cause of kidney stones (nephrolithiasis)

A

Calcium oxalate

- which forms more frequently in an alkaline urine

298
Q

Most common risk factor for kidney stones

A

Overexcretion of calcium in the urine

299
Q

A 46 y/o M comes to the ER 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

Katerolac

  • NSAID
  • more important to provide relief than specific diagnostic testing
300
Q

What is the most accurate diagnostic test for nephrolithiasis?

301
Q

Why does Crohn disease cause kidney stones?

A

Increased oxalate absorption

302
Q

Best initial therapy for acute renal colic

A
  • Analgesic and hydration
  • CT and sonography to detect obstruction
  • Stones < 5 mm pass spontaneously
  • Stones 5 - 7 mm get nifedipine and tamsulosin to help them pass
303
Q

Kidney stone etiology is determined with

A
  • Stone analysis
  • Serum calcium, NA, uric acid, PTH, Mg, and phosphate levels
  • 24 hr urine for volume, Ca, oxalate, citrate, cysteine
304
Q

Uric acid stones

A
  • not detectable on X-ray but seen on CT
305
Q

Cysteine stones

A
  • managed with surgical removal, alkalinizing the urine
306
Q

Woman with her 1st episode of renal colic is found to have a 1.8 cm stone in the L renal pelvis. She has no obstruction and her renal function is normal (normal BUN and Cr) What is the most appropriate next step in teh management of this patient?

A

Lithotripsy

307
Q

UTIs leave patients prone to which type of kidney stones?

A

Struvite stones (Mg/Al/ P)

308
Q

Long term management of nephrolithiasis

A

50% of those with kidneys stones will have reoccurence within 5 years

309
Q

Man with a Ca oxalate stone is managed with lithotripsy and the stone is destroyed and passes. His urinary calcium level is increased. Besides increasing hydration, which will most likely benefit this patient?

A

Hydrochlorothiazide

- removes calcium from urine

310
Q

Metabolic acidosis and stone formation

A

Metabolic acidosis removes Ca from bones and increases stone formation

  • acidosis decreases citrate levels
  • citrate binds calcium making it unavailable for stone formation
311
Q

Urinary Stress incontinence

A
  • older woman w/ painless urinary leakage with coughing, laughing, or lifting heavy objects
312
Q

Best test for urinary stress incontinence

A

have patient stand and cough

- observe for leakage

313
Q

Urinary stress incontinence: treatment

A
  1. Kegel exercises
  2. Local estrogen cream
  3. Surgical tightening of urethra
314
Q

Urinary urge incontinence

A
  • sudden pain in the bladder followed immediately by overwhelming urge to urinate
315
Q

Best test for urinary urge incontinence

A

pressure measurement in half full bladder

manometry

316
Q

Urinary urge incontinence: treatment

A
  1. Bladder training exercises
  2. Local anticholinergic therapy
    • oxybutinin
    • tolterodine
    • solifenacin
    • dariferancin
  3. Surgical tightening of urethra
317
Q

Hypertension

A
  • systolic pressure > 140 mm Hg
  • diastolic pressure > 90 mm Hg
  • diabetic patient or someone with CRD > 130/80 mm Hg
318
Q

Most common disease in the US

A

hypertension

319
Q

Most common risk factor for the most common cause of death

A

Myocardial infarction

320
Q

Causes of hypertension

A
  • Renal artery stenosis
  • Glomerulonephritis
  • Coarctation of the aorta
  • Acromegaly
  • Sleep apnea
  • Pheochromocytoma
  • Hyperaldosteronism
  • Cushing syndrome
  • Congenital adrenal hyperplasia
321
Q

Hypertension: symptomatic presentation

A
  • CAD
  • Cerebrovascular disease
  • CHF
  • Visual disturbance
  • Renal insufficiency
  • Peripheral arteru disease
322
Q

Renal artery stenosis: presentation

A
  • HTN
  • bruit is auscultated at the flank
  • continuous throughout systole and diastole
323
Q

Coaractation of the aorta

A
  • HTN

- upper extremities > lower extremities

First AId 2CK (22 decks)

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