Symptom To Diagnosis - Edema COPY Flashcards

1
Q

GENERALIZED edema due to a systemic cause - General etiologies:

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

Cardiovascular causes of edema:

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

Medications that cause generalized edema:

A
  1. Antidepressants: MAOIs.
  2. Antihypertensives: CCBs, hydralazine, minoxidil, beta-blockers.
  3. Hormones: Estrogens/progesterones, testosterone, steroids.
  4. NSAIDs and COX-2 inhibitors.
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4
Q

Limb edema - General etiologies:

A
  1. Venous diseases (obstruction + insufficiency).
  2. Lymphatic obstruction.
  3. Localized edema.
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5
Q

Venous disease as a cause of limb edema:

A
  1. OBSTRUCTION –> DVT, lymphadenopathy, pelvic mass.

2. INSUFFICIENCY.

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6
Q

Lymphatic obstruction as a cause of limb edema:

A
  1. PRIMARY –> (idiopathic, often bilateral), congenital, lymphedema praecox (onset in puberty) or tarda.
  2. SECONDARY –> (more common generally unilateral), neoplasm, surgery (esp. mastectomy), radiation, miscellaneous (TB, recurrent lymphangitis, filariasis).
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7
Q

Localized edema:

A
  1. Burns.
  2. Angioedema/hives.
  3. Trauma.
  4. Cellulitis, erysipelas.
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8
Q

MCC of cirrhosis:

A
  1. Alcohol.
  2. Chronic hep B, C.
  3. NAFLD.
  4. Hemochromatosis.
  5. Primary/secondary biliary cirrhosis.
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9
Q

Less common causes of cirrhosis:

A
  1. Drugs and toxins (isoniazid, methotrexate, amiodarone).
  2. Autoimmune hep.
  3. Genetic metabolic diseases (Wilson, alpha-1 antitrypsin def., glycogen storage diseases, porphyria).
  4. Infections (schistosomiasis, echinococcosis, brucellosis).
  5. Cardiac.
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10
Q

2 MCC of cirrhosis in the USA:

A
  1. Alcoholic liver disease.

2. Chronic hep C.

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11
Q

Risk factors for developing cirrhosis in patients with hep C:

A
  1. > 50.
  2. Regular alcohol.
  3. Male sex.
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12
Q

Risk factors for developing cirrhosis for those with NAFLD:

A
  1. Older age.
  2. Obesity.
  3. Insulin resistance.
  4. HTN.
  5. Hyperlipidemia.
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13
Q

Typical patient with ascites - Problem with daily living?

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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14
Q

Diagnostic criteria of hepatorenal syndrome:

A
  1. Cirrhosis with ascites.
  2. Serum Cr >1.5.
  3. Serum Cr stays above 1.5 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.
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15
Q

Type I hepatorenal syndrome:

A

Acute renal failure: Serum creatinine doubles or increases to >2.5 in less than 2 weeks.

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16
Q

Type II hepatorenal syndrome:

A

Refractory ascites: Serum creatinine 1.25-2.5 with a steady or slowly progressive course.

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17
Q

Hepatorenal syndrome - Incidence in patients with cirrhosis at 1yr and in 5yrs:

A

18% at 1 yr.

39% at 5 yrs.

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18
Q

Precipitants of type I hepatorenal syndrome:

A
  1. Bacterial infections (esp. SBP).
  2. GI bleeding.
  3. Alcoholic hep.
  4. Overdiuresis.
  5. Large volume paracentesis.
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19
Q

Hepatorenal syndrome - Mechanism:

A

Peripheral vasodilation –> Decreased systemic vascular resistance –> Renal arteriolar vasoconstriction –> Decreased renal blood flow and a reduced GFR.

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20
Q

SPB - Prevalence:

A

10-30% of hospitalized cirrhotic patients.

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21
Q

SBP - Recurrence rate in 1yr:

A

70%.

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22
Q

SBP - Mortality rate of:

A

20%.

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23
Q

3 common isolates in SBP:

A
  1. E.coli.
  2. Klebsiella.
  3. Pneumococci.
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24
Q

SBP - Symptoms:

A
50-75% --> Fever.
27-72% --> Abdominal pain.
16-29% --> Chills.
8-21% --> Nausea/vomiting.
Up to 50% --> Mental status changes.
33% --> Decreased renal function.
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25
Q

SBP - Percentage of patients who are asymptomatic:

A

13%.

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26
Q

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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27
Q

Criteria for performing a diagnostic paracentesis in patients with cirrhosis and ascites:

A
  1. Admission to the hospital.
  2. Change in clinical status.
  3. Development of leukocytosis, acidosis, or renal failure.
  4. Active GI bleeding.
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28
Q

Interpretation of ascitic fluid results - PMN >250 with single organism:

A

SPB.

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29
Q

Interpretation of ascitic fluid results - PMNs >250 with negative cultures:

A

Culture-negative neutrophilic ascites.

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30
Q

Interpretation of ascitic fluid results - PMN<250 with single organism:

A

Monomicrobial non neutrocytic bacterascites.

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31
Q

Interpretation of ascitic fluid - PMN >250 and polymicrobial:

A

Secondary bacterial peritonitis.

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32
Q

Interpretation of ascitic fluid - PMN<250 and polymicrobial:

A

Polymicrobial bacterascites.

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33
Q

LR + of SAAG >1.1 for the diagnosis of ascites due to portal HTN:

A

4.6.

34
Q

LR- of SAAG<1.1 for the diagnosis of ascites due to portal HTN:

A

0.06.

35
Q

Hepatic encephalopathy - Presents in …-…% of patients with chronic liver disease.

A

50-70%.

36
Q

Hypersplenism in cirrhosis - Textbook presentation:

A

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

37
Q

Splenomegaly is found in …-…% of patients with cirrhosis.
…-…% have the clinical syndrome of hypersplenism.

A

36-92%.

11-55%.

38
Q

Is there a rough correlation between spleen size and decrease in RBCs?

A

Yes.

39
Q

Mechanisms of thrombocytopenia in liver disease:

A
  1. Platelet sequestration in the spleen.
  2. Impaired bone marrow production.
  3. Decreased platelet survival.
40
Q

Mechanism of leukopenia in liver disease:

A

Sequestration in spleen - RARE compared to thrombocytopenia.

41
Q

Mechanism of anemia in liver disease:

A
  1. Increased destruction in spleen.
  2. Iron or folate deficiency.
  3. Decreased EPO production.
42
Q

Nephrotic syndrome - Textbook presentation:

A
  1. Edema.
  2. HTN.
  3. Hypoalbuminemia.
  4. Hyperlipidemia.
    at least 3.5g/24h of proteinuria.
43
Q

Infections that lead to nephrotic syndrome:

A
  1. Hep B,C, HIV.
  2. Syphilis.
  3. Malaria.
44
Q

Malignancies associated with nephrotic syndrome:

A
  1. Lung.
  2. Breast.
  3. Colon.
  4. HL.
45
Q

3 drugs that may cause nephrotic syndrome:

A
  1. NSAIDs.
  2. Captopril.
  3. Heroin.
46
Q

Risk factors for thromboembolism in nephrotic syndrome:

A
  1. Serum albumin 8g/24h.
47
Q

Lab evaluation of nephrotic syndrome:

A
  1. CBC.
  2. Comprehensive metabolic panel (renal and liver function, including serum albumin).
  3. Fasting glucose and HbA1c.
  4. ANA.
  5. HIV, hep B, C.
  6. Serum and urine electrophoresis.
48
Q

Normal pulmonary arterial pressure is:

A

12mmHg.

49
Q

Pulmonary HTN is defined?

A

As a mean PAP>25mmHg, with a mean pulmonary arterial occlusion pressure Mean PAP of at least 50mmHg.

50
Q

3 components of the pathophysiology of pulmonary HTN:

A
  1. Vascular remodeling with vascular inflammation and endothelial cell proliferation.
  2. Platelet dysfunction and thrombosis.
  3. Vasoconstriction due to 2 factors.
51
Q

Why vasoconstriction in pulmonary HTN?

A

Endothelial dysfunction resulting in:
1. OVERproduction of endothelin-1.
2. UNDERproduction of vasodilators such as NO, PGI2, VIP.
+ ABNORMAL voltage-gated K channels.

52
Q

Clinical classification of pulm. arterial HTN (PAH):

A
  1. Idiopathic.
  2. Familial.
  3. PAH associated with:
    a. Collagen vascular disease (esp. scleroderma, SLE, mixed connective tissue disease).
    b. Congenital pulmonary-systemic shunts.
    c. Portal HTN (1-6%).
    d. HIV (0.5%).
    e. Drugs and toxins.
53
Q

INITIAL Symptoms of PAH:

A
60% --> Dyspnea.
19% --> Fatigue.
7% --> Chest pain.
8% --> Syncope.
3% --> Edema.
54
Q

At the time the patients were given the diagnosis of PAH and were enrolled in the study:

A
98% --> Dyspnea.
73% --> Fatigue.
47% --> Chest pain.
37% --> Edema.
36% --> Syncope.
33% --> Palpitations.
55
Q

PAH - Physical exam:

A
  1. Accentuated pulm. component of S2.
  2. Sustained left lower parasternal movement.
  3. An early systolic click.
  4. Increased jugular a and v waves.
  5. TV regurgitation.
  6. Hepatojugular reflex.
  7. Pulsatile liver.
  8. Elevated jugular venous pressure.
  9. Edema.
56
Q

Sustained left parasternal movement for detecting a mean PAP>50mmHg:

A

Sens - 71%.
Spec - 80%.
LR+ 3.6.
LR- 0.4.

57
Q

A palpable P2 for detecting a mean PAP>50mmHg:

A
(studied in patients with MV stenosis).
Sens - 96%.
Spec - 73%.
LR+ 3.6.
LR- 0.05.
58
Q

ECG - Expected findings in PAH:

A
  1. Right axis deviation.
  2. RV hypertrophy.
  3. P-pulmonale pattern.
    NOT sensitive or specific enough to diagnose PAH.
59
Q

Venous insufficiency - Superficial or deep veins of the leg?

A

45% –> Superficial system.
40% –> Deep system + Superficial system.
Remainder –> Only deep system.

60
Q

Prevalence of varicose veins:

A

25-33% –> Women.

10-20% –> Men.

61
Q

Prevalence of skin changes in venous insufficiency:

A

3-11% –> Skin changes.

0.3-1% –> Skin ulcers.

62
Q

Risk factors for venous insufficiency:

A
  1. Age.
  2. Obesity.
  3. History of phlebitis or venous thrombosis.
  4. Serious leg trauma.
  5. Pregnancy.
  6. Prolonged standing.
  7. Greater height.
63
Q

Classification of venous insufficiency:

A

Class 1: Telangiectasias or reticular veins (non palpable subdermal veins up to 4mm in diameter).
Class 2: Varicose veins. (palpable >4mm in diameter).
Class 3: Edema without skin changes.
Class 4: Skin changes.
Class 5 and 6: Healed or non healed ulcers.

64
Q

Gold standard for venous insufficiency:

A

Venography.

65
Q

Best non invasive test for venous insufficiency:

A

Duplex US.

66
Q

Cellulitis definition:

A

An infection of the dermis and subcutaneous tissue.

67
Q

Erysipelas definition:

A

Superficial cellulitis with prominent lymphatic involvement.

68
Q

Risk factors for the development of cellulitis:

A
  1. Lymphedema.
  2. Peripheral edema.
  3. Venous insufficiency.
  4. Obesity.
  5. Diabetes.
  6. History of cellulitis.
  7. Breast cancer treatment.
69
Q

Cellulitis - Presence of systemic symptoms (fever, chills, myalgias)?

A

UNUSUAL –> Suggests concomitant bacteremia or a more serious infection such as necrotizing fasciitis.

70
Q

Risk factors for erysipelas:

A
  1. Similar to those for cellulitis.

2. Lymphedema and an identified portal of entry (primarily tinea pedis) are the 2 strongest risk factors in 1 study.

71
Q

Most common site for erysipelas?

A

Leg –> 90%.
5% –> Arm.
2.5% –> Face.

72
Q

BOTH cellulitis and erysipelas are … diagnoses.

A

Clinical.

73
Q

Erysipelas/cellulitis - Blood cultures are positive in …-…% of patients.

A

2-5%.

74
Q

Erysipelas/cellulitis - Skin biopsy cultures are positive in …-…% of patients.

A

5-40% - RARELY necessary.

75
Q

UPPER extremity DVT (UEDVT) - Textbook presentation:

A

Patients can be asymptomatic, but generally arm, shoulder, or neck discomfort or fullness as well as arm swelling are the presenting symptoms.

76
Q

Classification of UEDVT:

A

Primary (20%).

Secondary (80%).

77
Q

Effort thrombosis?

A

Paget-Schroetter syndrome:

  1. Young men after strenuous exercise, which causes microtrauma to the veins.
  2. May or may not find compression by hypertrophied muscles or a cervical rib.
78
Q

Secondary UEDVT - Etiology:

A
  1. Indwelling central venous catheter-associated UEDVT (up to 70% of cases).
  2. Malignancy (>40% of cases).
  3. Hypercoagulable states.
  4. Other miscellaneous causes (surgery, infection, immobility, concurrent lower DVT).
79
Q

UEDVT - Sites:

A

18-69% –> Subclavian.
5-42% –> Axillary.
8-29% –> Internal jugular vein.
4-13% –> Brachial.

80
Q

UEDVT - Clinical features:

A

80% –> Edema.
40% –> Pain.
Patients may note numbness, heaviness, paresthesias, pruritus, coldness.
Dilated cutaneous veins sometimes visible.

81
Q

UEDVT - Complications:

A
  1. PE –> 36%.
  2. Recurrent thrombosis –> 10%.
  3. Post thrombotic syndrome is seen in up to 4-34% of patients in different sites.
82
Q

How much must the interstitial volume be increased for edema to be clinically present?

A

2.5-3L.