MedInterne Flashcards

Question 1

Q

DxD arthrite à l’urgence

Question 2

Q

Décrire les trouvailles radiologiques selon le type d’arthrite

Answer

A

Arthrite septique tardive:

Subchondral bone destruction

Periosteal new bone

Loss of joint space, joint space narrowing

Osteoporosis

Arthrite pseudogoutte:

Linear calcification in cartilage

Asymmetrical joint space narrowing

Osteophyte formation / Subchondral cyst formation

Lack of osteoporosis

Ostéoarthrite dégénérative

Asymmetrical joint space narrowing

Sclerosis of juxta-articular bone

Bone spurs and cysts—adjacent to severe cartilage degeneration

No osteoporosis

Arthrite tuberculeuse:

Soft tissue swelling

Marked demineralization / Bone rarefaction / late bone destruction

Little reactive sclerosis

Joint space preserved

Arthrite rhumatoide tardive

Symmetrical joint space narrowing

Osteoporosis of periarticular bone

Marginal erosions (no overhanging margins as in gout)

Little reactive bone formation

Question 3

Q

Discuter de l’analyse du liquide articulaire lors d’une arthrite

Question 4

Q

Nommer des maladies associées à la pseudogoutte

Answer

A

CPPD is strongly associated with aging and joint surgery, but hemochromatosis, hypothyroidism, hyperparathyroidism, amyloidosis, hypomagnesemia, Wilson’s disease, and inflammatory osteoarthritis have also been implicated

Question 5

Q

Nommer 6 causes d’arthrite virale

Answer

A

Hépatite B, C

VIH

Parvovirus B19

Alphavirus (ex chikungunya)

Rubéole

Question 6

Q

Nommer les critères de Jones

Answer

A

Pour dx RAA

2 majeurs ou 1 majeur + 2 mineurs

et présence infection passée à SGA

Majeurs: Polyarthralgie, chorée, cardite, nodules sous-cutanées, érythème marginé

Mineurs: Fièvre, arthralgie, élévation CRP/VS, prolongement PR

Question 7

Q

Nommer les principaux effets secondaires des médicaments utilisés dans la PAR

Question 8

Q

DxD de la tendinopathie

Answer

A

Tendon rupture

Ligamentous injury

Inflammatory arthritis (eg, rheumatoid)

Fractures (eg, avulsion)

Tumors

Tenosynovitis

Osteochondrosis (eg, Osgood-Schlatter disease)

Bursitis

Septic arthritis

Osteoarthritis

Foreign bodies

Osteomyelitis

Nerve entrapment syndromes

Tendon sheath infections (eg, pyogenic)

Question 9

Q

Critères dx du lupus

Answer

A

MDSOAPBRAIN

malaire

discoid

serosite

oral ulceres

arthrite

photosensibilité

blood

renal

anticorps

immuno

neurologique

Question 10

Q

Quelle est la principale cause de douleur abdominale en lupus?

Answer

A

Entérite lupique (vasculite mésentérique)

Au TDM: épaississement des parois, engorgement des vaisseaux mésentérique, atténuation graisse mésentérique

Tx: stéroides IV

Question 11

Q

Nommer 7 médicaments causant un lupus

Answer

A

Procainamide

Hydralazine, méthyldopa

Isoniazide

Quinidine

Minocycline

Chlorpromazine

Question 12

Q

Question 13

Q

Classer les différentes vasculites selon la taille des vaisseaux atteints et nommer les 4 patterns

Answer

A

4 patterns

Occlusion vasculaire : Artérite à cellules géantes, Takayasu
Syndrome poumons-reins: Wegener, Churg-Struss, Goodpasture, Polyangiite microscopique
Manifestations cutanées: Érythème noueux, Purpura Henoch Schonlein, polyartérite noueuse, Behcet
Associées à exposition environnementale ou antigène: LEvamisole, cryoglobulinémie, Buerger

Question 14

Q

Artérite à cellules géantes

Answer

A

Aussi appelée artérite temporale.

Surtout femmes et x 6 si tabac +

Atteinte visuelle par occlusion artère ciliaire postérieure et moins svt, artère rétinienne.

Cause anévrysmes de l’aorte thoracique

Atteinte des artères vertébrales + basilaire avec ss/sx insuffisance vertébro-basilaire

Critères dx

age > 50 a
VS > 50
Céphalée nouvelle localisée
Sensibilité a/n artère temporale ou diminution du pouls temporal
Biopsie anormale avec infiltration mononuclées ou inflammation granulomateuse

Question 15

Q

Takayasu

Answer

A

Sx: claudication - surtout MS, HTA - sténose a rénale, carotidynie, étourdissement, TA asymétrique au MS, ischémie cérébrale, sx visuels.

Complications cardiaques: insuffisance aortique, myocardite, IC, ischémie

Dx: angioTDM

Tx: pred PO - suivi rhumato et chx vasculaire

Question 16

Q

Syndromes poumons-reins

Answer

A

Wegener

c- anca

Atteinte VRS - otite, sinusite, ulcérations muqueuses, épistaxis. Sténose sous-glottique fréquente

Autres: atteinte oculaire, myocardite, neuro, dermato…

Tx: cortico + MTX ou cyclophosphamide

Goodpasture

Anticorps anti GBM (qui cible collagène type 4)

Sx respiratoire +/- hémorragie pulmonaire et atteinte rénale type glomérulonéphrite

Tx: pred et cyclophosphamide, +/- échanges plasmatique en aigu

Polyangiite microscopique

Cause la + fréquente de poumons-reins

IR rapide ou progressive avec sx respi ad hémorragie alvéolaire

Tx: idem avec cortico et cyclophosphamide. Plasmaphérèse et IVIg pour cas réfractaires. Rémissions fréquentes

Churg-Strauss

Présence rhinite allergique/asthme et éosinophilie

Puis atteinte rénale et pulmonaire

Atteinte neuro fréquente

Tx: idem

Question 17

Q

Vasculites à atteinte cutanée

Answer

A

Érythème noueux

Conditions associées: infections respiratoires virales, strep, tuberculose, sarcoidose, MII, salmonelle/yersinia/chlamydia, coccidioidomycose, psitacose

Rx associés: phénytoine, sulfamidés, PNC, CO

Tx: tx support, AINS, +/- cortico/colchicine pour cas réfractaires

Purpura Henoch Schonlein

Attention au risque invagination iléo-iléale

Tx support- traitement agressif GMN

Polyartérite noueuse

Lésions cutanées, HTA et atteinte systémique = classique

Neuropathies périphériques fréquentes

Tx: cortico +/- immunosupresseur

Behcet

Triade: aphtes buccaux, génitaux et uvéites

Peau: erythema nodosum–like subcutaneous nodules, pyoderma gangrenosum, cutaneous thrombophlebitis, and pustular acne-like folliculitis.

Oeil: uvéite, iritis, névrite optique

Neuro: sx tronc cérébral, corticospinal, méningite aseptique, thrombose sinus veineux

Gastro: ulcères avec perforation

Arthrite: oligoarthrite

Question 18

Q

Cryoglobulinémie

Answer

A

Cryoglobuline: immunoglobulines qui précipitent au froid

Vasculite cryoglobulinémique: lorsque les cryoglobulines se lient aux antigènes et se déposent sur les parois vasculaires induisant une réaction inflammatoire causée par le complément

Type 1: associé au Waldenstrom et MM

types 2-3: majorité, 80%, associé à hépatite C/sjogren et LED

Triade: purpura, arthralgie et myalgies avec atteinte rénale et neurologique périphérique

Plasmaphérèse possible si life-threatening

Question 19

Q

Vasculites associés à antigène ou exposition exogène

Answer

A

Différencier Buerger, maladie sérique et vasculite d’hypersensibilité

Question 20

Q

Nommer les 4 types de réactions immunologiques

Answer

A

Type 1: libération de médiateurs par les mastocytes 2nd liaison de l’antigène aux IgE spécifiques. Anaphylactoide= libération directe des médiateurs par les mastocytes sans liaison par IgE. ex: anaphylaxie et rhinite allergique

Type 2: liaison anticorps - antigène induit cytotoxicité cellulaire avec activation du complément ex: réactions transfusionnelle

Type 3: dépôts de complexes immuns antigène-anticorps a/n parois vasculaires induisant une réaction inflammatoire ex: lupus et maladie sérique

Type 4: Lymphocytes sensibilités reconnaissent l’antigène et recrutent davantage de lymphocytes et début de la réaction inflammatoire ex: SSJ, TEN, dermatite de contact

Question 21

Q

Nommer les FR d’anaphylaxie et les FR de sévérité de la maladie

Answer

A

Risk Factors for Having Anaphylaxis

Pregnant women, infants, teenagers, elderly

Parenteral > oral

Higher social economic status

Summer and fall (the outdoor seasons)

History of atopy

Emotional stress

Acute infection

Physical exertion

History of mastocytosis

Risk Factors for Increased Anaphylaxis Severity and Mortality

Extremes of age

Very young (under-recognition)

Elderly

Comorbid conditions

Cardiovascular disease (heart failure, ischemic heart disease, hypertension)

Pulmonary disease (asthma, obstructive airway disease)

Others

Concurrent use of anti-hypertensive agents, specifically beta-blockers and angiotensin-converting enzyme (ACE) inhibitors

Concurrent use of cognition-impairing drugs (eg, alcohol, recreational drugs, sedatives, tranquilizers)

Recent anaphylaxis episode

Question 22

Q

Nommer 20 étiologies d’anaphylaxie et des cause IgE médiées et non IgE médiées

Answer

A

Immunologic Mechanisms (IgE-Dependent)

Foods: Egg, peanut, tree nut, milk, fruits, shellfish, soybean, sesame

Medications: Antibiotics, NSAIDs, chemotherapeutic agents, immunomodulators

Insect stings: Hymenoptera venoms, fire ant stings

Natural rubber latex

Hormones: Insulin, methylprednisolone, parathormone, estradiol, progesterone, corticotropin

Local anesthetics: Mostly ester family (procaine, tetracaine, benzocaine)

RCM

Occupational allergens: Enzymes, animal protein, plant protein

Aeroallergens: Pollen, dust, spores, per dander

Immunologic Mechanisms (IgE Independent)

RCM

NSAIDs

Dextrans

Biologic agents: Monoclonal antibodies, immunomodulators

Nonimmunologic Mechanisms (Direct Mast Cell Activations)

Physical factors: Exercise, cold, heat, sunlight

Ethanol

Medications: Some opioids

Question 23

Q

Nommer les 3 critères dx de l’anaphylaxie

Answer

A

Atteinte cutanée/muqueuse + 1/2 : sx respi ou HD
Apres exposition antigène, 2 ou plus de : cutanée/muqueuse, respi, GI, HD
Atteinte HD après exposition antigène connu

Question 24

Q

DxD flush syndrome (anaphylaxie)

Answer

A

Flushing associated with food

Alcohol

MSG

Sulfites

Scombroidosis

Carcinoid tumor

Peri-menopause

Thyrotoxicosis

Basophilic leukemia

Mastocytosis (systemic mastocytosis and urticaria pigmentosa)

Vasointestinal peptide tumors

Question 25

Q

Traitement de l’angioedème

Answer

A

Épi si associé à anaphylaxie

Tx support, concentrés de facteur C1 inhibitor, icatibant (inhibiteur récepteur bradykinin-2), FFP, inhibiteur Kallikrein (Ecallantide)

Question 26

Q

Nommer des causes de destruction massive de GR

Answer

A

Hémolyse intravasculaire 2nd réaction transfusionnelle

Hémolyse 2nd CIVD

Infection à malaria et clostridium

Anémie hémolytique auto-immune (ex quinidine)

Déficit en G6PD avec stress oxidatif

Brûlures massives

HPN

Toxines (araignées, serpent)

Hémolyse à hémaglutinine froides (mycoplasme pneumoniae, mono)

Question 27

Q

DxD anémie

Question 28

Q

Nommer les 3 types de thalassémie

Answer

A

Thalassémie beta hétérozygote et homozygote

Thalassémie alpha

Question 29

Q

Qu’est-ce que l’anémie sidéroblastique?

Answer

A

Déficit dans la synthèse de l’hème, plus précisément dans la synthèse des porphyrines

Corps d’inclusion de fer a/n GR

Forme idiopathique chez les PA le + fréquent.

Considéré forme préleucémique, avec transformation chez 5%

Intox au plomb est une cause fréquente réversible d’anémie sidéroblastique

Svt déficience concomittante en pyridoxine

Question 30

Q

Nommer 10 causes de déficit en folate

Answer

A

Inadequate dietary intake

Poor diet or overcooked or processed food diet

Alcoholism

Inadequate uptake

Malabsorption with sprue and other chronic upper intestinal tract disorders, drugs such as phenytoin and barbiturates, or blind loop syndrome

Inadequate use

Metabolic block caused by drugs, such as methotrexate or trimethoprim

Enzymatic deficiency, congenital or acquired

Increased requirement

Pregnancy

Increased red blood cell (RBC) turnover: Ineffective erythropoiesis, hemolytic anemia, chronic blood loss

Malignant disease: Lymphoproliferative disorders

Increased excretion or destruction or dialysis

Question 31

Q

Nommer 10 causes de déficit en B12

Answer

A

Inadequate dietary intake

Total vegetarianism: No eggs, milk, or cheese

Chronic alcoholism (rare)

Inadequate absorption

Absent, inadequate, or abnormal intrinsic factor, as seen in patients with pernicious gastrectomy and anemia; in anemia, autoimmune antibodies act against gastric parietal cells and intrinsic factor

Abnormal ileum, as can occur in sprue and inflammatory bowel disease

Inadequate use

Enzyme deficiency

Abnormal vitamin B12–binding protein

Increased requirement by increased body metabolism

Increased excretion or destruction

Question 32

Q

Différencier les types d’anémie mégaloblastiques

Question 33

Q

Nommer 8 médicaments responsable d’aplasie médullaire

Question 34

Q

DxD anémie hémolytique

Answer

A

Intrinsic

Enzyme defect

Pyruvate kinase deficiency

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Membrane abnormality

Spherocytosis

Elliptostomatocytosis

Paroxysmal nocturnal hemoglobinuria

Spur cell anemia

Hemoglobin abnormality

Hemoglobinopathies

Thalassemias (anemias)

Unstable hemoglobin

Hemoglobin M

Extrinsic

Immunologic

Alloantibodies

Autoantibodies

Mechanical

Microangiopathic hemolytic anemia

Cardiovascular, such as prosthetic heart valve disease

Environmental

Drugs

Toxins

Infections

Thermal

Abnormal sequestrations, as in hypersplenism

Question 35

Q

Nommer 4 médicaments induisant de l’hémolyse chez un pt avec déficit en G6PD

Answer

A

Analgesics and antipyretics: acetanilid, aspirin, phenacetin

Antimalarials: Primaquine, quinacrine, quinine

Nitrofurans

Sulfa drugs: Sulfamethoxazole, sulfacetamide, sulfones

Miscellaneous: Naphthalene, fava beans, methylene blue, phenylhydrazine, nalidixic acid

Question 36

Q

Nommer 10 maladiées associées à l’anémie hémolytique auto-immune

Answer

A

Neoplasms

Malignant: Chronic lymphocytic leukemia, lymphoma, myeloma, thymoma, chronic myeloid leukemia

Benign: Ovarian teratoma, dermoid cyst

Collagen Vascular Disease

Systemic lupus erythematosus

Periarteritis nodosa

Rheumatoid arthritis

Infections

Mycoplasma

Syphilis

Malaria

Bartonella

Virus: Mononucleosis, hepatitis, influenza, coxsackievirus, cytomegalovirus

Miscellaneous

Thyroid disorders, ulcerative colitis

Drug immune reactions

Question 37

Q

Nommer 4 médicaments causant une anémie hémolytique auto-immune et son mécanisme associé

Answer

A

Hapten type with antibodies to the drug

Complement-fixing antibody: Quinidine, quinine, phenacetin, ethacrynic acid, p-aminosalicylate, sulfa drugs, oral hypoglycemic agents

Non–complement-fixing antibody: Penicillin dosages >20 million units/day

Autoimmune type with antibodies to the red blood cell (RBC) membrane: D-methyldopa, L-dopa, mefenamic acid, chlordiazepoxide

Cephalosporins at dosages >4 g/day may cause hemolysis by direct membrane injury

Question 38

Q

Nommer 6 tests à faire lors de suspicion d’anémie hémolytique

Answer

A

Peripheral blood smear

Corrected reticulocyte index or reticulocyte production index

Haptoglobin levels

Plasma free and urinary hemoglobin

Lactate dehydrogenase level

Fractionated bilirubin level

Direct and indirect Coombs test

Red blood cell (RBC) membrane stability (osmotic fragility)

Frottis:

Hémolyse intravasculaire: shistocytes et helmet cells

Hémolyse 2nd défaut GR acquis Ex toxines = sphérocytes

Hyperslénisme: corps Howel-Jolly

Infections ex malaria = corps d’inclusion

Question 39

Q

Nommer 4 types d’hémoglobine

Answer

A

HbA (α2β2), HbA2 (α2δ2), and HbF (α2γ2)

HbS = anémie falciforme

et plusieurs combinaisons, avec sickle cell- b-thalassemie…

Question 40

Q

Tx anémie falciforme

Answer

A

2 principales manifestations: hémolyse et crises vaso-occlusives

Analgésie, hydratation

Tx stroke: rtpa idem, échanges plasmatiques

tx hydroxyurée

Viser HbS < 30%

Question 41

Q

Nommer 8 cause d’érythrocytose

Answer

A

Appropriately increased erythropoietin caused by tissue hypoxia

Congenital heart disease with a right-to-left shunt

Pulmonary disease (eg, bronchial-type chronic obstructive pulmonary disease)

Carboxyhemoglobinemia

High-altitude acclimatization

Decreased tissue oxygen release from hemoglobinopathies with high oxygen affinity

Inappropriate autonomous erythropoietin production

Renal origin: Carcinoma, hydronephrosis, cyst

Other lesions: Uterine fibroids, hepatoma of adrenal origin, cerebellar hemangioma

Congenital overproduction

Pure or essential erythrocytosis

Acquired immunodeficiency syndrome (AIDS) and zidovudine treatment

Question 42

Q

Décrire présentation et dx polycythémie vraie

Answer

A

Sx thromboses (IAM, EP, thrombose veineuse, AVC), saignement et ecchymoses

Critères

Category A

Increased RBC mass

In men: Hemoglobin >18.5 g/dL

In women: Hemoglobin >16.5 g/dL

Normal arterial oxygen saturation (>92%)

Splenomegaly

Category B

Thrombocytosis: Platelets >400,000/mm3

Leukocytosis: WBC count >12,000/mm3 (with no fever or infection)

Leukocyte alkaline phosphatase score >100

Vitamin B12 >900 pg/mL, unbound vitamin B12–binding capacity

Visons hématocrite inf 55% - phlébotomie et hydroxyurée, ASA

Question 43

Q

Nommer 4 causes de neutrophilie primaire

Answer

A

LMC, polycythémie vraie
neutrophilie héréditaire
neutrophilie idiopathique chronique
maladie myéloproliférative chronique

En cas d’hyperleucocytose sévère, leukaphérèse

Question 44

Q

3 types de leucémies adultes

Answer

A

Leucémie myéloide aigue - 60%

Leucémie lymphoide chronique - 30%

Leucémie myéloide chronique - 15% (sx constitutionnels, 20% asx, augmentation GB avec différentiel N, plt parfois augmentées, anémie associée)

Question 45

Q

Dxd leucopénie selon stade maturation GB

Question 46

Q

Expliquer le rôle des plaquettes dans l’hémostase

Answer

A

Adhesion to subendothelial connective tissue: Collagen, basement membrane, and noncollagenous microfibrils; serum factor VIII (von Willebrand’s factor [vWF]) permits this function; adhesion creates the initial bleeding arrest plug

Release of adenosine diphosphate, the primary mediator and amplifier of aggregation; release of thromboxane A, another aggregator and potent vasoconstrictor; release of calcium, serotonin, epinephrine, and trace thrombin

Platelet aggregation over the area of endothelial injury

Stabilization of the hemostatic plug by interaction with the coagulation system:

Platelet factor 3, a phospholipid that helps accelerate certain steps in the coagulation system

Platelet factor 4, a protein that neutralizes heparin

Pathway initiation and acceleration by thrombin production

Possible secretion of active forms of coagulation proteins

Stimulation of limiting reactions of platelet activity

Question 47

Q

Dessiner la cascade de la coagulation

Question 48

Q

Nommer les 3 groupes de facteurs de la coagulation

Answer

A

Thrombin-sensitive factors contributing to the metabolic response and local vasoconstriction: I, V, VIII, XIII

Vitamin K-sensitive factors: II, VII, IX, X

Sites of heparin activity: IIa, IXa, Xa (major site), XIa, platelet factor 3

Question 49

Q

Nommer 5 contrôles de la coagulation

Answer

A

Thrombin-sensitive factors contributing to the metabolic response and local vasoconstriction: I, V, VIII, XIII

Vitamin K-sensitive factors: II, VII, IX, X

Sites of heparin activity: IIa, IXa, Xa (major site), XIa, platelet factor 3

Question 50

Q

Nommer 3 médicaments associés au PTT

Answer

A

Quinine

Ticlopidine

Clopidogrel

Question 51

Q

3 grandes classes de thrombocytopathies et étiologies associées

Answer

A

Adhésion: déficit en VonWillebrand

Défaut de libération: plts normales mais libération aN de sérotonine, calcium, ADP …Ex ASA et inhibition cyclooxygenase et donc de la formation de thromboxane A2. Aussi urémie, dysprotéinémie

Agrégation: maladie récessive de thrombasthénie

Question 52

Q

DxD thrombocytopénie, thrombocytose et thrombocytopathie

Question 53

Q

Hémophilie A

Answer

A

Facteur 8 anormal (facteur 8 formé au foie)

Activité du facteur 8 = VIII:C activité

1-5% activité = sévère

5-10%= modéré

> 10% = léger

Traitement: facteur VIII, si non dispo - cryoprécipités, DDAVP 0.3mcg/kg

Cibles sgmt léger 25-40%, sgmt modéré 50%, sévère 80-100%

1 unités / kg augmente de 2% l’activité

1 unité = 1 mL de plasma d’un adulte normal

En urgence, assumer le niveau de facteur VIII à 0.

Because the half-life of factor VIII is 8 to 12 hours, the desired level is maintained by giving half the initial dose every 8 to 12 hours.

Cryoprecipitate is assumed to have 80 to 100 U of factor VIII:C per bag; factor VIII:C concentrates list the units per bottle on the label.

Possible développement AC inhibiteurs IgG , tx difficile, essai facteur VIIa,

Question 54

Q

VonWillebrand

Answer

A

Favorise l’Adhésion des plaquettes à l’endothélium vasculaire
Transporte le facteur VIII et permet de prolonger sa durée de vie

type 1 (75%) déficit quantitatif partiel vWF

type 2 déficit qualitatif vWF

type 3 déficit total en vWF

Tx: remplacement facteur VIII (idem à hémophilie A), DDAVP, dernier recours cryoprécipités, FFP

Question 55

Q

Hémophilie B

Answer

A

Déficit en facteur IX

Tx: concentrés de facteur IX, PCC, plasma frais

Concentrés de facteur IX

1 unité /kg = 1 % d’activité

Question 56

Q

Expliquer les changements de la coagulation lors CIVD

Question 57

Q

Nommer les doses de protamine

Answer

A

Héparine non fractionnée = 1 mg / 100 unités

HBPM: 1 mg / 1 mg HBPM

Question 58

Q

Compression néoplasie moelle osseuse

Néos les + fréquents

Tx

Answer

A

Néo: poumons, seins, prostate, rein, lymphome hodgkin, myélome multiple

Tx: chirurgie, decadron 10 IV puis 16 mg / jour

Radiothérapie

Question 59

Q

Nommer 4 étiologies d’épanchement péricardique néoplasique

Answer

A

Envahissement du péricarde par néo (poumons, seins, néo hématologiques, mélanome)

Épanchement 2nd obstruction lymphatique par ganglions lymphatiques obstrués

Hypoalbuminémie

Radiothérapie

Chimiothérapie

Question 60

Q

4 mécanismes d’hypercalcémie néoplasique

Answer

A

Production PTH-rp (néoplasies épidermoides poumons, oesophage, tête/cou, endomètre/col/ovaires)

Augmentation production calcitriol

Ostéolyse 2nd invasion osseuse

Production ectopique PTH

Question 61

Q

Question 62

Q

Tx hypercalcémie néoplasique

Answer

A

hydratation IV
biphosphonates (acide zolédronique ou pamidronique)
calcitonine si réfractaire
dialyse
denosumab
cortico si lymphome associé

Question 63

Q

Syndrome de lyse tumorale

Answer

A

FR: taille tumorale élevée, sensibilité à chimio élevée, réplication importante avec grossissement (LLA, burkitt), IRC, hypovolémie, hyperuricémie

sx:nausea, vomiting, lethargy, confusion, edema, seizure, myalgias, and tetany; dysrhythmias may result in cardiac arrest, changement ECG 2nd hypocalcémie et hyperkaliémie

Tx:

Hydratation IV

Hypocalcémie: tolérer sauf si arythmies ou confusion/convulsions

Tx standard hyperkaliémie

Dialyse PRN

Allopurinol ou rasburicase

Allopurinol : analogue de l’hypoxanthine et inhibite la xanthine oxidase, empêchant la production d’acide urique. Accumulation de xanthine et hypoxanthine (peut aussi induire IRA)

Rasburicase: analogue de l’enzyme urate oxidase et transforme l’acide urique en allantoine

Question 64

Q

Tx leucostase

Answer

A

hydratation IV

Éviter pRBC

Leukaphérèse

Hydroxyurée

Chimiothérapie

Answer 53

A

Acidose métabolique

1 PCO2 : 1,2 HCO3

Alcalose métabolique

1 PCO2 : 0,9 HCO3

Acidose respiratoire

HCO3 : 0,1 PCO2 / 0,35 PCO2

Alcalose respiratoire

HCO3 : 0,2 PCO2 / 0,5 PCO2

Answer 54

A

Hypoalbuminémie (anion gap corrigé = anion gap + 2.5 ( 4 - albumine sérique (g/dL)

Hypertriglycéridémie

Intoxication bromure

Intoxication lithium

Hypergammaglobulinémie

Myélome multiple

Answer 55

A

Hyperventilation caused by hypoxia

High altitude

Severe anemia

Ventilation-perfusion mismatch

Central hyperventilation

Voluntary or psychogenic

Cerebrovascular accident

Increased intracranial pressure (tumor, hemorrhage, trauma)

Toxic or pharmacologic

Salicylates

Caffeine, nicotine

Catecholamines

Thyroxine

Pulmonary

Pulmonary embolism

Pneumonia

Pulmonary edema

Asthma

Mechanical hyperventilation (iatrogenic)

Endocrine

Pregnancy

Hyperthyroidism

Septicemia

Hepatic encephalopathy

Hyponatremia

Answer 56

A

CAT MUDPILES

Answer 57

A

Winter’s equation (PaCO2 = [1.5 × serum HCO3] + [8 ± 2])

Answer 58

A

Spurious elevation: Hemolysis due to drawing or storing of the laboratory sample or post–blood sampling leak from markedly elevated white blood cells, red blood cells, or platelets

•

Renal failure: Acute or chronic

•

Acidosis: Diabetic ketoacidosis (DKA), Addison’s disease, adrenal insufficiency, type 4 renal tubular acidosis

•

Cell death: Rhabdomyolysis, tumor lysis syndrome, massive hemolysis or transfusion, crush injury, burn

•

Drugs: Beta-blockers, acute digitalis overdose, succinylcholine, angiotensin-converting enzyme inhibitors, angiotension receptor blockers, nonsteroidal anti-inflammatory drugs (NSAIDs), spironolactone, amiloride, potassium supplementation

Patients with severe hyperkalemia may present with neuromuscular findings, including muscle cramps, generalized weakness, paresthesias, tetany, and focal or global paralysis

Answer 59

A

Renal losses: Diuretic use, drugs, steroid use, metabolic acidosis, hyperaldosteronism, renal tubular acidosis, diabetic ketoacidosis (DKA), alcohol consumption

•

Increased nonrenal losses: Sweating, diarrhea, vomiting, laxative use

•

Decreased intake: Ethanol, malnutrition

•

Intracellular shift: Hyperventilation, metabolic alkalosis, drugs

•

Endocrine: Cushing’s disease, Bartter’s syndrome, insulin therapy

Answer 60

A

Hypernatremia with Dehydration and Low Total Body Sodium

Heatstroke

Increased insensible losses: Burns, sweating

Gastrointestinal loss: Diarrhea, protracted vomiting, continuous gastrointestinal suction

Osmotic diuresis: Glucose, mannitol, enteral feeding

Hypernatremia with Low Total Body Water and Normal Total Body Sodium

Diabetes insipidus

Neurogenic

Elderly with “reset” osmostat

Hypothalamic dysfunction

Suprasellar or infrasellar tumors

Renal disease

Drugs (amphotericin, phenytoin, lithium, aminoglycosides, methoxyflurane)

Sickle cell disease

Hypernatremia with Increased Total Body Sodium

Salt tablet ingestion

Salt water ingestion

Saline infusions

Saline enemas

IV sodium bicarbonate

Poorly diluted interval feedings

Primary hyperaldosteronism

Hemodialysis

Cushing’s syndrome

Conn’s syndrome

Answer 61

A

Central

Idiopathic

Familial disease

Cancer

Hypoxic encephalopathy

Infiltrative disorders

Post supraventricular tachycardia

Anorexia nervosa

Nephrogenic

Chronic renal insufficiency

Polycystic kidney disease

Lithium toxicitya

Hypercalcemia

Hypokalemia

Tubulointerstitial disease

Hereditary

Sickle cell disease

Answer 62

A

Pseudohyponatremia

Hyperlipidemia

Hyperproteinemia (multiple myeloma, macroglobulinemia)

Dilutional

Hyperglycemia*

Hypovolemic Hyponatremia: Decreased Total Body Water and Sodium, with a Relatively Greater Decrease in Sodium

Body fluid losses: Sweating, vomiting, diarrhea, gastrointestinal suction

Third spacing: Bowel obstruction, burns, pancreatitis, rhabdomyolysis

Renal causes: Diuretics, mineralocorticoid deficiency, osmotic diuresis, renal tubular acidosis, salt-wasting nephropathies

Hypervolemic Hyponatremia: Increased Total Body Sodium with a Relatively Greater Increase in Total Body Water

Heart failure

Chronic renal failure

Hepatic failure or cirrhosis

Euvolemic Hyponatremia: Increased Total Body Water with Nearly Normal Total Body Sodium

SIADH

Drugs causing SIADH (diuretics, barbiturates, carbamazepine, chlorpropamide, clofibrate, opioids, tolbutamide, vincristine)

Psychogenic polydipsia

Beer potomania

Hypothyroidism

Adrenal insufficiency

MDMA (ecstasy)

Accidental or intentional water intoxication

Answer 63

A

Lung Masses

Cancer (especially small cell)

Pneumonia

Tuberculosis

Abscess

Central Nervous System Disorders

Infection (meningitis, brain abscess)

Mass (subdural, postoperative, cerebrovascular accident)

Psychosis (with psychogenic polydipsia)

Drugs

Thiazide diuretics

Narcotics

Oral hypoglycemic agents

Barbiturates

Antineoplastics

Answer 64

A

Malignant Disease

Ectopic secretions of parathyroid hormone, multiple myeloma, cancer metastatic to bone

Most common: Breast, lung, hematologic, kidney, prostate

Endocrine

Hyperparathyroidism, multiple endocrine neoplasias, hyperthyroidism, pheochromocytoma, adrenal insufficiency

Granulomatous Disease

Sarcoidosis, tuberculosis, histoplasmosis, berylliosis, coccidioidomycosis

Pharmacologic Agents

Vitamins A and D, thiazide diuretics, estrogens, milk-alkali syndrome

Miscellaneous

Dehydration, prolonged immobilization, iatrogenic, rhabdomyolysis, familial, laboratory error

Answer 65

A

Pour chaque diminution d’albumine de 10, augmenter la calcémie de 0.2

Answer 66

A

Hypoalbuminemia

Hypoparathyroidism: inherited, postsurgical, autoimmune, infiltrative

Vitamin D deficiency and vitamin D resistance: Malabsorption syndrome, liver disease, malnutrition, sepsis, anticonvulsants, lack of sunlight exposure

Chronic renal failure

Hyperphosphatemia

Hypomagnesemia

Respiratory alkalosis

Severe pancreatitis

Drugs: Bisphosphonates, phenytoin, phosphate, calcitonin

Tumor lysis syndrome

Rhabdomyolysis

à l’urgence, le + fréquent:

Hyperventilation: Anxiety, sympathomimetics

Ethanol abuse, chronic malnutrition: Hypoalbuminemia

Massive blood transfusion: More than 10 units

Toxins: Hydrofluoric acid, ethylene glycol

Severe pancreatitis

Answer 67

A

Iatrogenic: IV administration, dialysate

•

Oral administration: Laxatives, antacids, vitamins, cathartics, dialysate, parental

•

Impaired elimination—hypomotility: Bowel obstruction, chronic constipation

•

Impaired elimination—medications: Anticholinergics, narcotics, lithium therapy

•

Miscellaneous: Hypothyroidism, tumor lysis syndrome, adrenal insufficiency, milk-alkali syndrome

Answer 68

A

Decreased deep tendon reflexes 1.5 - 2 mmol/L

Hypotension 2-3 mmol/L

Respiratory insufficiency 4 mmol/L

Heart block 4-6 mmol/L

Cardiac arrest 6-10 mmol/L

Answer 69

A

Cesser apport exogène

Hydratation IV

Diurétiques

Dialyse

si instable - calcium IV - 5mL gluconate de calcium

Answer 70

A

Decreased Phosphate Excretion

Acute and chronic renal failure

Increased Renal Tubular Reabsorption

Hypoparathyroidism

Thyrotoxicosis

Excess vitamin D administration

Excessive Phosphate Intake

Phosphate enemas or laxatives

IV or oral phosphate administration

Shift of Phosphate from Intracellular to Extracellular Space

DKA

Tumor lysis

Rhabdomyolysis

Spurious Hyperphosphatemia

Paraproteinemia

Hyperbilirubinemia

Hemolysis

Hyperlipidemia

Answer 71

A

Decreased Intake or decreased Absorptive States

Chronic alcoholism

Home parenteral nutrition

AIDS

Chemotherapy

Vomiting

Malabsorption syndromes

Secretory diarrhea

Vitamin D deficiency

Hyperventilatory States

Sepsis

Alcohol withdrawal

Salicylate poisoning

Neuroleptic malignant syndrome

Panic attacks

DKA

Hepatic coma

Hormonal and Endocrine Effects

Insulin loading

Glucose loading

Exogenous epinephrine

Hyperparathyroidism

Medicationsa

Diuretics

Chronic antacid ingestion

Steroids

Phosphate binders

Xanthine derivatives

Beta2-agonists

Disease States

Trauma

Severe thermal burns

Acute renal failure

Gout

Answer 72

A

Central Nervous System

Irritability

Confusion

Paresthesias

Depression

Dysarthria

Seizure

Coma

Cardiovascular

Cardiomyopathy

Depressed myocardial contractility

Arrhythmias

Respiratory

Acute respiratory failure

Depressed myocardial contractility

Gastrointestinal

Ileus, dysphagia

Hematologic

Depressed levels of 2,3-diphosphoglycerate and adenosine triphosphate

Leukocyte dysfunction

Hemolysis

Platelet dysfunction

Renal

Acute tubular necrosis

Metabolic acidosis

Hypercalcemia

Endocrine

Insulin resistance

Hyperparathyroidism

Rhabdomyolyse

Answer 73

A

HbA1C > 6.5%

Glycémie aléatoire > 11.1

Glycémie à jeun > 7

2hr post 75g glucose > 11.1

Answer 74

A

Biguanides (ex metformine)

Sulfonylurées (Ex glyburide, glyclazide)

Thiazolidinediones ( Actos, Avandia, CI insuffisance cardiaque)

Inhibiteurs de l’alpha-glucosidase : acarbose

Meglinitides: sécrétagogues non sulfonylurées (ex repaglinide)

Analogues GLP-1 (ex victoza)

Inhibiteurs DPP-4 - qui dégrade GLP-1 (sitagliptin (Januvia), saxagliptin (Onglyza), and linagliptin (Tradjenta)

Inhibiteurs SGLT2 - protéine qui permet réabsorption tubulaire de glucose: canagliflozine (invokana)

Answer 75

A

Ajouter 3 de natrémie pour chaque augmentation de 10 de la glycémie

Answer 76

A

Pour chaque augmentation de pH de 0,1, la kaliémie augmente de 0,5

Answer 77

A

osmolarité > 350

glycémie > 33

svt atteinte fonction rénale

sx neuro

Acidose métabolique possible si acidose lactique par hypoperfusion ou atteinte rénale

Answer 78

A

increased cytoplasmic calcium concentration, leading to myocyte destruction, with the release of muscle components into the circulation. There are two primary mechanisms whereby calcium pathologically accumulates in the cell, direct cell membrane damage and ATP depletion

Na+,K+-ATPase pump dysfunction leads to increased intracellular Na+, causing a temporary increase in Na+-Ca2+ exchanger function and resultant increase in intracellular Ca2+

4 principes pathophysio de base

Impairment of the muscle’s production or use of ATP at the cellular level. ATP concentrations within the cell fall; energy-dependent mechanisms falter, including Na+,K+-ATPase pumps, leading to disruption of chemical gradients, sarcolemma and cell membrane compromise, and cell destruction.
Disruption in the delivery of oxygen, glucose, and other nutrients to skeletal muscle
Increases in metabolic demands beyond the ability of the organism to deliver oxygen and nutrients
Direct myocyte damage

Answer 79

A

Immobilisation prolongée

Ischémie musculaire

Activité musculaire intense

Extrêmes de température (hypothermie, SNM, coup de chaleur, hyperthermie maligne)

Électrisation

aN électrolytiques: hyponatrémie, hypophosphatémie, hypokaliémie, hypernatrémie

Drogues: LSD, opiacés, cannabinoides (par mécanismes divers)

Médications: statine, antipsychotiques

Infections: influenza A, legionnelle

Myopathies héréditaires

Maladie du tissu conjonctif / maladies autoimmune

Toxines : serpent

Hypothyroidie

Answer 80

A

Hyperkaliémie, hyperphosphatémie, hypocalcémie

Hyperuricémie

Acidose métabolique

Hypercalcémie tardive ( par libération du calcium accumulé intracellulaire)

Answer 81

A

Wolff-Chaikoff : l’excès d’iode induit une inhibition de la libération d’hormones thyroidiennes (inhibition transitoire)

Jod-Basedow: induction d’hyperthyroidie par excès d’iode chez pt avec goitre ou maladie de Graves

Answer 82

A

Maladie de Graves : AC anti récepteurs TSH - augmente la production/libération d’hormones

Goître multinodulaires toxique: multiples nodules qui produisent les hormones , surtout femmes de plus de 50 ans

Adénome toxique: nodule unique

Thyroidite: + svt autoimmune, hashimoto

Thyroidite post-partum: svt 3 phases; thyrotoxicose, hypothyroidie puis euthyroidie

Thyroidite De Quervain ( ou subaigue): post viral, svt avec hypothyroidie au long cours, mais parfois thyrotoxicose initiale

Thyroidite suppurative: infection aigue de la glande

Thyroidite induite par Rx: amiodarone, lithium, trithérapie

hyperthyroidie factice: prise d’hormones ou médicaments pour mai

Hyperthyroidie subclinique: TSH diminuée, hormones N

Answer 83

A

Constitutional: Weight loss despite hyperphagia, fatigue, generalized weakness

Hypermetabolic: Heat intolerance, cold preference, excessive perspiration

Cardiorespiratory: Palpitations, dyspnea, dyspnea on exertion, chest pains, poor exercise tolerance

Gastrointestinal: Nausea, vomiting, diarrhea, dysphagia

Neuropsychiatric: Anxiety, restlessness, hyperkinesis, emotional lability, confusion, insomnia, poor attention

Neuromuscular: Myopathy, myalgias, tremor, proximal muscle weakness (difficulty getting out of a chair or combing hair)

Ophthalmologic: Tearing, irritation, wind sensitivity, diplopia, foreign body sensation

Thyroid gland: Neck fullness, dysphagia, dysphonia

Dermatologic: Flushed feeling, hair loss, pretibial swelling

Reproductive: Oligomenorrhea, amenorrhea, menometrorhaggia, decreased libido, gynecomastia, erectile dysfunction, infertility

Vital signs: Tachycardia, widened pulse pressure, bounding pulses, fever

Cardiac: Hyperdynamic precordium, systolic flow murmur, prominent heart sounds, systolic rub (Means-Lerman scratch), tricuspid regurgitation, atrial fibrillation, evidence of heart failure

Ophthalmologic: Widened palpebral fissures (stare), lid lag, globe lag, conjunctival injection, periorbital edema, proptosis, limitation of superior gaze

Neurologic: Fine tremor, hyperreflexia, proximal muscle weakness

Psychiatric: Fidgety, emotionally labile, poor concentration

Dermatologic: Warm, moist, smooth skin; rosy cheeks, blushing face; fine brittle hair; alopecia, flushed facies; palmar erythema; hyperpigmented pretibial plaques, nodules, or induration that is nonpitting; onycholysis (Plummer’s nails, separation of the distal portion of the fingernail from the nail bed)

Neck: Diffuse symmetric thyroid enlargement, sometimes with a bruit and palpable thrill; thyroid with multiple irregular nodules or a prominent single nodule; tracheal deviation, venous prominence with arm elevation (Pemberton’s sign

Answer 84

A

Hyperpyrexie

Tachycardie importante

Altération état conscience

Insuffisance cardiaque

Sx GI (avec atteinte fonction hépatique)

facteur précipitant (svt avec atteinte thyroide préexistante): chirurgie, stress, trauma, accouchement, charge iodée, infection, SCA, EP, acidocétose…

Answer 85

A

Hyperthyroidie factice: thyroglobuline basse (p/r toutes les autres causes) et captation iode diminuée (comme thyroidite)

Answer 86

A

β-Adrenergic Blockade

Propranolol 60–80 mg PO every 4 hours

Metoprolol, 25–50 mg PO qid

If IV route is required—propranolol, 0.5–1.0 mg IV slow push test dose, then repeat 1–2 mg every 15 min as tolerated to desired effect, then 1–2 mg every 3 hr ou

Esmolol, 50–100 µg/kg/min infusion

Strict contraindication to beta blocker—reserpine 2.5–5 mg IM every 4 hr

Inhibition of Thyroid Hormone Synthesis

Propylthiouracil, 500–1000 mg loading dose, then 250 mg every 4 hr

or

Methimazole, 60–80 mg/day in divided doses

Preferred route, PO or nasogastric (NG); alternative route: PR (in rectum), enema prepared by pharmacy; same dose for all routes

Inhibition of Thyroid Hormone Release

Seulement après thionamides (peuvent augmenter production)

Saturated solution of potassium iodide (SSKI, 50 mg iodide/drop), 1–2 drops PO or PR tid

or

Lugol’s solution (8 mg iodide/drop), 5–7 drops PO or PR tid

or

Sodium iodide, 500 mg IV bid in solution prepared by pharmacy

or

If allergic to iodine, lithium carbonate, 300 mg PO or NG qid

Administration of Corticosteroids

Inhibit T4 to T3 conversion; treat relative adrenal insufficiency.

Hydrocortisone, 300 mg IV, followed by 100 mg tid

or

Dexamethasone, 2–4 mg IV qid

Diagnosis and Treatment of Underlying Precipitant

Consider empirical antibiotics if critical.

Supportive Measures

Volume resuscitation and replacement of glycogen stores

D5/0.9 NS, 125– 000 mL/hr, depending on volume status and CHF

Tylenol, with caution

Cooling blanket, fans, ice packs, ice lavage

Miscellaneous

Lorazepam or diazepam as anxiolytic and to decrease central sympathetic outflow

Cholestyramine (blocks enterohepatic recirculation of thyroid hormone), 1–4 g PO twice daily for severe or refractory thyrotoxicosis (surtout tx en externe)

Considérer plasmaphérese ou dialyse

Conditions spéciales

Thyroiditis (Subacute)

NSAIDs for inflammation and pain control

Prednisone, 40 mg/day, if refractory to NSAIDs

Beta blockade to control thyrotoxic symptoms

No role for PTU, methimazole, or iodides

Factitious Thyrotoxicosis

Beta blockade for thyrotoxic symptoms

Cholestyramine to block absorption of ingested thyroid hormone

No role for PTU, methimazole, or iodides

Answer 87

A

Factors that may result in primary hypothyroidism include autoimmune disorders, infiltrative disorders, congenital thyroid dysfunction, pregnancy, radiotherapy, medications, infection, surgery, inadequate dietary iodine intake, thyroid medication noncompliance, and previous treatment of thyrotoxicosis.

Hypothyroidism may also be associated with other autoimmune diseases, such as diabetes mellitus, pernicious anemia, Addison’s disease, and hyperparathyroidism.

+ fréquent: thyroidite d’hashimoto

Lithium: inhibe libération T3 et T4

Amiodarone: inhibe conversion T4 en T3

En grossesse, augmentation TBG, donc diminution T4 libre. HCG ressemble à TSH, donc stimulation T3-T4 avec TSH abaissée. Augmentation métabolisme périphérique en grossesse

Answer 88

A

Vital Signs

Systolic blood pressure, normal or low

Diastolic blood pressure, normal or elevated

Slow pulse to sinus bradycardia

Respirations, normal or slow, shallow

Temperature, normal, but prone to hypothermia with stress

Hypometabolic Complaints

Cold intolerance

Fatigue

Weight gain, but decreased appetite

Cutaneous

Coarse, brittle hair

Alopecia

Dry skin, decreased perspiration

Pallor, cool hands and feet

Coarse, rough skin

Yellow tinge from carotenemia

Thin, brittle nails

Lateral thinning of the eyebrows

Neurologic

Slow mentation and speech

Impaired concentrating ability and attention span

Lethargy

Decreased short-term memory

Agitation, psychosis

Seizures

Ataxia, dysmetria

Mononeuropathy

Carpal tunnel syndrome

Sensorineural hearing loss

Peripheral neuropathy, paresthesias

Muscular

Proximal myopathy

Pseudohypertrophy

Delayed relaxation of reflexes (hung up or pseudomyotonic)

Cardiac

Decreased exercise capacity

Dyspnea on exertion

Sinus bradycardia

Long QT with increased ventricular arrhythmia

Chest pain, accelerated coronary disease

Diastolic heart failure (delayed ventricular relaxation)

Pericardial effusion (asymptomatic)

Peripheral edema

Respiratory

Dyspnea on exertion

Obstructive sleep apnea

Primary pulmonary hypertension

Gastrointestinal

Constipation

Ileus

Gastric atrophy

Reproductive

Oligomenorrhea and amenorrhea

Menorrhagia

Decreased fertility

Early abortions

Decreased libido

Erectile dysfunction

Rheumatic

Polyarthralgias

Joint effusions

Acute gout or pseudogout

Head, Ear, Eyes, Nose, and Throat

Hoarseness

Deep husky voice

Macroglossia

Hearing loss

Periorbital swelling

Broad nose

Swollen lips

Goiter

Answer 89

A

Infection, sepsis (especially pneumonia)

Exposure to cold

Cerebrovascular accident

Drug effect

Altered sensorium—sedative-hypnotics, narcotics, anesthesia, neuroleptics

Decreased T4 and T3 release—amiodarone, lithium, iodides

Enhanced elimination of T4 and T3: phenytoin, rifampin

Inadequate thyroid hormone replacement: noncompliance; interference with absorption (iron, calcium, cholestyramine)

Myocardial infarction

Gastrointestinal bleeding

Trauma, burns

Congestive heart failure

Hypoxia

Hypercapnia

Hyponatremia

Hypoglycemia

Hypercalcemia

Diabetic ketoacidosis

Présentation typique

Patient profile—older woman in the winter

Known hypothyroidism; thyroidectomy scar

Hypothermia—temperature usually <95.9° F (36° C); <90° F (32° C) is poor prognostic sign; as low as 75° F (24° C) reported; nearly normal in presence of infection

Altered mental status—lethargy and confusion to stupor and coma, agitation, psychosis, and seizures (myxedema madness)

Hypotension—refractory to volume resuscitation and pressors unless thyroid hormone administered

Slow, shallow respirations with hypercapnia and hypoxia; high risk of respiratory failure

Bradycardia (sinus), long QT and ventricular arrhythmias

Myxedema facies—puffy eyelids and lips, large tongue, broad nose

Evidence of severe chronic hypothyroidism—skin, hair, reflexes, bradykinesis, voice

Acute precipitating illness (eg, pneumonia)

Drug toxicity (eg, sedative, narcotic, neuroleptic)

Hyponatremia

Answer 90

A

Protect airway, ventilatory support; monitor for alkalosis

Fluid resuscitation

0.9 NS or D5/0.9 NS if hypoglycemia

Watch for unmasking of CHF

Thyroid hormone replacement

T4 200–400 µg IV (give lower doses to patients who are smaller, have coronary artery disease or a history of arrythmia) loading dose

Subsequent daily replacement of 1.6 µg/kg body weight PO, give 75% of this dose if given IV

Hydrocortisone—100 mg IV every 8 hrs

Hyponatremia

Consider fluid restriction.

Avoid hypotonic fluids; use only 0.9 NS or D5/0.9 NS.

If <120 mEq/L, consider 3% saline, 50- to 100-mL boluses.

Passive rewarming

Regular blankets; prevent heat loss

If heating blankets are considered, pretreat with IV fluids and monitor blood pressure closely.

Avoid mechanical stimulation.

Treatment of any precipitating illness, with special attention to infectious causes

Answer 91

A

Zones du cortex : GFR

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