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Surgery > spleen > Flashcards

spleen Flashcards

1
Q

what “tickles” the spleen

A

tail of pancreas

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2
Q

functions of the spleen

A

-filters abn rbc(not store)
-stores platelets
-produces tuftsin and properdin (opsins)
produces antibodies and site of phagocytosis

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3
Q

delayed splenic rupture

A

subcapsular hematoma or pseudoaneurysm may rupture some time after blunt trauma, causing delayed splenic supture; rupture classically occurs about 2 wks after injury and presents with shock and abd pain

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4
Q

s/sx ruptured/injured spleen

A

hemoperitoneum and kehr’s sign; luq abd pain; ballances sign

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5
Q

kehr’s sign

A

left shoulder pain seen w splenic rupture

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6
Q

ballance’s sign

A

luq dullness to percussion

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7
Q

seagesser’s sign

A

phrenic nerve compression causing neck tenderness in splenic rupture

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8
Q

dx spleen injury

A

abd ct (stable); dpl or fast exam if unstable

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9
Q

tx stable pt w spleen injury

A

nonop in stable w an isolated splenic injury without hilar involvement/complete rupture

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10
Q

tx pt unstable spleen injury

A

dpl/fast lap w splenorrhaphy or splenectomy

embolization in select pt

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11
Q

splenorrhaphy

A

splenic salvage operation:wrapping vicryl mesh, aid of topical hemostatic agents or partial splenectomy, sutures

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12
Q

malignant ds that need splenectomy

A

hodgkins, splenic tumors, hypersplenism

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13
Q

anemias need splenectomy

A

medullary fibrosis w myeloid metaplasia, hereditary elliptocytosis, sickle cell, pyruvate kinase def, auto hemolytic anemia, hereditary spherocytosis, thalassemias

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14
Q

thrombocytopenia need splenectomy

A

ITP, TTP

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15
Q

is g6pd def an indication for splenectomy

A

no

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16
Q

postsplenectomy complications

A

thrombocytosis, subphrenic abscess, atelectasis, pancreatitis, gastric dilation, overwhelming postsplenectomy sepsis (OPSS), pancreatic injury of tail

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17
Q

s/sx of overwhelming postsplenectomy sepsis (OPSS)

A

fever, lethargy, common cold, sore throat, uri followed by confusion, shock, come w death ensuing within 24hr in up to 50%pt

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18
Q

common organisms assoc w opss

A

encapsulated: strep pneumo, neisseria meningitides, h infl

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19
Q

mc bacteria cause opss

A

strep pneumo

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20
Q

prevention of opss

A

vaccines for pneumococcus, h infl, meningococcus; prophylactic penicillin for all minor infx/illness and immediate med care if febrile illness develops

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21
Q

best time to give immunizations to splenectomy pt

A

preop but if emergent 2 weeks postop

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22
Q

what tests are abn after splenectomy

A

wbc count inc by 50% over baseline; marked thrombocytosis occurs; rbc smear

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23
Q

findings on postsplenectomy rbc smear

A

peripheral smear will show pappenheimer bodies, howell jolly bodies and heinz bodies

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24
Q

when and how should thrombocytosis be tx

A

platelet count >1million, tx w aspirin

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25
Q

mc cause splenic vein thrombosis

A

pancreatitis

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26
Q

what opsonins does the spleen produce

A

properdin, teftsin

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27
Q

mc cause of isolated gastric varices

A

splenic vein thrombosis (usually from pancreatitis)

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28
Q

tx of gastric varices caused by splenic vein thrombosis

A

splenectomy

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29
Q

which pt develop hyposplenism

A

pt w ulcerative colitis

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30
Q

what vaccinations should every pt w splenectomy receive

A

pneumococcus, meningococcus, h inf type B

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31
Q

hypersplenism

A

hyperfunctioning spleen; doc loss of blood elements; large spleen; hyperactive bone marrow (trying to keep up w loss of blood elements)

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32
Q

define splenomegaly

A

enlarged spleen

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33
Q

idopathic thrombocytopenic purpure (ITP)

A

autoimm platelet destruction leading to troublesome bleeding and purpura

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34
Q

mc cause of failure to correct thrombocytopenia after splenectomy for ITP

A

missed accessory spleen

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35
Q

I’s of ITP

A

immune etiology (IgG); immunosuppressive tx; immune globulin; improvement w splenectomy

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36
Q

tx TTP

A

plasmapheresis; splenectomy as last resort

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37
Q

mc pe finding of portal htn

A

splenomegaly

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38
Q

what arteries and veinous supply the spleen

A

splenic artery and short gastric arteries; portal vein, splenic vein, left gastroepiploic vein

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39
Q

accessory spleens

A

result from failure of separate splenic masses in the dorsal mesogastrium to fuse; buds are then carried to various locations

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40
Q

polysplenia

A

presence of multiple small spleens with no normal spleen

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41
Q

functions of the spleen

A

hematopoiesis, blood filtering, immune modulation

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42
Q

what raises suspicion of an accessory spleen

A

after splenectomy, nuclear remnants should be present on peripheral blood smear; if not =accessory spleen

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43
Q

what are opsonins and what ones are produced by the spleen

A

proteins that bind to particulate and bacterial antigen and facilitate phagocytosis; properdin (complement system), tuftsin (macrophage phagocytosis), fibronectin

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44
Q

the spleen is the body’s largest source of which Ig

A

IgM

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45
Q

size of a normal adult spleen

A

12cm long and 7cm wide

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46
Q

axr of spleen

A

rarely show normal spleen; splenomegaly is suggested when there is displacement of the colon inferiorly, stomach medially, or left diaphragm is elevated; splenic shadow

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47
Q

what can US/ sonography show

A

splenomegaly, splenic cysts, or splenic abscesses; best way to evaluate trauma pts for presence of blood in the abdomen

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48
Q

CT scan w iv and oral contrast

A

most useful to determine splenic size and detect splenic injury

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49
Q

radionuclide scans

A

colloid suspensions of technetium are taken up by the reticuloendothelial system and imaging gives info about size and function; helpful in searching for missed accessory spleens

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50
Q

what has replaced splenic artery catheterization for evaluation of the spleen in stable patients after sonography shows intra-abd fluid in cases of trauma

A

CT angiography

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51
Q

mc reason for splenectomy

A

trauma (blunt compressive then penetrating then blunt deceleration)

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52
Q

grade 1 of splenic trauma

A

hematoma (subcapsular

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53
Q

grade 2 of splenic trauma

A

hematoma (subcapsular 10-15% sa), parenchymal (

54
Q

grade 3 of splenic trauma

A

hematoma (subcap >50% sa), parenchymal (>5cm diameter), any expanding or ruptured laceration (>3cm deep or involving trabecular vessels)

55
Q

grade 4 splenic trauma

A

laceration: segmental vessels involved w devascularization

56
Q

grade 5 splenic trauma

A

completely shattered spleen or hilar vascular injury w devascularization

57
Q

what is the scale of splenic trauma used for

A

predicting which patients will stabilize initially; once they stabilize it has no use

58
Q

name of signs of peritoneal irritation that include lug tenderness and pain medial to at the top of left shoulder

A

Kehr’s sign/omalgia

59
Q

name of percussion dullness of left flank that suggests intraperitoneal bleeding

A

Ballance’s sign

60
Q

hemodynamically unstable pts who have signs of blunt abd trauma require

A

prompt laparotomy

61
Q

stable pt w signs of abd injury and those neuro status is impaired require

A

eval w us, ct, and rarely w dx peritoneal lavage

62
Q

when is a splenectomy performed

A

spleen is extensively injured (grade 5) or pt is profoundly unstable

63
Q

how much of the splenic volume needs to be preserved for the immune function of the spleen to remain intact

A

50%

64
Q

splenorrhaphy

A

operative repair of the spleen by debridement of devitalized tissue followed by compression w microcrystalhne collagen, pledgeted suture repair, and creation of polyglycolic acid mesh slings to provide hemostatic compression

65
Q

what two conditions should splenorrhaphy be abandoned

A

persistent hypotension or extensive additional intra abd injuries

66
Q

hyposplenism

A

diminished splenic function; usually increases susceptibility to infx, particularly w encapsulated bacteria

67
Q

hypersplenism

A

excess splenic function manifested by cytopenia which is a dec number of cells and normal/hyperplastic cellular precursors in the bone marrow

68
Q

3 hematologic disorders of splenic function for which splenectomy may be helpful

A

hemolytic anemia, immune thrombocytopenic purpure (ITP), and cytopenia assoc w splenomegaly from other ds

69
Q

hereditary spherocytosis

A

autosomal dominant trait, is characterized by abnormally shaped, rigid red cells as a result of a deficiency in membrane proteins essential for deformability, such as spectrin, ankyrin, or band 3. These rigid erythrocytes cannot pass through the splenic sinuses and become sequestered in the red pulp. Splenectomy is usually indicated because it allows red cells to survive and hematocrit to reach near-normal values postoperatively
.

70
Q

sickle cell disease

A

auto rec, mild hetero, severe homo;hemolytic anemia, sickle cells cause an increase in blood viscosity that leads to stasis and subsequent thrombocytosis. Ischemia occurs as a result and leads to fibrosis in a variety of organs

71
Q

thalassemias

A

characterized by deficits in the synthesis of one or more subunits of hemoglobin. There are many varied types. In thalassemia major (homozygous β-thalassemia), splenectomy is beneficial in reducing the requirements for transfusion, the physical discomfort from massive splenomegaly, and the potential for rupture. In thalassemia minor (heterozygous β-thalassemia), splenectomy can decrease the need for transfusion and the problems associated with iron overload. In general, patients who have thalassemia and undergo splenectomy are at the highest risk for OPSI.

72
Q

positive direct Coomb’s test

A

Red blood cells from patients with autoimmune hemolytic anemias are coated with immunoglobulin, complement, or both

73
Q

tx positive coombs

A

coritcosteroid therapy and tx any underlying disorders; splenectomy if steroids are ineffective or require high does

74
Q

tx neg coombs

A

secondary to drugs, toxins, or infectious agents and tx by removing the agent

75
Q

anemias assoc w warm reactive antibodies (usually IgG)

A

no complement activation; assoc w splenic sequestration and respond to splenectomy

76
Q

anemias assoc w cold reactive antibodies (IgM)

A

complement binding and agglutination; hemolysis occurs inperipheral locations in response to cool environmental temps so splenectomy is not indicated

77
Q

what are the only types of thrombocytopenias in which a splenectomy is appropriate

A

idiopathic, immune mediated (another cause can’t be found)

78
Q

what do pt w thrombocytopenia often have

A

multiple petechiae

79
Q

when does acute immune thrombocytopenic purpura (ITP) usually occur

A

after an acute viral infection

80
Q

tx ITP

A

corticosteroids; if don’t respond w an elevated platelet count and are refractory to adv medical therapy such as a gamma globulin or monoclonal antibody, splenectomy is performed ; vincristine and y globulin; gamma globulin

81
Q

thrombotic TP (TTP)

A

ds of arteries or capillaries; thrombotic episodes and low platelet counts; fever, purport, hemolytic anemia, neuro manif, signs renal ds

82
Q

tx ttp

A

plasma pheresis +/- whole blood exchange transfusions, steroids, and anti platelet therapy

83
Q

splenectomy is indicated for hypersplenism if

A

platelet count

84
Q

tx of choice when there is significant postsplenectomy thrombocytosis

A

hydroxyurea

85
Q

congestive splenomegaly

A

enlargement of the spleen as a result of vascular engorgement (ex portal htn); tx htn > splenectomy; tx splenorenal shunt procedure

86
Q

felty’s syndrome

A

leg ulcers or chronic infx assoc w splenomegaly and neutropenia in pt w rheumatoid arthritis

87
Q

is splenectomy indicated for acute leukemia

A

no

88
Q

after splenectomy when does the abc count return to normal from being elevated

A

5-7days; beyond this may be a sign of infection

89
Q

absence of howell jolly bodies, nucleated red cells, heinz bodies, pappenheimer bodies, and pitted red cells on peripheral smear after splenectomy suggest

A

accessory spleen was missed

90
Q

when does platelet count return to normal after splenectomy

A

within 2 weeks; if not tx w platelet inhibitors (aspirin, dipyridamole) until returns to normal; avoid anticoag w heparin or warfarin

91
Q

pt who undergo splenectomy for what reason are at highest risk for OPSI

A

hematologic disorders

92
Q

mc causes of infections

A

strep pneumoniae*, h influ, neisseria meningititdis, beta hemolytic strep, staph aureus, echoli, pseudomonas

93
Q

what vaccine given after total splenectomy or conservative splenic operation for trauma

A

polyvalent pneumococcal polysaccharide vaccine

94
Q

abx prophylaxis for immuno comp, receiving chemo, kids

A

oral penicillin

95
Q

mc complication after splenectomy

A

atelectasis

96
Q

fever, luq pain, omalgia, left pleural effusion, prolonged atelectasis, pneumonia, prolonged leukocytosis

A

subphrenic abscess- secondary to bleeding, inflammation, or leakage of pancreatic fluid as result to tail of pancreas

97
Q

enlarged spleen w lymphadenopathy suggests

A

mononucleosis, lymphoma, leukemia

98
Q

what are tender, hard, and rubbery nodes assoc w

A

tender=acute infx skin/soft tissue;

hard=cancer

rubbery= lymphomas

99
Q

right supraclavicular adenopathy

A

cancers of right lung or esophagus

100
Q

left supraclavicular adenopathy (virchow’s node)

A

gi and abd malig

101
Q

axillary lymphadenopathy

A

cat scratch ds or malignancy (breast)

102
Q

dx lymphadenopathy

A

cbc w diff; ct or mri, cxr, FNA, bx

103
Q

order of bx for generalized lymphadenopathy

A

cervical, supraclav, axillary, and inguinal

104
Q

Hodgkin’s ds

A

malignant lymphoma marked by chronic enlargement of the lymph nodes that is often local at onset and later generalized, together with enlargement of the spleen and often of the liver, no pronounced leukocytosis, and often anemia and continuous or remittent fever; associated with inflammatory infiltration of lymphocytes and eosinophilic leukocytes and fibroses.

105
Q

non hodgkin’s lymphoma

A

lymphoma other than Hodgkin’s disease; classified by Rappaport according to pattern (nodular or diffuse) and cell type; a working or international formulation separates lymphomas into low, intermediate, and high grades and into cytologic subtypes that reflect follicular center cell or other origin.

106
Q

avg age of person with hodgkins

A

32 (late 20s and mid 70s)

107
Q

s/sx hodgkins

A

usually asymp cervical lymphadeno, (fever,night sweats, wl) worse prognosis

108
Q

dx hodgkins

A

cxr, excisional bx of enlarged abnormal lymph node, bone marrow bx, evaluation of liver, spleen and retroperioneal nodes w ct

109
Q

REAL/WHO classification system group of Hodgkins 5 categories

A

nodular lymphocyte predominate, lymphocyte rich, nodular sclerosis*, mixed cellularity, lymphocyte depleted

110
Q

large reactive background of lymphocytes, eosinophils, and plasma cells with few malignant mononuclear cells and multinuclear giant cells “Reed stern berg”

A

hodgkins; owl eye

111
Q

cotswolds stage 1 hodgkins

A

Involvement of a single lymph node region or lymphoid structure (e.g., spleen, thymus, Waldeyer’s ring) or a single extralymphatic organ or site

112
Q

cotswolds stage 2 hodgkins

A

Involvement of two or more lymph node regions on the same side of the diaphragm (hilar nodes, when involved on both sides, constitute stage II disease); localized contiguous involvement of only one extralymphatic organ or site and lymph node region on the same side of the diaphragm (HE). The number of anatomic regions involved should be indicated by a subscript (e.g., II3)

113
Q

cotswolds stage 3 hodgkins

A

Involvement of lymph node regions on both sides of the diaphragm (III), which may be accompanied by involvement of the spleen (Ills), of or by localized contiguous involvement of only one extralymphatic organ site (IIIE), or both (lllSE)

114
Q

cotswolds stage 3-1 hodgkins

A

With or without involvement of splenic, hilar, celiac, or portal nodes

115
Q

cotswolds stage 3-2 hodgkins

A

with involvement of splenic, hilar, celiac, or portal nodes

116
Q

cotswolds stage 4 hodgkins

A

Diffuse or disseminated involvement of one or more extralymphatic organs or tissues, with or without associated lymph node Involvement (Involved organs should be identified by a symbol)

117
Q

what is used to stage hodgkins

A

cotswolds: a (asymp) or b (fever, night sweats, wl), x (bulky ds), e (involve extranodal site), cs (clinical stage), ps (pathologic stage)

118
Q

tx hodgkins

A

stage 1-2 (radiation- doses of 30-40Gy) other stages is chemo +/- radiation

119
Q

chemo for hodgkins

A

nitrogen mustard, vincristine, procarbazine and prednisone (MOPP); and doxorubicin (adriamycin), bleomycin, vinblastine, and dacarbazine (ABVD)

120
Q

who is at inc risk for nonhodgkins

A

AIDS and those who undergo organ transplantation

121
Q

what type of lymphoma is Epstein barr virus assoc w

A

Burkitts

122
Q

s/sx nonhodgkins

A

most asymp; can have fever/night sweats/wl; enlarged node with n/v, bleeding; tends to be disseminated

123
Q

MALT

A

lymphomas occur outside the lymph nodes (GI tract, thyroid, breast, or skin)

124
Q

dx nonhodgkins

A

cbc, lft, cxr, ct of chest/abd/pelvis, bm bx, (if inter/high bm involvement need lumbar puncture)

125
Q

what is used in staging nonhodgkins

A

REAL/WHO, Ann Arbor, or International NHL prognostic factors project

126
Q

tx nonhodgkins

A

surgery, radiation, or chemo depending on histologic subtype, stage, and risk relapse

127
Q

A 27-year-old woman is brought to the emergency department by her husband 16 hours after the onset of fever, malaise, sweats, vague abdominal pain, and increasing confusion. She has no chronic illnesses and takes no medications. Ten years ago, she underwent splenectomy for a ruptured spleen sustained when she was kicked by a horse. She recalls receiving vaccinations at that time when she was discharged from the hospital. Now her temperature is 39°C. Vital signs are pulse—125/mlnute, blood pressure (BP)—85/40 mm Hg, and respirations—30/minute. She Is confused. There are diffuse petechiae over her trunk. Her abdomen Is soft and nontender with a long, well-healed midline incisional scar. Laboratory values are WBC—26,000 mm3, sodium—125 mEq/dL, potassium of 6.0 mEq/dL, and glucose of 60 mg/dL.

After the patient is stabilized, a CT scan Is performed, which shows bilateral adrenal Infarcts with adrenal hemorrhage. Infection with which of the following microorganisms Is the most likely cause for her current infection?

A

Overwhelming postsplenectomy infection (OPSI) is most often caused by encapsulated organisms such as the Pneumococcus. She received vaccination after splenectomy, and therefore she is still at higher risk for developing OPSI with pneumococcus than someone who was vaccinated prior to splenectomy. Pneumococcal sepsis can lead to adrenal infarction (Waterhouse-Friderichsen syndrome). While the other organisms can cause severe infections, her clinical presentation is most likely due to pneumococcal sepsis.

128
Q

A 45-year-old woman comes to clinic because of bleeding gums when she brushes her teeth and heavy menstrual bleeding. She has a history of Immune thrombocytopenic purpura that was unresponsive to corticosteroids at that time and underwent splenectomy 15 months ago. Her platelet count 2 months after splenectomy was 175,000/mm3. Her physical exam today reveals scattered petechiae and a few purpuric lesions on her forearms. Platelet count today is 30,000/mm3. A peripheral smear shows normal red cell morphology and no red cell Inclusions. What is the next best step in management?

A

The correct answer is to obtain a radionuclide spleen scan to look for a missed accessory spleen. Accessory spleens can hypertrophy and sequester platelets just like a normal spleen. For this reason, It is important to look for and remove all accessory splenic tissue at the time of splenectomy. Platelet pheresis has no role at this time. If no accessory splenic tissue is identified on a radionuclide scan, further evaluation with a bone marrow aspirate may be necessary but not at this time. She did not respond initially to steroids so it is unlikely she will respond at this time. Platelet transfusion Is not indicated at this time as she Is not actively bleeding.

129
Q

A 23-year-old man is brought to the emergency department 30 minutes after a motorcycle crash. He Is awake and complaining of severe abdominal and left chest pain. Oxygen therapy and IV fluids were started at the scene. Blood pressure on admission was 90/60 with a pulse of 110/minute and respirations were 18/minute. A chest tube was placed on the left that yielded only a small amount of bloody fluid. Breath sounds are only slightly diminished at the left base and there is no tracheal deviation. After 2 L of normal saline, his BP is 80/50. A FAST exam shows a large amount of fluid in the abdomen and what appears to be a fractured spleen. In addition to blood transfusion, the most appropriate management Is

A

The correct answer Is to perform an exploratory laparotomy. This patient Is in shock and appears to have a severe splenic injury with continued hemorrhage. This Is not amenable to no operative treatment. Admission to the intensive care unit is necessary to monitor patients for nonoperative management; however, this patient is too unstable. It takes time to organize an angiography team, and this patient is too unstable. A CT scan is needed before an attempt at angiographic control of splenic hemorrhage in order to rule out other injuries. This patient remains hypotensive because of continued rapid intra-abdominal hemorrhage and needs control of the bleeding, which Is best accomplished at the time of laparotomy. Dopamine will not stop the bleeding.

130
Q

A 29-year-old woman is seen In clinic with fatigue and weakness. She recently had a urinary tract infection treated for 7 days with trimethoprim/sulfamethoxazole and stopped taking this 2 days ago. She takes no other medications. She has a history of glucose-6-phophate dehydrogenase deficiency. Her pulse is 100. She appears pale. Otherwise her physical exam is normal. Hematocrit Is 22%. What is the most likely mechanism for her anemia?

A

Glucose-6-phosphate dehydrogenase deficiency is a sex-linked recessive trait. The pentose phosphate shunt is blocked and red cell membranes are Injured by oxidation injury from certain drugs such as sulfamethoxazole, aspirin, phenacetin, or nitrofurantoin. Spectrin deficiency, a membrane component essential for deformabillty, is seen in spherocytosis. Sensitization of red cell membranes by membrane-bound antibody is the result of acquired hemolytic anemia. Conformational change in hemoglobin is seen in sickle cell anemia. Decreased production of ATP leading to membrane destruction Is the mechanism by which pyruvate kinase deficiency causes hemolysis.

131
Q

A 19-year-old man comes to clinic because of a left neck mass. He first noticed a firm nontender mass just above his clavicle about a month ago. He has not had any recent Infections. He has a cat that has been a pet for 4 years. He has also had nighttime sweats, but he has not taken his temperature. He does not use tobacco products and does not drink alcohol. He is now afebrile. On physical exam, there is a 3-cm, firm, nontender mass in the supraclavicular fossa. The rest of the physical exam is normal. What is the most likely diagnosis?

A

The correct answer is Hodgkin’s disease. The presence of night sweats and the identification of a large, nontender firm node suggest Hodgkin’s disease as opposed to a benign reactive adenopathy. Cat scratch disease usually presents with painful, suppurative adenopathy. There Is usually generalized mild lymphadenopathy associated with Addison’s disease. He has no risk factors for esophageal cancer, and the node is firm rather than hard, which would be more characteristic of metastatic cancer.

Surgery (21 decks)

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