MedInterne Flashcards

(108 cards)

1
Q

DxD arthrite à l’urgence

A
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2
Q

Décrire les trouvailles radiologiques selon le type d’arthrite

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

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3
Q

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

A
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4
Q

Nommer des maladies associées à la pseudogoutte

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

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5
Q

Nommer 6 causes d’arthrite virale

A

Hépatite B, C

VIH

Parvovirus B19

Alphavirus (ex chikungunya)

Rubéole

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6
Q

Nommer les critères de Jones

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

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7
Q

Nommer les principaux effets secondaires des médicaments utilisés dans la PAR

A
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8
Q

DxD de la tendinopathie

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)

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9
Q

Critères dx du lupus

A

MDSOAPBRAIN

malaire

discoid

serosite

oral ulceres

arthrite

photosensibilité

blood

renal

anticorps

immuno

neurologique

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10
Q

Quelle est la principale cause de douleur abdominale en lupus?

A

Entérite lupique (vasculite mésentérique)

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

Tx: stéroides IV

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11
Q

Nommer 7 médicaments causant un lupus

A

Procainamide

Hydralazine, méthyldopa

Isoniazide

Quinidine

Minocycline

Chlorpromazine

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12
Q
A
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13
Q

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

A

4 patterns

  1. Occlusion vasculaire : Artérite à cellules géantes, Takayasu
  2. Syndrome poumons-reins: Wegener, Churg-Struss, Goodpasture, Polyangiite microscopique
  3. Manifestations cutanées: Érythème noueux, Purpura Henoch Schonlein, polyartérite noueuse, Behcet
  4. Associées à exposition environnementale ou antigène: LEvamisole, cryoglobulinémie, Buerger
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14
Q

Artérite à cellules géantes

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
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15
Q

Takayasu

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

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16
Q

Syndromes poumons-reins

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

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17
Q

Vasculites à atteinte cutanée

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

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18
Q

Cryoglobulinémie

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

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19
Q

Vasculites associés à antigène ou exposition exogène

A

Différencier Buerger, maladie sérique et vasculite d’hypersensibilité

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20
Q

Nommer les 4 types de réactions immunologiques

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

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21
Q

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

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

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22
Q

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

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

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23
Q

Nommer les 3 critères dx de l’anaphylaxie

A
  1. Atteinte cutanée/muqueuse + 1/2 : sx respi ou HD
  2. Apres exposition antigène, 2 ou plus de : cutanée/muqueuse, respi, GI, HD
  3. Atteinte HD après exposition antigène connu
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24
Q

DxD flush syndrome (anaphylaxie)

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

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25
Traitement de l'angioedème
Épi si associé à anaphylaxie - Tx support, concentrés de facteur C1 inhibitor, icatibant (inhibiteur récepteur bradykinin-2), FFP, inhibiteur Kallikrein (Ecallantide)
26
Nommer des causes de destruction massive de GR
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)
27
DxD anémie
28
Nommer les 3 types de thalassémie
Thalassémie beta hétérozygote et homozygote Thalassémie alpha
29
Qu'est-ce que l'anémie sidéroblastique?
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
30
Nommer 10 causes de déficit en folate
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
31
Nommer 10 causes de déficit en B12
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
32
Différencier les types d'anémie mégaloblastiques
33
Nommer 8 médicaments responsable d'aplasie médullaire
34
DxD anémie hémolytique
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
35
Nommer 4 médicaments induisant de l'hémolyse chez un pt avec déficit en G6PD
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
36
Nommer 10 maladiées associées à l'anémie hémolytique auto-immune
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
37
Nommer 4 médicaments causant une anémie hémolytique auto-immune et son mécanisme associé
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
38
Nommer 6 tests à faire lors de suspicion d'anémie hémolytique
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
39
Nommer 4 types d'hémoglobine
HbA (α2β2), HbA2 (α2δ2), and HbF (α2γ2) HbS = anémie falciforme et plusieurs combinaisons, avec sickle cell- b-thalassemie...
40
Tx anémie falciforme
2 principales manifestations: hémolyse et crises vaso-occlusives Analgésie, hydratation Tx stroke: rtpa idem, échanges plasmatiques tx hydroxyurée Viser HbS \< 30%
41
Nommer 8 cause d'érythrocytose
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
42
Décrire présentation et dx polycythémie vraie
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
43
Nommer 4 causes de neutrophilie primaire
- LMC, polycythémie vraie - neutrophilie héréditaire - neutrophilie idiopathique chronique - maladie myéloproliférative chronique En cas d'hyperleucocytose sévère, leukaphérèse
44
3 types de leucémies adultes
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)
45
Dxd leucopénie selon stade maturation GB
46
Expliquer le rôle des plaquettes dans l'hémostase
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
47
Dessiner la cascade de la coagulation
48
Nommer les 3 groupes de facteurs de la coagulation
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
49
Nommer 5 contrôles de la coagulation
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
50
Nommer 3 médicaments associés au PTT
Quinine Ticlopidine Clopidogrel
51
3 grandes classes de thrombocytopathies et étiologies associées
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
52
DxD thrombocytopénie, thrombocytose et thrombocytopathie
53
Hémophilie 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,
54
VonWillebrand
1. Favorise l'Adhésion des plaquettes à l'endothélium vasculaire 2. 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
55
Hémophilie B
Déficit en facteur IX Tx: concentrés de facteur IX, PCC, plasma frais Concentrés de facteur IX 1 unité /kg = 1 % d'activité
56
Expliquer les changements de la coagulation lors CIVD
57
Nommer les doses de protamine
Héparine non fractionnée = 1 mg / 100 unités HBPM: 1 mg / 1 mg HBPM
58
Compression néoplasie moelle osseuse Néos les + fréquents Tx
Néo: poumons, seins, prostate, rein, lymphome hodgkin, myélome multiple Tx: chirurgie, decadron 10 IV puis 16 mg / jour Radiothérapie
59
Nommer 4 étiologies d'épanchement péricardique néoplasique
Envahissement du péricarde par néo (poumons, seins, néo hématologiques, mélanome) Épanchement 2nd obstruction lymphatique par ganglions lymphatiques obstrués Hypoalbuminémie Radiothérapie Chimiothérapie
60
4 mécanismes d'hypercalcémie néoplasique
Production PTH-rp (néoplasies épidermoides poumons, oesophage, tête/cou, endomètre/col/ovaires) Augmentation production calcitriol Ostéolyse 2nd invasion osseuse Production ectopique PTH
61
62
Tx hypercalcémie néoplasique
- hydratation IV - biphosphonates (acide zolédronique ou pamidronique) - calcitonine si réfractaire - dialyse - denosumab - cortico si lymphome associé
63
Syndrome de lyse tumorale
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
64
Tx leucostase
hydratation IV Éviter pRBC Leukaphérèse Hydroxyurée Chimiothérapie
65
Compensations acidobasique
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
66
Nommer 5 causes d'anion gap faussement bas
Hypoalbuminémie (anion gap corrigé = anion gap + 2.5 ( 4 - albumine sérique (g/dL) Hypertriglycéridémie Intoxication bromure Intoxication lithium Hypergammaglobulinémie Myélome multiple
67
Nommer 15 étiologies d'alcalose respiratoire
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
68
DxD acidose métabolique anion gap élevé
CAT MUDPILES
69
DxD acidose métabolique anion gap normal
70
Nommer l'équation de Winter
Winter’s equation (PaCO2 = [1.5 × serum HCO3] + [8 ± 2])
71
5 catégories les plus fréquentes d'hyperkaliémie
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
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Nommer 5 causes d'hypokaliémie
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
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Nommer 10 causes d'hypernatrémie
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
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Nommer 10 causes de diabète insipide
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
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Nommer 15 causes d'hyponatrémie
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
76
Nommer les 3 principales causes de SIADH avec 3 exemples pour chacun
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
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Nommer 10 causes d'hypercalcémie
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
78
Expliquer la correction du calcium avec l'albumine
Pour chaque diminution d'albumine de 10, augmenter la calcémie de 0.2
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Nommer 10 causes d'hypocalcémie
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
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Nommer 5 causes d'hypermagnésémie
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
81
Nommer ss/sx hypermagnésémie selon le niveau sérique
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
82
Tx hypermagnésémie
Cesser apport exogène Hydratation IV Diurétiques Dialyse si instable - calcium IV - 5mL gluconate de calcium
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Nommer 10 causes d'hyperphosphatémie
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
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Nommer 15 causes d'hypophosphatémie
**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
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Nommer 15 ss/sx d'hypophosphatémie
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
86
Nommer les seuils dx du diabète
HbA1C \> 6.5% Glycémie aléatoire \> 11.1 Glycémie à jeun \> 7 2hr post 75g glucose \> 11.1
87
Nommer les classes d'hypoglycémiants oraux
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)
88
Expliquer la correction de la natrémie selon la glycémie
Ajouter 3 de natrémie pour chaque augmentation de 10 de la glycémie
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expliquer le changement de kaliémie selon le pH
Pour chaque augmentation de pH de 0,1, la kaliémie augmente de 0,5
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dx syndrome hyperglycémie hyperosmolaire
osmolarité \> 350 glycémie \> 33 svt atteinte fonction rénale sx neuro Acidose métabolique possible si acidose lactique par hypoperfusion ou atteinte rénale
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Décrire physiopatho de la rhabdomyolyse
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 1. 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. 2. Disruption in the delivery of oxygen, glucose, and other nutrients to skeletal muscle 3. Increases in metabolic demands beyond the ability of the organism to deliver oxygen and nutrients 4. Direct myocyte damage
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Nommer 10 étiologies de rhabdomyolyse
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
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94
Expliquer les mécanismes physiopathologiques de l'atteinte rénale en rhabdomyolyse et les anomalies électrolytiques associées
Hyperkaliémie, hyperphosphatémie, hypocalcémie Hyperuricémie Acidose métabolique Hypercalcémie tardive ( par libération du calcium accumulé intracellulaire)
95
Nommer les 2 effets possibles induit par l'excès d'iode
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
96
Nommer les principales causes d'hyperthyroidie
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
97
Nommer les sx et signes à EP d'une hyperthyroidie
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
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Ss/sx tempête thyroidienne
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...
99
Dx selon tests de fonction thyroidienne
Hyperthyroidie factice: thyroglobuline basse (p/r toutes les autres causes) et captation iode diminuée (comme thyroidite)
100
Tx hyperthyroidie
**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
101
Nommer 10 causes d'hypothyroidie
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
102
Nommer 25 ss/sx d'hypothyroidie
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
103
Nommer 10 facteurs précipitants ou aggravants reliés au coma myxoedémateux
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
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Tx coma myxoedémateux
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
105
Décrire la production d'hormones par les glandes surrénales
Zones du cortex : GFR
106
Dessiner l'axe surrénalien avec les diverses causes d'insuffisance surrénalienne primaire/secondaire/tertiaire
107
Nommer ss/sx d'insuffisance surrénalienne primaire et secondaire
108