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Internal Medicine > Symptom to Diagnosis - Edema > Flashcards

Symptom to Diagnosis - Edema Flashcards

1
Q

What are the features of generalized edema?

A
  1. Bilateral leg edema
  2. +/- presacral edema
  3. Ascites
  4. Pleural effusion
  5. Pulmonary edema
  6. Periorbital edema
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2
Q

What are the general causes of generalized edema?

A
  1. Cardiovascular
  2. Hepatic (cirrhosis)
  3. Renal
  4. Anemia
  5. Nutritional deficiency
  6. Medications
  7. Refeeding edema
  8. Myxedema
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3
Q

What are the specific cardiovascular causes of generalized edema?

A
  1. Systolic or diastolic dysfunction, or both.
  2. Constrictive pericarditis
  3. Pulmonary HTN
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4
Q

What are the specific renal causes of generalized edema?

A
  1. Advanced renal failure of any cause

2. Nephrotic syndrome

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5
Q

What are the MC systemic causes of edema?

A
  1. Cardiac
  2. Renal
  3. Hepatic
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6
Q

What medications may cause edema?

A
  1. Antidepressants –> MAOIs
  2. Antihypertensives –> CCBs, hydralazine, minoxidil, beta-blockers.
  3. Hormones –> Estrogens/Progesterone, testosterone, corticosteroids.
  4. NSAIDs and COX-2 inhibitors.
  5. Rosiglitazone, pioglitazone
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7
Q

What are the causes of limb edema?

A
  1. Venous disease –> Obstruction/Insufficiency.

2. Lymphatic obstruction –> Primary/Secondary.

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8
Q

What are the main causes of venous obstruction that produces limb edema?

A
  1. DVT
  2. Lymphadenopathy
  3. Pelvic mass
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9
Q

What are the causes of primary lymphatic obstruction (lymphedema)?

A
  1. Congenital

2. Lymphedema praecox (onset in puberty) or tarda (onset after 20).

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10
Q

What are the causes of secondary lymphatic obstruction?

A
  1. Neoplasm
  2. Surgery (especially following mastectomy)
  3. Radiation therapy
  4. Miscellaneous (TB, recurrent lymphangitis, filariasis)
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11
Q

What are the main causes of localized edema?

A
  1. Burns
  2. Angioedema, hives
  3. Trauma
  4. Cellulitis, erysipelas
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12
Q

What are the most common causes of cirrhosis?

A
  1. Alcohol
  2. Chronic Hep B/C
  3. NAFLD
  4. Hemochromatosis
  5. Primary/Secondary biliary cirrhosis
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13
Q

Mention some less common causes of cirrhosis.

A
  1. Drugs + Toxins –> Isoniazid, methotrexate, amiodarone.
  2. Autoimmune hep.
  3. Genetic metabolic diseases (Wilson, α1-antitrypsin def., glycogen storage diseases, porphyria)
  4. Infections –> Schistosomiasis, echinococcosis, brucellosis.
  5. Cardiac
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14
Q

Why is there incr. risk for HCC in background of cirrhosis?

A

Due to regenerative activity.

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15
Q

What are the risk factors for developing cirrhosis in patients with chronic hep C?

A
  1. Age over 50
  2. Regular alcohol consumption
  3. Male sex
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16
Q

What are the risk factors for developing cirrhosis in patients with NAFLD?

A
  1. Older age
  2. Obesity
  3. Insulin resistance
  4. HTN
  5. Hyperlipidemia
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17
Q

What is the 5-yr mortality in cirrhosis after decompensation if transplantation is not performed?

A

85%

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18
Q

What is the gold standard in diagnosing cirrhosis?

A

Percutaneous liver biopsy, although due to sampling error, the sensitivity has been reported to be as low as 70-80%.

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19
Q

Mention some physical findings associated with chronic liver disease.

A
  1. Spider angiomata
  2. Palmar erythema
  3. Dupuytren contracture
  4. Gynecomastia
  5. Testicular atrophy
  6. Jaundice
  7. Ascites
  8. Peripheral edema
  9. Hepatomegaly
  10. Splenomegaly
  11. Caput medusae
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20
Q

What is the textbook presentation of ascites?

A

Patient complains of an inability to fasten her pants due to increasing abdominal girth, sometimes accompanied by dyspnea and edema.

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21
Q

What is the epidemiology of ascites?

A
  1. Develops over 5yrs in 30% of patients with compensated cirrhosis, defined as the absence of manifestations of portal HTN.
  2. 1-yr survival rates drop significantly once ascites develops.
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22
Q

Mention some major complications of ascites.

A
  1. Respiratory compromise due to compression of lung volumes.
  2. Hepatorenal syndrome (HRS)
  3. Spontaneous bacterial peritonitis (SBP)
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23
Q

What are the diagnostic criteria for HRS?

A
  1. Cirrhosis with ascites
  2. Serum creatinine >1.5 mg/dL
  3. Serum creatinine stays above 1.5mg/dL after at least 2 days of diuretic withdrawal and volume expansion with albumin.
  4. Absence of shock
  5. No current or recent treatment with nephrotoxic drugs.
  6. Absence of parenchymal kidney disease (<50 RBC/hpf, abnormalities on renal US).
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24
Q

What are the two types of HRS?

A

Type I –> ARF –> serum Cr doubles or incr. to >2.5 mg/dL in less than 2 weeks.
Type II –> Refractory ascites –> serum Cr 1.25-2.5mg/dL –> Steady or slowly progressive course.

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25
Q

What is the incidence of HRS in patients with cirrhosis at 1yr and at 5yrs?

A

18% at 1yr.

39% at 5yrs.

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26
Q

Mention some precipitants of type I HRS?

A
  1. Bacterial infections –> especially SBP
  2. GI bleeding
  3. Alcoholic hep
  4. Overdiuresis
  5. Large volume paracentesis
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27
Q

What is the basis of HRS?

A

Due to peripheral vasodilation –> Decr. systemic vascular resistance –> Renal arteriolar vasoconstriction –> Decr. renal blood flow –> Decr. GFR.

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28
Q

What is the definitive treatment for both types of HRS?

A

Liver transplantation.

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29
Q

What is the prevalence of SBP in hospitalized cirrhotic patients?

A

10-30% –> 1yr recurrence rate of 70%.

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30
Q

What is the mortality of SBP?

A

20%.

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31
Q

What is the mechanism for SBP?

A

Overgrowth intestinal bacteria + incr. intestinal permeability lead to movement of bacteria into mesenteric lymph nodes –> Can enter systemic circulation and colonize the ascitic fluid.

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32
Q

What are the 3 most common isolates in SBP?

A
  1. E.coli
  2. K.pneumoniae
  3. Pneumococci
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33
Q

What are the symptoms of SBP?

A
  1. Fever (50-75%)
  2. Abdominal pain (27-72%)
  3. Chills (16-29%)
  4. Nausea/vomiting (8-21%)
  5. Mental status changes (up to 50%)
  6. Decr. renal function (33%)
  7. About 13% are ASYMPTOMATIC
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34
Q

Mention risk factors for SBP.

A
  1. Ascitic fluid total protein level <1g/dL.
  2. Upper GI bleeding
  3. Prior episode of SBP
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35
Q

If more than 1 organism is cultured from the ascitic fluid, what should be considered?

A

Secondary peritonitis.

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36
Q

What is the best-studied drug for SBP?

A

IV cefotaxime - also augmentin.

37
Q

What is the condition if PNM count of ascitic fluid is >250 with a single organism?

A

SBP

38
Q

What is the condition if the PMN count in ascitic fluid is >250 with negative culture results?

A

Culture-negative neutrophilic ascites.

39
Q

What is the condition if PMN count is <250 with a single organism?

A

Monomicrobial non neutrocytic bacterascites.

40
Q

What is the conditions if the PMN count is >250 and the culture results show multiple organisms?

A

Secondary bacterial peritonitis.

41
Q

What is the condition if the PMN count is <250 and the culture results show multiple organisms?

A

Polymicrobial bacterascites.

42
Q

In the treatment of ascites what has interestingly been shown to reduce mortality and development of renal impairment?

A

IV albumin!

43
Q

Should liver transplantation be considered in patients with SBP?

A

YES - 2yr survival is only about 30%.

44
Q

What is the best test for distinguishing ascites due to portal HTN and ascites due to other causes?

A

Serum-ascites albumin gradient.

45
Q

What is the diuretic of choice in ascites?

A

Spironolactone –> Also treat the aldosterone-driven salt and water retention –> 75% respond.

46
Q

In order to avoid hypovolemia and renal impairment what should be the rate of weight loss in patients with ascites +/- edema?

A

Should not exceed 0.5kg/d in the ABSENCE of peripheral edema.
Or 1kg/d in the presence of edema.

47
Q

What drugs should be avoided in patients with ascites?

A

NSAIDs and aspirin –> Blunt natriuretic effect of diuretics.

48
Q

What percentage of patients with chronic liver disease have hepatic encephalopathy?

A

50-70%.

49
Q

What may precipitate encephalopathy?

A
  1. Incr. ammonia production
  2. Reduced metabolism of toxins because of hepatic hypoxia
  3. Incr. central venous depressant effect with use of benzodiazepines or other psychoactive drugs.
  4. Reduced metabolism of toxins because diversion of portal blood, due to surgical or intrahepatic shunts.
50
Q

What may increase ammonia production?

A
  1. Excess dietary protein.
  2. Constipation
  3. GI bleeding
  4. Infection
  5. Azotemia
  6. Hypokalemia
  7. Systemic alkalosis
51
Q

What may induce hepatic hypoxia?

A
  1. Dehydration
  2. Arterial hypotension
  3. Anemia
52
Q

What are two complications of lactulose therapy used in encephalopathy?

A
  1. Hypovolemia

2. Hyponatremia

53
Q

Do we consider liver transplantation in patients with hepatic encephalopathy?

A

Yes

54
Q

What is the textbook presentation of hypersplenism?

A

Cytopenias are found on routine blood test in a patient with cirrhosis.

55
Q

What percentage of patients with cirrhosis have splenomegaly?

A

36-92%

56
Q

What percentage of patients with cirrhosis have the clinical syndrome of hypersplenism?

A

11-55%

57
Q

What is more common in hypersplenism, thormbocytopenia or leukopenia?

A

By far thrombocytopenia.

58
Q

What is the textbook presentation of nephrotic syndrome?

A

Classically present with edema (often periorbital), hypertension, hypoalbuminemia, hyperlipidemia, and at least 3.5g/d of proteinuria.

59
Q

What are the 2 general categories of etiology for nephrotic syndrome?

A
  1. Primary glomerular disease

2. Systemic causes

60
Q

Mention some common causes of nephrotic syndrome with primary glomerular basis.

A 
In adults:
1. Membranous
2. Focal glomerulosclerosis 
33% each.
Less common:
1. Minimal change disease (15%)
2. IgA nephropathy (10%)
3. MPGN
61
Q

Mention some common systemic causes of nephrotic syndrome?

A
  1. Diabetes is the MC.
  2. SLE
  3. Amyloidosis + MM (in those over 40)
  4. Infections –> HIV, hep B/C, syphilis, malaria
  5. Malignancies
  6. Many drugs - NSAIDs, captopril, heroin.
62
Q

Mention some major clinical consequences of nephrotic syndrome?

A
  1. Primary sodium retention by the kidney causes edema and HTN.
  2. Albumin excretion –> Hypoalbuminemia –> Contributes to edema formation.
  3. Alteration in lipoprotein production + catabolism –> UP LDL + sometimes TGs.
  4. Ig excretion causes incr. susceptibility to infection.
  5. Thromboembolic complications.
63
Q

What should lab evaluation of nephrotic syndrome include?

A
  1. CBC
  2. Comprehensive metabolic panel (renal/liver function, incl. serum albumin).
  3. Fasting glucose + HbA1c
  4. ANA
  5. HIV
  6. Hep B surface antigen + core antibody.
  7. Hep C antibody
  8. Serum + Urine electrophoresis.
  9. Renal biopsy is OFTEN necessary.
64
Q

What is the role of ACE inhibitors in nephrotic syndrome?

A

Reduce proteinuria in BOTH hypertensive + normotensive patients.

65
Q

When does the antiproteinuric effect of ACE inhibitors become maximal?

A

In 28 days.

66
Q

What may incr. the effect of ACEIs in nephrotic syndrome?

A
  1. Low-salt diet
  2. Diuretic treatment
  3. Both
67
Q

What is the textbook presentation of pulmonary HTN?

A
  1. Complain of long standing dyspnea that progresses over months and years.
  2. Syncope
  3. Exertional chest pain
  4. Edema
  5. Impaired RV function
    (the latters with more severe pulmonary HTN).
68
Q

What is the definition of pulmonary HTN?

A

Normal mean PAP is 12mmHg.
Defined as mean PAP >25mmHg with a mean pulmonary arterial OCCLUSION pressure <15mmHg.
SEVERE is defines as a mean PAP of at least 50mmHg.

69
Q

What are the 3 factors responsible for the incr. pulmonary vascular resistance?

A
  1. Vascular remodeling with vascular inflammation and endothelial cell proliferation.
  2. Platelet dysfunction and thrombosis.
  3. Vasoconstriction due to 2 factors.
    a. Endothelial dysfunction (imbalance between vasoconstrictors/vasodilators).
    b. Abnormal voltage-gated K channels.
70
Q

Mention the different types of pulmonary HTN.

A
  1. Idiopathic
  2. Familial
  3. PAH associated with collagen vascular disease (scleroderma, SLE, mixed connective tissue disease).
  4. PAH associated with congenital systemic-pulmonary shunts.
  5. PAH due to portal HTN (1-6%)
  6. PAH due to HIV (0.5%)
  7. PAH due to drugs/toxins
  8. PAH due to LH disease
  9. PAH due to lung disease or hypoxemia
  10. PAH due to chronic thromboembolic disease (proximal, or distal)
  11. Miscellaenous –> Sarcoidosis, compression due to adenopathy, tumor, fibrosing mediastinitis.
71
Q

What are the main initial symptoms of PAH?

A
  1. Dyspnea
  2. Fatigue
  3. Chest pain
  4. Syncope
  5. Edema
72
Q

In a patient with PAH, what would the physical exam show?

A

Characteristic findings include:

  1. Accentuated pulmonary component of S2.
  2. Sustained left lower parasternal movement.
  3. Early systolic click.
  4. Incr. jugular α and v waves.
  5. Tricuspid regurgitation murmur.
  6. Hepatojugular reflex
  7. Pulsatile liver
  8. Elevated jugular venous pressure
  9. Edema
73
Q

What are the expected findings in the ECG in a patient with PAH?

A
  1. Right axis deviation
  2. RVH
  3. RA enlargement - P-pulmonale pattern.
74
Q

Is ECG sensitive or specific enough to diagnose PHTN?

A

NO.

75
Q

Is a chest film sensitive or specific enough to diagnose PTHN?

A

NO.

76
Q

What is the MC NON-invasive way to estimate pulmonary pressure?

A

Transthoracic echocardiogram.

77
Q

What is the GOLD standard for diagnosing PHTN?

A

Right heart catheterization.

78
Q

Mention some causes of PHTN that can be corrected.

A
  1. For OSA –> Continuous positive airway pressure.
  2. For chronic thromboembolism –> Begin anticoagulation + consider thromboendarterectomy.
  3. For valvular disease –> Replace valve.
  4. For congenital heart disease –> Repair surgically.
  5. For left ventricular dysfunction –> Optimize medical regimen.
79
Q

What does the treatment of PHTN involve?

A
  1. Most patients require loops.
  2. Endothelin blockers –> Bosentan.
  3. Sildenafil
  4. Prostacyclins - such as epoprostenol (parenteral)
  5. or iloprost (inhaled).
80
Q

What is the textbook presentation of venous insufficiency?

A
  1. May be asymptomatic
  2. Manifested by small visible, but nonpalpable veins.
  3. In more severe cases, the patient has large varicose veins + skin changes ranging from edema to fibrosing panniculitis to ulceration.
  4. Leg fullness or heaviness.
  5. Aching leg pain
  6. Nocturnal leg cramps
81
Q

Reflux in the veins of the leg occur mostly in the superficial system or in the deep vein system?

A

45% –> Superficial
40% –> Both
15% –> Deep

82
Q

Varicose veins are more common in women or men?

A

25-33% –> Women

10-20% –> Men

83
Q

Mention some risk factors for venous insufficiency?

A
  1. Advancing age
  2. Obesity
  3. History of phlebitis or venous thrombosis
  4. Serious leg trauma
  5. Pregnancy
  6. Prolonged standing
  7. Greater height
84
Q

What is the post thrombotic syndrome?

A

Venous insufficiency after a DVT.

85
Q

How many classes does the classification of venous insufficiency have?

A

6

86
Q

What happens in class 1 classification of venous insufficiency?

A

Telangiectasias or reticular veins (non palpable subdermal veins up to 4mm in diameter).

87
Q

What happens in class II classification?

A

Varicose veins (palpable subcutaneous veins >4mm in diameter).

88
Q

What is the volume of the edema in order to become clinically apparent?

A

At least 2.5-3L.

Internal Medicine (106 decks)

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