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MRCEM Primary Exam > Pathologia > Flashcards

Pathologia Flashcards

1
Q

Hvenær í sáralokunarferli gerist inflammatory phase og hvaða 3 frumur eru aðalleikarar þar?

A

Gerist innan klukkustunda og aðal frumurnar eru:

  • macrophagar
  • neutrophilar
  • lymphocytar
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2
Q

Hvenær í sáralokunarferlinu birtast neutrophilar? Hvað gera þeir?

A

Neutrophils start to appear almost immediately and are the predominant cell type for the first 48 hours after the injury has occurred.

  • They cleanse the wound site of bacteria and necrotic matter
  • release inflammatory mediators and bactericidal oxygen free radicals.
  • The absence of neutrophils does not prevent healing, however, and they not appear essential to the wound-healing process.
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3
Q

Hvað gerist ef neutrophila vantar í sáralokunarferlið?

A

Sárið lokast samt!

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4
Q

Hvenær birtast macrophagar í sáralokunarferlinu og hvað gera þeir?

A

Macrophages appear 24-48 hours after the injury has occurred. They are the most important cells in the early stage of wound healing and are essential to the wound healing process.

  • They phagocytose debris and bacteria, and also secrete collagenases and elastases, which break down injured tissue and release cytokines.
  • In addition, macrophages release PDGF, an important cytokine that stimulates the chemotaxis and proliferation of fibroblasts and smooth muscle cells.
  • Finally, macrophages secrete substances that attract endothelial cells to the wound and stimulate their proliferation to promote angiogenesis. Macrophage-derived growth factors play a pivotal role in new tissue formation.
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5
Q

Hvenær birtast T-lymphocytar í sáralokunarferlinu og hvað gera þeir?

A

T-lymphocytes migrate into the wound approximately 72 hours following injury. They are attracted to the wound by the cellular release of interleukin 1, which also contributes to the regulation of collagenase.

  • Lymphocytes secrete lymphokines such as heparin-binding epidermal growth factor and basic fibroblast growth factor.
  • They also play a role in cellular immunity and antibody production.
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6
Q

Hver eru 2 helstu einkenni aplastiskrar krísu í sickle-cell sjúkdómi?

A
  • Syndrome of severe anaemia with a lower reticulocyte count and bilirubin level than is usual for the patient
  • Usually due to parvovirus B19 infection (erythrovirus), which causes ‘slapped cheek’ syndrome in healthy individuals
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7
Q

Hvað gerist þegar einstaklingur með sickle cell fær parvovirus B19?

A

Parvovirus B19 interrupts erythropoiesis in sickle-cell patients, causing a precipitous drop in haemoglobin levels

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8
Q

Hvers konar galla í ónæmi veldur neutropenia? Sérstaklega hvaða 6 kríp?

A

Veldur auknu næmi fyrir bakteríu- og sveppasýkingum, sérstaklega:

  • Enterobacteriae spp
  • Streptococcus spp
  • Pseudomonas spp
  • Enterococcus spp
  • Candida spp
  • Aspergillus spp
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9
Q

Hvaða ónæmisgalli tengist gastric cancer?

A

Humoral immune deficiency getur valdið auknum líkum á gastric cancer!

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10
Q

Hvað er humoral immune deficiency?

A

These are deficiencies in B-cell, plasma cells or antibody

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11
Q

Fyrir hvaða 5 krípum verður einstaklingur með humoral immune deficiency veikari?

A
  • Streptococcal spp
  • Haemophilus influenzae
  • Pneumocystic jirovecii
  • Giardia
  • Cryptosporidium
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12
Q

Fyrir hvernig krípum verður einstaklingur með T-cell deficiency viðkvæmari? Fjögur dæmi.

A

Intracellular krípum!

  • herpes simplex virus
  • Mycobacterium
  • Listeria
  • intracellular fungal infections.
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13
Q

Fyrir hvernig krípum eru miltislausir viðkvæmari? 3 dæmi.

A

Increases the risk of infection from polysaccharide-encapsulated bacteria such as

  • Pneumococcus
  • Haemophilus influenzae
  • Meningococcus
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14
Q

Fyrir hvernig krípum eru þeir viðkvæmari sem vantar C3 komplement og hvers vegna?

A

C3 complement is important for opsonisation, therefore deficiency in C3 results in a susceptibility to infections caused by encapsulated bacteria.

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15
Q

Hvað er opsonization?

A

Opsonization is an immune process which uses opsonins to tag foreign pathogens for elimination by phagocytes.

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16
Q

Dæmi um 3 kríp sem einstaklingar án C3 komplement eru viðkvæmari fyrir:

A
  • Streptococcus pneumoniae
  • Streptococcus pyogenes
  • Haemophilus Influenzae
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17
Q

Hvar er Glucose-6-phosphate dehydrogenase (G6PD) algengast?

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency, which is common in Africa and the Mediterranean region.

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18
Q

Hvað er Glucose-6-phosphate dehydrogenase (G6PD) og hvernig erfist það?

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive inherited disorder characterised by a defect in the enzyme G6PD. This enzyme is important in red blood cell metabolism and the defect can result in haemolytic crises. It is the most common human enzyme defect

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19
Q

Haemolytic crises in patients with G6PD deficiency most commonly occur in response to:

A
  • Illness, most notably infection and DKA
  • Drugs including certain antibiotics, antimalarials, sulphonamides and aspirin
  • Foods, most notably fava beans
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20
Q

Dæmi um 4 sýklalyf sem eru triggerandi fyrir sjúklinga með G6PD skort og 2 sýklalyf sem eru örugg.

A

Several antibiotics are recognised to trigger haemolysis in patients with G6PD deficiency including nitrofurantoin, quinolones (such as ciprofloxacin), trimethoprim and chloramphenicol. The use of penicillins and cephalosporins is safe however, and does not trigger haemolysis.

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21
Q

Hvernig er greining polycythemia vera?

A

The diagnosis of PCV requires two major criteria and one minor criterion, or the first major criterion and two minor criteria:

Major criteria:

  • HB > 18.5 g/dl in men, 16.5 g/dl in women
  • Elevated red cell mass > 25% above mean normal predicted value
  • Presence of JAK2 mutation

Minor criteria:

  • Bone marrow biopsy showing hypercellularity with prominent erythroid, granulocytic and megakaryocytic proliferation
  • Serum erythropoietin level below normal range
  • Endogenous erythroid colony formation in vitro
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22
Q

Hverjar eru þrjár major criteria fyrir greiningu polycythemia vera?

A

Major criteria:

  • HB > 18.5 g/dl in men, 16.5 g/dl in women
  • Elevated red cell mass > 25% above mean normal predicted value
  • Presence of JAK2 mutation
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23
Q

Hverjar eru þrjár minor criteria fyrir greiningu polycythemia vera?

A
  • Bone marrow biopsy showing hypercellularity with prominent erythroid, granulocytic and megakaryocytic proliferation
  • Serum erythropoietin level below normal range
  • Endogenous erythroid colony formation in vitro
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24
Q

Hver eru meginmarkmið meðferðar við polycythemiu vera og hver er meðferðin?

A

The main aim of treatment is to normalize the full blood count and prevent complications such as thrombosis. Venesection is the treatment of choice but hydroxyurea can also be used to help control thrombocytosis.

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25
Q

Hvað er polycythemia vera og á hvaða aldri greinist hún helst?

A

Polycythaemia vera (PCV), which is also referred to as polycythaemia rubra vera, is a clonal haematological malignancy in which the bone marrow produces too many red blood cells. It may also result in the overproduction of white blood cells and platelets. It is most commonly seen in the elderly and the mean age at diagnosis is 65-74 years.

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26
Q

Hver eru helstu einkenni polycythemia vera?

A

Patients can be completely asymptomatic and it is often discovered as an incidental finding on a routine blood count. Approximately 1/3 of patients present with symptoms due to thrombosis, of these 3/4 have arterial thrombosis and 1/4 venous thrombosis. Features include stroke, myocardial infarction, deep vein thrombosis and pulmonary embolism.

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27
Q

10 einkenni polycythemia vera.

A
  • Einkenni tengt thrombosu, svo sem DVT, arteríal thrombar, stroke, MI, emb. pulm.
  • Plethoric appearance
  • Lethargy and tiredness
  • Splenomegaly (common)
  • Pruritis (in 40% – particularly after exposure to hot water)
  • Headaches, dizziness and sweating (in 30%)
  • Gouty arthritis (in 20%)
  • Budd-Chiari syndrome (in 5-10%)
  • Erythromyalgia (in <5% – burning pain and red/blue discolouration of hands and feet)
  • Increased incidence of peptic ulcer disease (possibly related to increased histamine release from mast cells)
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28
Q

6 dæmi um microcytiska anemiu (MCV undir 80)

A
  • Iron deficiency anaemia
  • Thalassaemia
  • Anaemia of chronic disease (can also be normocytic)
  • Sideroblastic anaemia (can also be normocytic)
  • Lead poisoning
  • Aluminium toxicity (affects some haemodialysis patients but now rare)
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29
Q

8 dæmi um normocytiska anemiu (MCV 80-100):

A
  • Haemolysis
  • Acute haemorrhage
  • Bone marrow failure
  • Anaemia of chronic disease (can also be microcytic)
  • Mixed iron and folate deficiency
  • Pregnancy
  • Chronic renal failure
  • Sickle-cell disease
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30
Q

9 dæmi um macrocytiska anemiu (MCV yfir 100):

A
  • B12 deficiency
  • Folate deficiency
  • Hypothyroidism
  • Reticulocytosis
  • Liver disease
  • Alcohol abuse
  • Myeloproliferative disease
  • Myelodysplastic disease
  • Drugs e.g. methotrexate, hydroxyurea, azathioprine
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31
Q

Hvaða immunoglobulin finnast í öllum vökvum líkamans?

A

IgG

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32
Q

Hvað eru immunoglobulin? Hvaða hlutverki gegna þau?

A

Öðru nafni antibodies.
They are glycoprotein molecules produced by plasma cells. They act as a critical part of the immune response by specifically recognizing and binding to particular antigens, such as bacteria or viruses and aiding in their destruction.

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33
Q

Hvaða 5 týpur eru til af immunoglobulinum?

A

A, G, D, M, E

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34
Q

Hvað gera IgA mótefni og hvar er þau helst að finna?

A
  • Protect body surfaces that are exposed to outside foreign substances.
  • Found in the nose, respiratory tract, digestive tract, eyes, ears and vagina. Also found in saliva, tears and blood.
  • 10-15% of all antibodies present in body.
  • A small number of people do not produce IgA.
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35
Q

Hvað gera IgD mótefni?

A

These are expressed in the plasma membranes of immature B-lymphocytes.
How they work is not clearly understood.
Constitute < 1% of all antibodies.

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36
Q

Hvað gera IgE mótefni? Hvar er þau helst að finna?

A

These antibodies cause the body to react to foreign substances, such as pollen, fungus, spores and animal dander.
They are found in the lungs, skin and mucous membranes.
Antibody levels are often high in patients with a history of allergy.
In normal, healthy individuals constitute only 0.05% of all antibodies.

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37
Q

Hvað gera IgG mótefni og hvar er þau að finna?

A

Very important in combating viral and bacterial infections.
The smallest but commonest antibody – 75%-80% of all antibodies found in the body.
They are found in all body fluids.
The only antibody type that can cross the placenta and help to protect the fetus.

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38
Q

Hvaða mótefni fer yfir fylgju?

A

IgG

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39
Q

Hvað gera IgM mótefni?

A

The first type of antibody made in response to an infection. They also cause other immune system cells to destroy foreign substances.
They are the largest antibody found in the body and constitute 5-10% of all antibodies.

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40
Q

Hvað eru margir fasar í sáralokunarferlinu?

A

Fjórir:

  1. Hemostasis
  2. Inflammatory phase
  3. Proliferative phase
  4. Maturation phase
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41
Q

Hvernig lýsir fyrsta stig sáralokunarferlisins sér?

A

Fyrsta stigið er hemostasis.
Hemostasis is the process of the wound being closed by clotting. It begins with the leakage of blood from the body. The first step of hemostasis is when blood vessels constrict to restrict the blood flow. Next, platelets stick together in order to seal the break in the wall of the blood vessel. Finally, coagulation occurs and reinforces the platelet plug with threads of fibrin, which are like a molecular binding agent.

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42
Q

Hversu hratt gerist hemostasis í sári?

A

The hemostasis stage of wound healing happens very quickly. The platelets adhere to the sub-endothelium surface within seconds of the rupture of a blood vessel’s epithelial wall. After that, the first fibrin strands begin to adhere in about sixty seconds. As the fibrin mesh begins, the blood is transformed from liquid to gel through pro-coagulants and the release of prothrombin. The formation of a thrombus or clot keeps the platelets and blood cells trapped in the wound area.

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43
Q

Hvað gerist í inflammatory phase í sáralokunarferlinu og hvaða tíma tekur það?

A

The inflammatory phase (up to 48 hours after injury) – Blood vessels dilate to allow antibodies, white blood cells, growth factors, enzymes and nutrients to reach the wounded area. The characteristic signs of inflammation are seen. The predominant cell types seen are neutrophils and macrophages, which serve to autolyse devitalized necrotic tissue.

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44
Q

Hvað gerist í proliferative phase í sáralokunarferli og hvaða tíma tekur það?

A

The proliferative phase (up to 3 weeks after injury) – New granulation tissue, comprised of collagen and extracellular matrix develops. Epithelialisation occurs during this phase. During epithelialisation epithelial cells develop at the wound margins and then divide and migrate towards the centre of the wound. Angiogenesis occurs with fibroblasts and capillaries growing into the necrotic areas. Healing wound mass is greatest after 3 weeks.

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45
Q

Hvað gerist í maturation phase í sáralokunarferlinu og hvaða tíma tekur það?

A

The maturation phase (up to 1 year after injury) – The final phase occurs when the wound has closed. This phase involves remodeling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regresses and decreases. Wound remodeling continues for up to 1 year.

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46
Q

Af hverju eru nýfædd börn náttúrulega með meira bilirubin en fullorðnir?

A

Bilirubin levels are higher in neonates than in adults because newborn babies have a higher concentration of red blood cells, which also have a shorter lifespan. It is usually a short-lived and harmless condition, but there are also some potentially serious causes that need to be assessed for.

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47
Q

Í hvaða tvo hópa skiptist neonatal gula?

A
  1. Unconjugated hyperbilirubinaemia (can be physiological or pathological)
  2. Conjugated hyperbilirubinaemia (always pathological)
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48
Q

Einkenni neonatal gulu (5)

A
  • Gula í augum (sést ef bilirubin fer yfir 35 micromól/L) og jafnvel búk (þarf að vera komið yfir 225 micromól/L til að sjást þar)
  • Poor feeding
  • Excessive sleepiness
  • Faltering growth
  • Features of the underlying cause
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49
Q

4 adverse atburðir sem geta gerst við blóðgjöf:

A

Immunological complications
Administration errors (‘wrong blood’ episodes)
Infections (bacterial, viral, possibly prion)
Immunodilution

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50
Q
A
  • Febrile transfusion reaction
  • Acute haemolytic reaction
  • Delayed haemolytic reaction
  • Allergic reaction
  • TRALI (Transfusion Related Acute Lung Injury)
  • TACO (Transfusion Associated Circulatory Overload)
  • GVHD (Graft-vs-Host Disease)
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51
Q

Einkenni og meðferð Febrile transfusion reaction við blóðgjöf:

A
  • Presents with 1 degree rise in temperature from baseline. Patient may also have chills and malaise.
    Most common reaction (1 in 8 transfusions).
    Usually caused by cytokines from leukocytes in transfused red cell or platelet components.
  • Supportive only. Paracetamol helpful.
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52
Q

Einkenni og meðferð Acute haemolytic reaction við blóðgjöf:

A
  • Fever, chills, pain at transfusion site, nausea, vomiting, dark urine.
    Feeling of ‘impending doom’ often reported early on.
    Most serious type of reaction. Often ABO incompatibility due to administration error.
  • STOP THE TRANSFUSION. Administer IV fluids. Diuretics may be required.
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53
Q

Einkenni Delayed haemolytic reaction við blóðgjöf:

A
  • Most commonly occurs 4-8 days after a blood transfusion.
    Patient presents with fever, anaemia, jaundice and haemoglobuinuria.
    Direct antiglobulin (Coombs) test positive.
    Due to low titre antibody too weak to detect in cross-match and unable to cause lysis at time of transfusion.
  • Most delayed haemolytic reactions have a benign course and require no treatment.
    Monitor anaemia and renal function and treat as required.
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54
Q

Einkenni og meðferð Allergic reaction við blóðgjöf:

A
  • Usually caused by foreign plasma proteins but may be due to anti-IgA.
    Allergic type reactions usually present with urticaria, pruritis, hives. May be associated with laryngeal oedema or bronchospasm.
    Anaphylaxis rare.
  • For allergic reactions treat symptomatically with antihistamines. There is no need to stop transfusion.
    If anaphylaxis occurs the transfusion should be stopped and the patient should be administered adrenaline and treated as per the ALS protocol.
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55
Q

Einkenni og meðferð TRALI (Transfusion Related Acute Lung Injury) við blóðgjöf:

A
  • Abrupt onset non-cardiogenic pulmonary oedema within 6 hours of transfusion.
    Associated with the presence of antibodies in the donor blood to recipient leukocyte antigens.
    This is the most common cause of death associated with transfusion reactions.
  • STOP THE TRANSFUSION. Oxygen should be administered. Approximately 75% of patients require aggressive respiratory support.
    Diuretic usage should be avoided
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56
Q

Einkenni og meðferð TACO (Transfusion Associated Circulatory Overload) við blóðgjöf:

A
  • Acute or worsening respiratory distress within 6 hours of transfusion of a large volume of blood. Evidence of pulmonary and peripheral oedema and fluid overload. Rapid increases in blood pressure common. BNP is usually elevated to at least 1.5 times pre-transfusion value. Most commonly occurs in the elderly and those with chronic anaemia.
  • Blood transfusion should be slowed so that the unit is given over 3-4 hours. Diuretics should be administered with the transfusion.
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57
Q

Einkenni og meðferð GVHD (Graft-vs-Host Disease) við blóðgjöf:

A
  • Rash, fever, diarrhoea, and liver dysfunction 1-4 weeks after transfusion.
    Viable T lymphocytes in blood components are transfused, engraft and react against the recipient’s tissues and the recipient is unable to reject the donor lymphocytes because of immunodeficiency, severe immunosuppression, or shared HLA antigens.
  • Treatment is supportive and there is no proven effective treatment for transfusion-associated GVHD.
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58
Q

Hver er munurinn á primary og secondary wound healing?

A
  • Primary: týpískt healing eftir skurðaðgerð t.d. - hreint sár sem við lokum og það byrjar strax að gróa
  • Delayed primary: oft notað í óhreinum sárum. Þá koma neutrophilar fyrst inn og hreinsa sárið í 2-3 daga og svo er því lokað.
  • Secondary primary: vefur hefur tapast úr sárinu, t.d. necrosa eða biti farið úr. Granulationsvefur kemur þá fyrst inn í sárið.
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59
Q

Lýsa 4 stigum sáralokunarferlisins.

A
  1. Haemostasis: platelets losa út growth factors sem hefja healing cascade.
  2. Inflammatory: Complement cascade er activerað. Neutrophils koma að eftir nokkrar klst og hreinsa bakteríur og necrosu. Monocytar koma svo og breytast í macrophaga á sólarhringum 2-3, leysa alls konar cytokin.
  3. Proliferative: fibroblastar koma 2-4 dögum eftir áverkann. Háræðar byrja að myndast og granulationsvefur.
  4. Remodeling: epithel vex yfir sárið. Þessi fasi getur verið í ár eða meira. Myofibroblastar draga sárið saman.
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60
Q

Hvers vegna skreppa sár saman eftir að þau eru gróin?

A

Út af því að myofibroblastar eru teygjanlegir og draga sárið saman.

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61
Q

Hvernig er beingróandi í mismunandi stigum?

A
  1. Reactive phase: dagar 1-7. Blæðing og hematóma myndast, platelets safnast fyrir. Akút bólga, fibroblastar migrera á staðinn og granulationsvefur myndast.
  2. Soft callus phase frá degi 4 út viku 3. Chondroblastar (búa til brjósk) og fibroblastar mígrera inn í granulationsvefinn sem var búinn til í fyrsta fasa. Þeir leggja þar niður hyaline cartilage og “woven bone”.
  3. Hard callus phase: mánuðir 1-3. Osteoblastar frá periosteum koma inn og leggja niður bæði woven og trabecular bone. Callusinn er sjáanlegur eftir ca 6 vikur.
  4. Remodelling phase: Ár+. Osteoclastar og osteoblastar remodela beinið hægt og rólega í sinni upprunalegu mynd. Trabecular beini er skipt út fyrir sterkara bein.
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62
Q

Hvernig gróa sinar?

A
  • Fibroblastar framleiða týpu 3 collagen á fyrstu vikunni.
  • Mikið magn af illa skipulögðu kollageni komið á 3 vikum.
  • Gradually svo remondelað í týpu I kollagen á allt að 18 mánuðum.
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63
Q

3 mismunandi týpur af skaða á taugar og hvernig það grær:

A
  • Neuropraxia: vægur skaði eftir þrýsting á taug.
  • Axonotmesis: axon degenerast en nærliggjandi vefur er heill. Tekur mánuð að vaxa 2cm.
  • Neurotmesis: neural integrity er lost og recovery limited.
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64
Q

Hvernig grær hjartavöðvinn?

A

Necrotiskur vöðvi er invaded af granulation vef og fibroblöstum og fáum svo ör.

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65
Q

Hvernig grær heilinn?

A

Þar eru engir fibroblastar.
Necrotiskt svæði er yfirleitt fjarlægt með gliosis og þar með tapast hluti heilans. Neuroplasticity getur komið með eitthvað af því til baka.
Fáum hins vegar ekki ör, það gæti haft mjög slæm áhrif á heilann.

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66
Q

7 atriði sem seinka wound closure:

A
  • Sýking
  • Ischemia
  • Bjúgur
  • Lélegt blóðflæði
  • Hypoxia
  • Næringarskortur
  • Meira trauma á sama svæði
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67
Q

3-faldur tilgangur inflammationar:

A
  • Deal with cause if possible (drepa t.d. veiru eða bakteríur)
  • Fjarlægja skemmdan vef
  • Hefja gróning
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68
Q

Hvaða fruma losar histamín í vefjaskaða?

A

Mast frumur

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69
Q

Hvaða fruma losar TNFalfa í vefjaskaða?

A

Macrophagar

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70
Q

Hvaða frumur losa nitric oxide og prostacyclin í vefjaskaða? Hvaða áhrif hafa þau?

A

Endothelial frumur innan á æðunum.
Hafa æðavíkkandi áhrif og æðarnar verða “lekar” til að polymorph frumur komist út í vefina (neutrophilar festast líka á viðtaka á endothelial frumunum og virkja sama ferli).

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71
Q

Monocytar geta orðið að… í sáraheilunarferli?

A

macophögum. Koma eftir nokkrar klst.

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72
Q

Í sáralokunarferli gefa neutrophilar og macrophagar frá sér hvaða cytokin?

A

IL6
IL1
TNF alfa

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73
Q

IL6, IL1 og TNF alfa hafa áhrif á m.a. hvaða 3 atriði í akút fasa sáralokunarferlis?

A
  • Adrenal/pituitary axis: ACTH og í kjölfarið glucocorticoids
  • Inducar PG: fáum febrile response frá hypothalamus
  • Aukin framleiðsla í lifur: fáum akút fasa prótín eins og CRP og serum amyloid
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74
Q

4 hlutverk complement kerfisins:

A
  • Lysis á bakteríum með MAC (bindast bakteríunum og merkja þær þannig)
  • Chemotactic fyrir leucocyta
  • Opsonisation
  • Inflammation
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75
Q

3 triggerar fyrir complement kerfið:

A
  • Classical pathway IgG eða IgG antigen complex
  • Alternate pathway C3b binds to pathogen surface
  • Lectin pathway
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76
Q

Hvað gerir kallikrein?

A

Breytir kininogen í bradykinin.

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77
Q

Hvenær losnar kallikrein?

A

Við vefjaskaða

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78
Q

Hvað er það sem eyðir kallikrein og hvað gerist ef maður er ekki með þann mekanisma?

A
  • C1 esterasa inhibitor eyðir því

- Ef maður er ekki með hann þá fær maður hereditary angioedema því kallikreinið safnast upp.

79
Q

Hvað gerir bradykinin?

A
  • Festist við B1 viðtaka: aktiverar sensory nerves fyrir sársauka og stimulerar mitogenesis
  • Festist við B2 viðtaka: vasodilation og eykur háræðaleka
80
Q

Hvernig er bradykinin brotið niður?

A

Með ACE í lungum og verður þá að óvirku kinin.

Ef við notum ACE inhibititora þá safnast bradykinin hins vegar upp og þess vegna fá margir hósta af ACE inhb.

81
Q

Hvar eru leukotrienes framleidd og úr hverju?

A

Framleidd í leukocytum frá arachidonic acid.

82
Q

Hvað gera leukotrienes? Í hvaða sjúkdómum eru þau offramleidd?

A

Hafa ýmis hlutverk í inflammation.
LTD4 er t.d. mikilvægt fyrir samdrátt sléttra vöðva.
Offramleitt í astma og alergiskum rhinitis.

83
Q

Hvar eru prostaglandin framleidd?

A

Af COX 1 og 2.

84
Q

Hvaða COX er það sem hefur slæm áhrif á hjartað að blokka?

A

COX 2.

85
Q

Hvar eru thromboxanes framleidd og hvað gera þau? Hvað lyf er það sem hindrar þau?

A
  • Framleidd af activated platelets.
  • Promotera platelet aggregation og samdrátt æða (í raun alveg andstæðan við prostacyclin)
  • Lyfið sem hindrar þau er aspirin
86
Q

Hvar eru prostacyclin framleidd og hvað gera þau?

A
  • Released í vascular endothelium

- Eru vasodilator og hindra platelet aggregation (í raun alveg öfugt við thromboxanes)

87
Q

Hypersensitivity týpa I, lýsið:

A
  • Antigen reactar við IgE antibody á sensitised mast frumu
  • Hún sleppir histamínum og vasoactivum efnum
  • Getur orðið lokal eða systemic
88
Q

Hvenær sjáum við týpu I hypersensitivity?

A

Í anaphylaxa og atopiskum sjúkdómum, t.d. ofnæmi.

89
Q

Type II hypersensitivity, lýsið:

A
  • Cytotoxic og antibody mediated
  • Circulerandi antibody (IgM og IgG) bindast á eitthvað sem þau eiga ekki að bindast á.
  • Í kjölfarið virkjast komplement kerfið og phagocytosa verður og fruman (sem var blásaklaus) er drepin
90
Q

Hvenær sjáum við type II hypersensitivity?

A

T.d. í blóðgjöfum, transfusion reaction

Líka myasthenia gravis, RA, SLE og Goodpastures.

91
Q

Mótefni við hverju sjáum við í Myasthenia gravis?

A

Mótefni gegn Ach receptors

92
Q

Mótefni við hverju sjáum við í RA?

A

erum með rheumatoid factor

93
Q

Mótefni við hverju sjáum við í SLE?

A

Mótefni gegn antigeni í nucleus

94
Q

Mótefni við hverju sjáum við í Goodpastures?

A

Mótefni gegn GBM og alveolar háræðum.

95
Q

Lýsa Type III hypersensitivity:

A
  • Circulerandi antigen og antibody sameinast og falla út sem immune complexes
  • Þeir valda svo skaða á smáum æðum
96
Q

2 dæmi um Type III hypersensitivity:

A
  • Farmers lung

- Serum sickness

97
Q

Lýsa Type IV hypersensitivity:

A
  • Er cell mediated og tekur því 12 klst eða meira að koma fram.
  • Antigen stimulerar næmda T-lymphocyta sem veldur losun lymphokines og bólgumiðla.
  • Ekkert antibody.
98
Q

3 dæmi um type IV hypersensitivity:

A
  • late graft rejection
  • contact dermatitis
  • tuberculin skin reaction
99
Q

4 týpur af mismunandi sjokki og dæmi um hvert og eitt:

A
  • Cardiogenic: pump failure
  • Hypovolaemic: blæðing
  • Distributive: sepsis, anaphylaxi
  • Obstructive: PE, cardiac tamponade
100
Q

3 progresserandi stig af sjokki:

A
  • Compensated: erum byrjuð að sjá laktat og catecholamin en einstaklingurinn viðheldur homeostasis
  • Decompensated: homeostasis út um gluggann
  • Irreversible (eða refractory): myocardial skaði, intravascular coagulation og lekar æðar
101
Q

Eðlilegt magn basophila í blóði

A

The reference range for basophils is up to 0.01 x 109/L, comprising 0-1% of white blood cells. Basophilia is a basophil count higher than this range.

102
Q

9 ástæður basophiliu:

A
  • Viral infections e.g. chickenpox, influenza
  • Urticaria
  • Hypothyroidism
  • Post-splenectomy
  • Haemolysis
  • Polycythaemia rubra vera
  • Chronic myeloid leukaemia
  • Ulcerative colitis
  • Systemic mastocytosis
103
Q

Eðlilegt magn eosinophila í blóði:

A

The reference range for eosinophils is to 0.02-0.5 x 109/L, comprising 1-6% of white blood cells. Eosinophilia is an eosinophil count higher than this range.

104
Q

8 ástæður fyrir eosinophiliu:

A
  • Allergic conditions e.g. asthma, hayfever, eczema (commonest cause in the U.K.)
  • Parasitic infections e.g. helminth infections (commonest cause worldwide)
  • Drug hypersensitivity e.g. anticonvulsants, allopurinol, sulfonamides
  • Connective tissue diseases e.g. Churg-Strauss syndrome, rheumatoid arthritis, polyarteritis nodosa
  • Haematological malignancy e.g. Hodgkin and non-Hodgkin lymphoma, chronic myeloid leukaemia
  • Other malignancies e.g. gastric cancer, lung cancer
  • Endocrine disorders e.g. Addison disease
  • Post-splenectomy
105
Q

Hvað eru teardrop cells og í hvaða 3 sjúkdómum sjáum við þær:

A

Teardrop cells are also known as dacrocytes and have a characteristic teardrop like shape. When a large number of these cells are present it is referred to as dacrocytosis.

Dacrocytes are seen in the following conditions:

  • Myelofibrosis
  • Beta thalassaemia major
  • Myelophthisic anaemia (casued by myelofibrosis)
106
Q

Hvert er algengasta form hemophiliu og hvaða clotting factor er það sem klikkar?

A

Haemophilia A is a bleeding disorder caused by a deficiency of clotting factor VIII. It is the commonest of form of haemophilia.

107
Q

Hvernig erfist hemophilia A?

A

The vast majority of cases are inherited in an X-linked recessive fashion, affecting males born to carrier mothers. Females born to affected fathers can also, rarely, be affected due to homozygosity for the gene, where there is marriage to close relatives.

108
Q

Hver er munurinn á orsök gout og pseudogout?

A

Gout and pseudogout are both characterised by crystal deposition in the affected joints. Gout is caused by the deposition of urate crystals, whilst pseudogout is caused by the deposition of calcium pyrophosphate crystals.

109
Q

Hvar er líklegast að finna gout vs pseudogout?

A

Gout can affect almost any joint but most commonly presents (around 50% of cases) with an affected hallux metatarsophalangeal joint. Pseudogout predominantly affects the large joints e.g. the knee.

110
Q

Munurinn á kristöllunum í gout vs pseudogout

A

Gout: urate crystals sem eru negatively birefringent needle-shaped crystals.

Pseudogout: calcium pyrophosphate crystals sem eru positively birefringent brick-shaped crystals.

111
Q

Einkenni G6PD deficiency:

A

Most individuals with G6PD deficiency are asymptomatic. Symptomatic patients are almost exclusively male but females can occasionally be affected due to unfavourable lyonisation.

Í köstum fær fólk hemolytiska krísu.

112
Q

Hvaða sýklalyf eru þekkt fyrir að triggera hemolytiska krisu í G6PD deficiency og hver eru safe?

A

Several antibiotics are recognised to trigger haemolysis in patients with G6PD deficiency including nitrofurantoin, quinolones (such as ciprofloxacin), trimethoprim and chloramphenicol. The use of penicillins and cephalosporins is safe however, and does not trigger haemolysis.

113
Q

Hvað er G6PD deficiency, hvernig erfist það og 3 atriði sem geta triggerað hemolytiskar krísur hjá þessum einstaklingum:

A

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive inherited disorder characterised by a defect in the enzyme G6PD. This enzyme is important in red blood cell metabolism and the defect can result in haemolytic crises. It is the most common human enzyme defect.

Haemolytic crises in patients with G6PD deficiency most commonly occur in response to:

  • Illness, most notably infection and DKA
  • Drugs including certain antibiotics, antimalarials, sulphonamides and aspirin
  • Foods, most notably fava beans
114
Q

The complement system og Interleukin-1 eru dæmi um…

A

…humoral barriers sem eru hluti af meðfæddu ónæmiskerfi.

115
Q

Dæmi um 4 frumur sem eru hluti af meðfæddu ónæmiskerfi og 1 fruma sem er sérhæfð.

A 
Neutrophils
Macrophages
Dendritic cells
Natural killer cells
... eru allar partur af meðfædda systeminu.

T-lymphocytar eru hins vegar í sérhæfðu deildinni.

116
Q

Hvenær sjáum við caseating necrosis í heilanum?

A

Caseating necrosis often occurs in TB (mycobacterium tuberculosis) injections and results in a cheese like substance within a necrotic core of granuloma.

117
Q

Hvað er liquefactive degeneration, hvenær gerist það?

A

Following major injury such as stroke, the brain undergoes a process of liquefactive degeneration, which leaves cystic spaces within the brain.

118
Q

3 frumur sem taka þátt í liquefactive degeneration í heilanum (t.d. eftir stroke) og hvað þær gera:

A
  • Neurones undergo central chromatolysis, in which the cell body becomes pale centrally and the nucleus moves peripherally and is accompanied with increased protein synthesis. Following neuronal injury, the axon undergoes anterograde degeneration starting at the cell body and progressing distally, with the axon becoming fragmented and degenerating.
  • Astrocytes undergo hypertrophy and hyperplasia in a process termed reactive gliosis, leaving behind a firm translucent barrier around sites of damage.
  • Microglia act as phagocytes, ingesting the cellular breakdown products alongside recruited blood monocytes.
119
Q

4 frumur sem histamín er losað frá:

A

Mast cells
Basophils
Eosinophils
Platelets

120
Q

Tvennt sem histamín gerir:

A

Vasodilatation

Increase vascular permeability

121
Q

3 staðir sem nitric oxide er losað frá:

A

Endothelium
Macrophage
Free radicals

122
Q

2 hlutverk nitric oxide:

A

Toxic to bacteria

Major factor in endotoxic shock

123
Q

4 staðir/frumur sem prostaglandín eru losuð frá:

A

Platelets
Endothelium
Monocytes
Macrophages

124
Q

3 hlutverk prostaglandína:

A 
Increase vascular permeability
Platelet aggregation (pA2)
Platelet disaggregation (pI2)
125
Q

4 staðir sem leukotrienes eru mynduð á og úr hverju:

A 
Synthesised from arachidonic acid in:
Neutrophils
Mast cells
Basophils
Macrophages
126
Q

4 hlutverk leukotrienes:

A

Increase vascular permeability
Sustain inflammatory actions in allergic reactions
Chemotactic effect on migrating neutrophils
Bronchoconstriction

127
Q

5 dæmi um frumur sem cytokin eru losuð frá:

A 
Many cells including:
Mast cells
Monocytes
Macrophages
Dendritic cells
T-cells
128
Q

Hlutverk cytokina:

A

Attract neutrophils to site of inflammation

129
Q

Hvar eru lysosomal compounds losuð? Hvað örvar losunina?

A

Neutrophils (release stimulated by bacteria and damaged tissue)

130
Q

2 hlutverk lysosomal compounds:

A

Increase vascular permeability

Activate complement

131
Q

Hvaða immunoglobulin kemst yfir placentu?

A

IgG

132
Q

Hver er algengasta arfgenga storkutruflunin í heimi? Hvaða faktor kemur við sögu og hver eru áhrifin á APTT, PT tíma og flögufjölda?

A

Von Willebrand disease (vWD) is the most common hereditary coagulation disorder occurring in approximately 1 in 100 of the population. It arises from a deficiency in Von Willebrand factor (vWF). This causes a reduction in factor VIII levels as vWF binds to factor VIII to protect it from rapid breakdown within the blood. vWF is also required for platelet adhesion and a deficiency of it will also result in abnormal platelet function. It therefore prolongs both the APTT and the bleeding time. The platelet count and thrombin time are unaffected.

133
Q

Hver eru áhrif von Willebrandt sjúkdóms á APTT tíma, blæðingatíma, PT tíma og fjölda blóðflagna?

A

Prolongs both the APTT and the bleeding time. The platelet count and thrombin time are unaffected.

134
Q

Einkenni von Willebrandt sjúkdóms:

A

Many patients with vWD are asymptomatic and are diagnosed following a coincidental check of the clotting profile. If symptomatic the most common symptoms are easy bruising, epistaxis and menorrhagia. In severe cases more severe bleeding and haemarthroses can occur.

135
Q

Meðferð við von Willebrandt sjúkdómi:

A

Desmopressin can be used to treat bleeding in mild cases of von Willebrand disease. This works by raising the patient’s own levels of vWF by releasing vWF that is stored in the Weibel-Palade bodies in the endothelial cells. The Weibel-Palade bodies are the storage granules of endothelial cells that form the inner lining of the blood vessels and the heart. More severe cases are treated with replacement therapy using cryoprecipitate infusions or Factor VIII concentrate. Replacement therapy is advised for patients with severe von Willebrand’s disease that are having moderate or major surgical procedures performed.

136
Q

6 einkenni TRALI, transfusion related lung injury og hvenær það kemur fram:

A
  • Hypoxia
  • Breathlessness
  • Cough (can be non-productive)
  • Frothy sputum
  • Fever
  • Hypotension or hypertension
    Kemur fram innan við 6 klst eftir að blóðgjöf lýkur.
    Algengasta ástæða dauða eftir blóðgjöf - stoppa blóðið strax, gefa súrefni en forðast þvagræsilyf.
137
Q

Hvað er nýrnabilun?

A

Acute kidney injury (AKI) (previously known as acute renal failure) is a sudden loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.

138
Q

Skilgreining á 1. stigs nýrnabilun:

A
  • Creatinine rise of 26 micromol/L or more within 48 hours, or
  • Creatinine rise of 50-99% from baseline within 7 days (1.5-1.99 x baseline), or
  • Urine output <0.5 mL/kg/hour for more than 6 hours
139
Q

Skilgreining á 2. stigs nýrnabilun:

A
  • Creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 x baseline), or
  • Urine output <0.5 mL/kg/hour for more than 12 hours
140
Q

Skilgreining á 3. stigs nýrnabilun:

A
  • Creatinine rise of 200% or more from baseline within 7 days (3.0 or more x baseline), or
  • Creatinine rise to 354 micromol/L or more with acute rise of 26 micromol/L or more within 48 hors or 50% or more rise within 7 days, or
  • Urine output <0.3 mL/kg/hour for 24 hours or anuria for 12 hours
141
Q

Meðaltími fyrir grónin á fingurbroti:

A

Phalanges: 3 weeks

142
Q

Meðaltími sem það tekur metacarpus að gróa:

A

Metacarpals: 4-6 weeks

143
Q

Meðaltími sem það tekur distal radius brot að gróa:

A

Distal radius: 4-6 weeks

144
Q

Meðaltími sem það tekur humerusbrot að gróa:

A

Humerus: 6-8 weeks

145
Q

Meðaltími sem það tekur tibiu brot að gróa:

A

Tibia: 10 weeks

146
Q

Meðaltími sem það tekur brot í femur hálsi eða skafti að gróa:

A

Femoral neck: 12 weeks

Femoral shaft: 12 weeks

147
Q

7 helstu ástæður lokastigsnýrnabilunar í UK:

A
  • Diabetic nephropathy (20-30%)
  • Chronic glomerulonephritis (10-15%)
  • Unknown aetiology (10-15%)
  • Chronic reflux nephropathy (10-15%)
  • Renovascular disease (5-10%)
  • Polycystic kidney disease (5-10%)
  • Hypertension (5-10%)
148
Q

Hvar eru Langerhan´s frumur?

A

Langerhan’s cells are antigen presenting monocytic cells found in the skin.

149
Q

4 týpur af frumum sem finnast í granuloma:

A

A typical granuloma contains giant multinucleated cells (Langhan’s cells - ath. EKKI langerhans!) surrounded by epithelioid cell aggregates (activated macrophages), T lymphocytes and fibroblasts.

150
Q

Skilgreining á akút nýrnaskaða:

A
  • A rise in serum creatinine of 26 μmol/L or greater within 48 hours.
  • 50% or greater increase in serum creatinine (1.5 fold from baseline) within the preceding seven days.
  • A fall in urine output to less than 0.5 mL/kg/hour for more than six hours.
151
Q

Hvað er algengasta birtingarmynd sickle cell sjúkdóms hjá börnum og oft fyrsta merki sjúkdómsins?

A

Sickle dactylitis is most commonly seen in children and is often the earliest manifestation of the condition.

152
Q

5 einkenni sickle dactylitis (sem er oft fyrsta birtingarmynd sickle cell sjúkdóms):

A
  • Infarction of small bones of hands and/or feet, which contain active red marrow in childhood
  • Can be the earliest manifestation of sickle-cell disease
  • Most commonly seen in childhood
  • Presents with local pain and swelling
  • Can cause long-term deformity
153
Q

Hver er ástæða hereditary angioedema?

A

C1-inhibitor deficiency (not C3 deficiency!) is the cause of hereditary angioedema.

154
Q

Fyrir utan það að einstaklingurinn verði viðkvæmari fyrir S. pyogenes, S. pneumoniae og Haemophilus influenzae, þá er C3 skortur einnig tengdur…

A

…C3 deficiency is also associated with an increased risk of systemic lupus erythematosus and membranous glomerulonephritis.

155
Q

Normal fjöldi blóðflaga:

A

The normal reference range for the platelet count is 150-450 x 109/L.

156
Q

Hvers vegna fá einstaklingar með von Willebrand sjúkdóm thrombocytopeniu?

A

In von Willebrand disease platelet production is unaffected. It arises from a deficiency in von Willebrand factor (vWF). This causes a reduction in factor VIII levels as vWF binds to factor VIII to protect it from rapid breakdown within the blood. vWF is also required for platelet adhesion and a deficiency of it will also result in abnormal platelet function.

157
Q

5 dæmi um meðfæddar platelet framleiðslutruflanir:

A
  • Wiskott-Aldrich syndrome
  • Bernard-Soulier syndrome
  • May-Heggin anomaly
  • Fanconi’s anaemia
  • Megakaryocytic hypoplasia
158
Q

7 dæmi um Decreased platelet production

(Bone marrow disorders):

A
  • Viral infections e.g. HSV, CMV, EBV, HIV
  • Aplastic anaemia
  • Malignancy e.g. leukaemia, lymphoma
  • Myelofibrosis
  • Drug induced e.g. chemotherapy, alcohol
  • Paroxysmal nocturnal haemoglobinuria
  • Megaloblastic anaemia
159
Q

9 dæmi um sjúkdóma þar sem er decreased platelet survival:

A
  • Idiopathic thrombocytopaenic purpura (ITP)
  • Thrombotic thrombocytopaenic purpura (TTP)
  • Connective tissue disease e.g. SLE, RA
  • Anti-phospholipid syndrome
  • Post-transfusion thrombocytopaenic purpura (PTTP)
  • Drug induced e.g. heparin, carbemazepine
  • Pregnancy – HELLP syndrome
  • Splenomegaly and hypersplenism
  • Disseminated intravascular coagulation
160
Q

4 dæmi um erfðasjúkdóma þar sem blóðflöguvirkni er trufluð:

A

Glanzmann’s thrombasthenia (GT)
Von Willebrand disease
Chediak-Higashi syndrome
Receptor defects e.g. TXA2 receptor defect

161
Q

4 dæmi um acquired platelet disorders:

A
  • Drug induced e.g. NSAIDs, Aspirin, clopidogrel
  • Chronic kidney disease
  • Myeloproliferative disorders
  • Paraproteins (especially multiple myeloma and Waldenstrom’s macroglobulinaemia)
162
Q

Hvaða immunoglobulin er algengast í serum?

A

IgG is the commonest type of immunoglobulin class for in the serum, representing approximately 75% of the immunoglobulin concentration.

163
Q

Hvaða 4 ávextir eru með krossofnæmi við latexofnæmi:

A

Banana
Avocado
Chestnut
Kiwi fruit

(fleiri sem eru moderate risk en sítrusávextir og perur eru í lagi)

164
Q

Hver er genotýpa sickle cell anemiu?

A

Sickle-cell anaemia has the genotype HbSS.

In heterozygous people with one normal haemoglobin gene and one sickle gene the genotype is HbAS, this is referred to as sickle-cell trait.

165
Q

Hver er líftími rauðra blóðkorna hjá heilbrigðum vs. þeim sem eru með sickle cell sjúkdóm?

A

Sickle shaped red blood cells have a shorter life span (10-20 days) than normal red blood cells (90-120 days).

166
Q

Hvernig erfist sickle cell?

A

Sickle-cell anaemia shows autosomal recessive inheritance.

167
Q

Hvaða stökkbreyting veldur sickle cell anemiu?

A

Sickle-cell anaemia is caused by a point mutation in the beta-globin chain of haemoglobin, causing glutamic acid to be replaced by valine at the sixth position.

168
Q

Hvers vegna eru einstaklingar með sickle cell líklegri en aðrir til að fá gallsteina?

A

Cholelithiasis is a recognized complication of sickle-cell disease. It results from excessive bilirubin production secondary to haemolysis of red blood cells.

169
Q

Hvað eru anti-nuclear antibodies?

A

Anti-nuclear antibodies (ANAs) are autoantibodies that bind to contents of the cell nucleus. They are also referred to as anti-nuclear factors (ANFs). Geta verið af hvaða immunoglobulin flokki sem er.

170
Q

Hvernig eru ANA mótefni greind?

A

Indirect immunofluoresence is the routine method for detecting ANA. It is highly sensitive and the fluorescence pattern can give some indication of the disease type present. ELISA testing is a cheaper alternative but is less reliable.

171
Q

Hvernig ANA staining patterns eru suggestive fyrir lupus, mixed connective tissue disease, scleroderma og CREST sx? (allt mismunandi staining)

A

A number of different staining patterns are seen and each is suggestive of different disorders, although none are specific enough to be diagnostic.

  • Homogenous staining is suggestive of lupus
  • speckled staining is suggestive of mixed connective tissue disease
  • nucleolar staining is suggestive of scleroderma
  • centromere staining is suggestive of CREST syndrome.
172
Q

Hvað eru margir SLE sjúklingar með anti-dsDNA antibodies?

A

Anti-double stranded DNA (Anti-dsDNA) antibodies are highly associated with systemic lupus erythematosus (SLE) and are present in 80-90% of patients with SLE.

173
Q

Hvað er Felty´s sx og hvaða gigtarsjúkdómi og mótefni tengist það?

A

Felty’s syndrome is characterized by the combination of rheumatoid arthritis (RA), splenomegaly and neutropenia.

It is more likely to be present in long-term sufferers of RA but only affects less than 1% of patients with it. The presence of ANAs in rheumatoid arthritis is highly suggestive of Felty’s syndrome.

174
Q

Hvað köllum við súbtýpur ANA mótefna og dæmi um 6 þeirra:

A

There are many subtypes of ANAs that bind to different proteins or protein complexes within the nucleus. These are referred to as extractable nuclear antigens (ENAs). These all have different and distinct disease associations and include:

  • Anti-Ro antibodies
  • Anti-La antibodies
  • Anti-Sm antibodies
  • Anti-Scl-70 antibodies
  • Anti-centromere antibodies
  • Anti-histone antibodies
175
Q

Hvaða 2 sjúkdómum tengjast Anti-Ro antibodies?

A

Sjögren’s syndrome

Congenital heart block

176
Q

Hvaða sjúkdómi tengist Anti-La antibodies?

A

Sjögrens

177
Q

Hvaða sjúkdómi tengist Anti-Sm antibodies?

A

Systemic lupus erythematosus

conferring high-risk of renal disease

178
Q

Hvaða sjúkdómi tengist Anti-Scl-70 antibodies

A

Progressive systemic sclerosis

179
Q

Hvaða sjúkdómi tengist Anti-centromere antibodies?

A

CREST syndrome

180
Q

Hvaða sjúkdómi tengist Anti-histone antibodies?

A

Drug induced lupus

181
Q

Hvað er transudate og hvers vegna myndast það?

A

A transudate is a fluid emanating from the intravascular compartment due to an imbalance of between oncotic and hydrostatic pressures across the walls of the microcirculation.

182
Q

6 mismunandi flokkar ástæðna fyrir transudate:

A
  • Cardiac: congestive cardiac failure
  • Renal: nephrotic syndrome
  • Hepatic: cirrhosis, ascites
  • Ovarian: Meig’s syndrome
  • Endocrine: myxoedema
  • Autoimmune: sarcoidosis
183
Q

Hvað er exudat og hvernig myndast það?

A

An exudate is an inflammatory fluid emanating from the intravascular space due to changes in the permeability of the microcirculation.

184
Q

6 ástæðnaflokkar fyrir exudat:

A
  • Infection: pneumonia, empyema
  • Malignancy: lung, breast, pleural
  • Autoimmune: SLE, rheumatoid arthritis
  • Cardiac: pericarditis
  • Abdominal: subphrenic abscess
  • Respiratory: chylothorax
185
Q

Hvaða hvítblæði er algengast að hrjái börn?

A

Acute lymphoblastic leukaemia (ALL) predominantly affects children and is the most common cancer of childhood. The peak age of incidence is between 2 and 4 years of age, and ALL is rare in adulthood.

186
Q

2 algengustu sýkingarvaldarnir í heilahimnubólgu hjá neonates?

A

Group B Streptococcus

Escherichia coli

187
Q

4 algengustu sýkingarvaldarnir í heilahimnubólgu hjá börnum?

A

Escherichia coli
Listeria monocytogenes
Haemophilus influenza type B
Streptococcus pneumoniae

188
Q

2 algengustu sýkingarvaldarnir í heilahimnubólgu hjá unglingum:

A

Neisseria meningitidis

Streptococcus pneumoniae

189
Q

4 algengustu sýkingarvaldarnir í heilahimnubólgu hjá fullorðnum:

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenza type B
Listeria monocytogenes

190
Q

Algengasti sýkingarvaldur í heilahimnubólgu hjá ónæmisbældum:

A

Listeria monocytogenes

191
Q

Hver er nýja skilgreiningin á sepsis?

A

In February 2016 the Society of Critical Care Medicine published a JAMA article reformatting the definitions of sepsis in an attempt to overcome the shortcomings of the old definitions.

The main changes are a new definition of sepsis, the replacement of the SIRS criteria with the quick Sepsis-related Organ Failure Assessment (qSOFA), and the complete removal of “severe sepsis” as an entity.

The new definition of sepsis is that it is “life-threatening organ dysfunction caused by a dysregulated host response to infection.”

192
Q

Hver er skilgreiningin á septic shock?

A

Septic shock is “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to increase mortality.”

In essence this means that septic shock is sepsis plus the following, despite adequate fluid resuscitation:
Vasopressors required to maintain a MAP > 65 mmHg
Serum lactate > 2 mmol/l

193
Q

Hvað er qSOFA og hvaða klínísku þýðingu hefur þaðÐ

A

The qSOFA score is a bedside prompt designed to identify patients with suspected infection who are at greater risk for a poor outcome outside of the intensive care unit. It uses the following three criteria:

  • Hypotension (SBP < 100 mmHg)
  • Tachypnoea (RR > 22)
  • Altered mental status (GCS < 15)

The presence of 2 or more of the qSOFA criteria near the onset of infection is associated with greater risk of death or a prolonged intensive care unit stay.

MRCEM Primary Exam (21 decks)

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