PROTEINA S-100

PRESENTACION CLASE IMPARTIDA POR EL DR. NESTOR AMARO GUTIERREZ

ROTACION PATOLOGIA CLINICA

MODULO MEDICINA INTERNA

DEPARTAMENTO DE MEDICINA Y NUTRICION

UG CAMPUS LEON

Marcador proteina s 100

View more presentations from Hector Marrufo

FUNCION TUBULAR

PRESENTACION CLASE PRUEBAS DE FUNCIONAMIENTO RENAL

ROTACION DE PATOLOGIA CLINICA

MODULO MEDICINA INTERNA

DEPARTAMENTO DE MEDICINA Y NUTRICION

ALUMNO: FRANCISCO JAVIER ARMAS ZARATE

FDA Prepares for Nanomedicine Revolution

June 21, 2011 — New technology now makes it possible to create atomic-scale drug particles, diagnostic tools, and biological medical devices -- and the FDA is struggling to regulate the fast-growing field.

Noting the "critical need to learn more" about the impact of nanotechnology on medicines and medical devices, the FDA has issued a warning that it intends to regulate the field -- and has asked for help in understanding the impact the new technology will have on FDA-regulated products.

It's a welcome development, says nanomedicine developer Gang Bao, PhD, director of the Center for Pediatric Nanomedicine, a joint project of the Georgia Institute of Technology, Emory University, and Children's Healthcare of Atlanta.

"It is a great thing that FDA now pays attention to nanotechnology," Bao tells WebMD. "We can always publish scientific papers, but what we really want to do is have nanomedicine used in the clinic: for drug delivery, diagnosis, or treatment using nanomachines. Without FDA approval we cannot do that. So therefore this is a very important advance."

Nanotechnology already is a trillion-dollar industry spanning fields from agriculture to product packaging. It springs from new technology that makes it possible to manipulate matter at the atomic scale. The application of this technology to medicine is truly revolutionary, says Jamey Marth, PhD, director of the Sanford Burnham Center for Nanomedicine at the University of California, Santa Barbara.

"It will be comparable to what occurred 50 or so years ago when Watson and Crick discovered the structure of DNA and its role in biology," Marth tells WebMD. "We are going to witness a huge increase in the understanding of disease and in the ability to treat, detect, and ultimately cure disease with nanomedicine."

What Is Nanomedicine?

It's difficult, but important, to grasp the scale of the nano world. A nanometer (nm) is a billionth of a meter. A single sugar molecule is 1 nm in diameter; the DNA helix is 2 nm in diameter. A typical virus is 75 nm in size. A red blood cell is 7,000 times larger than a nanometer.

"Why this size? Inside a living cell we have proteins, we have DNA molecules, etc., all on a nanoscale," Bao says.

"Just a few decades ago, a computer used to be the size of a room," says Marth. "Now everyone has a laptop. It's the same thing in biology. We are seeing the miniaturization of biology, which will rapidly change the way we do research and develop drugs."

By allowing scientists to take such a close look at biological processes, nanotechnology offers new tools to understand what causes disease. We've been able to learn a lot by cracking the DNA code. But genetics doesn't tell us all the biology we need to know.

"We have not been able to answer all of the questions about a lot of important diseases -- grievous diseases such as diabetes, cardiovascular disease, diseases of aging, cancer. All these diseases have some genetic underpinning, but the genetic role is partial," says Marth. "What nanomedicine is able to do is to begin to identify and interrogate those processes which are outside our genetic inheritance."

That's only part of the story. Nanotechnology also offers powerful new tools to treat disease.

The FDA already has approved two cancer drugs based on nanotechnology: Abraxane and Doxil, which package cancer drugs into nanoscale lipid droplets and allow higher chemotherapy doses with fewer side effects.

Second-generation drugs of this type will carry nanoparticles on their surfaces that not only target the drugs to cancer cells, but also allow them to penetrate deep into tumors. The FDA has given the green light to clinical trials of Cornell dots -- nanoscale silicon cages that carry nanoparticles to tumor cells.

Marth says that nanomedicine will speed the discovery of biomarkers that identify diseased cells. Once these biomarkers are found, they can be used to bind therapeutic nanoparticles only to the cells that need them, leaving normal cells alone.

Bao's team is pioneering another approach: using nanoparticles to repair genetic mutations. Their first target will be the mutation that causes sickle cell disease.

"We are trying to develop nanodevices to fix this mutation," Bao says. "We use a nanoscissors -- technically a zinc finger nuclease -- to cut the DNA at a pre-described location. At the same time, we supply a piece of DNA that has no mutation. In repairing the DNA cut, the cell actually uses the template we supply."

Is Nanomedicine Safe?

A major task for the FDA will be to set guidelines for demonstrating that new nanomedicines are safe. But Marth says there are both toxic and nontoxic approaches to nanomedicine.

"We will have to do clinical trials, but we are not adding poisonous materials to the body," he argues. "The way forward is to take natural products, rearrange them in ways that do new things, but allow them to be degraded normally in the body."

Even so, Bao says the FDA guidance will be important, as materials that behave one way on a normal scale can behave quite differently at a nanoscale.

"There might be some unique features of nanoparticles that induce some toxic effects," Bao suggests. "If they could get into the body, stay in the cells, not be cleared, there might be some harmful effects down the road, and we need to understand that. We do not think the particles we use have any intrinsic toxicity, but we need to know this for sure."

Daniel J. DeNoon

From WebMD Health News

SOURCES:

Jamey Marth, PhD, director and professor, Center for Nanomedicine, Sanford-Burnham Medical Research Institute, University of California, Santa Barbara.

Gang Bao, PhD, professor of biomedical engineering, Georgia Institute of Technology; director, Center for Pediatric Nanomedicine, Emory University/Georgia Institute of Technology/Children's Hospital of Atlanta.

RETROALIMENTACION CASO CLINICO NEFROLOGIA

What is the most likely diagnosis?
Prerenal ARF due to volume depletion.

How to confirm the diagnosis?
UA.

Urinary sodium and creatinine to calculate the fractional excretion of sodium (FENA).

What other tests would you order?
BMP in 6 and 24 hours.

Renal ultrasound to rule out urinary obstruction and nephrolithiasis.

What treatment would you start for this patient?
Insulin 10 units IV with D50, 1amp. IV x 1.
Kayexalate 45 gm po x 1.
Foley catheter.
Strict I/O.
NS at 150 cc/hr x 2 L, then 125 cc/hr, adjust the rate of IVF according to I/O, avoid fluid overload.
Hold ACEi and NSAIDs

What happened?
FENA of 0.77 % confirmed the diagnosis of prerenal failure.
Renal U/S ruled out urinary obstruction.
The patient had good urine output with IVF and was in a positive fluid balance.
Potassium normalized after treatment with Kayexalate, Insulin and D50.
There was a downward trend in BUN and creatinine.

Final diagnosis
Prerenal Acute Renal Failure due to Volume Depletion.

What did we learn from this case?
ARF is frequently defined as an acute increase of the serum creatinine level by 25 % from baseline.

The fractional excretion of sodium (FENa) is useful in diagnosing pre-renal ARF. FENa is less than 1 % in many patients with prerenal ARF. Intravenous hydration is the mainstay of treatment.

VAGINITIS DIAGNOSIS

Open publication - Free publishing - More diagnostico

NT-proBNP Beats CRP at Predicting CV Risk in Older Patients

June 22, 2011 (London, United Kingdom) — N-terminal pro-brain natriuretic peptide (NT-proBNP) was better than C-reactive protein (CRP) at predicting major cardiovascular events in older men with and without preexisting cardiovascular disease in a new prospective study [1].

The study, published in the June 28, 2011 issue of the Journal of the American College of Cardiology, was led by Dr Goya Wannamethee (University College London, UK).

Wannamethee commented to heartwire : "Other studies have shown that BNP can predict cardiovascular events, but the novel thing in our study is that we have shown that it is useful in stratifying patients when added on top of the risk factors we already use, ie, the Framingham score."

She noted that this particular study's results were applicable only to the older population (over 60). "We are saying than NT-proBNP seems particularly useful in this older population, where blood pressure and cholesterol are not as reliable predictors as they are in middle-aged people. Also, our study was only in men and mostly Europeans, so we would like to see confirmation in other populations. But our results do appear to suggest that BNP more useful than CRP for risk prediction in this older population. I would say it is the best marker of risk so far in this population."

This is the second study showing NT-proBNP to be a useful risk predictor to be reported this week, with an analysis from ASCOT presented at the European Society of Hypertension (ESH) European Meeting on Hypertension 2011 this past weekend showing the marker to predict cardiovascular events in a hypertensive population without preexisting cardiovascular disease.

In this study, 3649 men age 60 to 79 years were followed for a mean of nine years, during which there were 608 major cardiovascular events. Results showed that NT-proBNP was significantly associated with risk of all major cardiovascular outcomes after adjustment for cardiovascular risk factors in both men with and without cardiovascular disease, whereas CRP was associated with cardiovascular outcomes only in men without preexisting cardiovascular disease and was a weaker predictor than NT-proBNP.

Adjusted Hazard Ratios (95% CI) for Future Cardiovascular Events

Measure	Men without preexisting CV disease	Men with preexisting CV disease
NT-proBNP	1.49 (1.33–1.65)	1.52 (1.33–1.75)
CRP	1.22 (1.10–1.34)	1.00 (0.86–1.38)

When incorporated into a model including Framingham data, NT-proBNP significantly improved the ability to predict cardiovascular events, as shown by an improvement in the C statistic, whereas CRP did not improve prediction.

Net Reclassification Improvement in C Statistic (%) When Added to Framingham Data

Measure	Men without preexisting CV disease	Men with preexisting CV disease
NT-proBNP	8.8	8.2
CRP	3.8	0.6

Wannamethee said: "NT-proBNP has traditionally been thought of a marker of heart failure. But this study was done in the general population, so it is obviously picking up something else here--not just heart failure. It predicts CHD events and stroke as well as heart failure."

She noted: "It's still at an early stage. It's not going to be used routinely any time soon, but I would hope that this study will stimulate further research to look at its potential role in general practice. This would involve thinking about how it would fit in with other tests and who it would best be used in." She also pointed out that NT-proBNP was also more specific for cardiovascular disease than CRP, which tended to be elevated in most major diseases

References

1. Wannamethee SG, Welsh P, Lowe GD, et al. N-terminal pro-brain natriuretic peptide is a more useful predictor of cardiovascular disease risk than C-reactive protein in older men with and without preexisting cardiovascular disease. J Am Coll Cardiol 2011; 58:56–64.

Statin Therapy Tied to Lower Prostate Cancer Risk

Statin Therapy Tied to Lower Prostate Cancer Risk
Lower risk of cancer detected at initial biopsy, reduced risk of moderate to high-grade cancer

THURSDAY, June 23 (HealthDay News) -- Statin therapy may decrease the risk and severity of prostate cancer, according to a study published in the July issue of The Journal of Urology. Nelly Tan, M.D., from the Yale-New Haven Hospital in Connecticut, and colleagues investigated the association between statin therapy and prostate cancer in men who underwent prostate biopsy. Between 2000 and 2007, 4,204 men underwent biopsy, including 1,022 men on statin therapy and 3,182 men not on statin therapy. Statin use was assessed on the basis of pharmacy records. Multivariate logistic regression analysis was used to determine the effects of statins and the duration of use. The investigators found that men diagnosed with prostate cancer while on statin therapy were significantly less likely to have digital rectal examination positivity (odds ratio [OR], 0.7), high-grade prostate cancer (Gleason score 7 or greater; OR, 0.78), and high-volume prostate cancer, compared to nonstatin users. Prostate-specific antigen was significantly lower in statin users compared to nonstatin users. After adjustments, the risk ratio (RR) was significantly lower for prostate cancer diagnosis, high-grade prostate cancer, and high-volume (three or more cores positive) in statin users (RR, 0.92, 0.76, and 0.86, respectively). Length of use was associated with a lower rate of high-grade cancer. "This study provides evidence that patients screened for prostate cancer who use statins are less likely to have cancer detected at the time of initial biopsy, less likely to have moderate to high-grade prostate cancer and more likely to have lower prostate cancer volume compared to nonstatin users," the authors write. One of the study authors disclosed financial ties to the pharmaceutical and medical device industries.

Copyright © 2011 HealthDay. All rights reserved.

APREDIZAJE BASADO EN PROBLEMAS (CASO CLINICO)

A 67-year-old African American male is admitted to the hospital with chief complaint of generalized weakness and potassium level of 6.5 mEq/L. His laboratory results show acute renal failure (ARF). The patient has severe osteoarthritis and takes high-dose nonsteroidal antiinflammatory drugs (NSAIDs). In the recent heat wave, he noticed that he did not go to bathroom as often as he used to for the last 2-3 days.
Past medical history (PMH)
Obesity, obstructive sleep apnea (OSA), hypertension (HTN), osteoarthritis (OA).

Medications
Motrin (ibuprofen), Percocet (oxycodone with acetaminophen), oxycodone, lisinopril.

Physical examination
VSS.
HEENT: Dry mucosal membranes (MM).
Chest: CTA (B).
CVS: Clear S1S2.
Abdomen: Soft, NT, ND, +BS.
Extremities: no c/c/e.

Laboratory results
BUN/Cr were normal several months ago.

What is the most likely diagnosis?

How to confirm the diagnosis?

What other tests would you order?

What treatment would you start for this patient?

RETROALIMENTACION CASO CLINICO NEFROLOGIA

CASO CLINICO:

Insuficiencia renal e hipertensión

En ausencia de tratamiento antihipertensivo, la lesión renal es muy frecuente en pacientes con hipertensión arterial esencial. En este sentido, Perera et al describió cómo la proteinuria estaba presente en el 42 % y la insuficiencia renal crónica en el 18 % de una serie de 500 hipertensos no tratados, seguidos hasta su fallecimiento (1). El desarrollo del tratamiento antihipertensivo ha supuesto una mejoría espectacular en el pronóstico renal y cardiovascular de los pacientes hipertensos (2,3).

Sin embargo, algunas evidencias indican que el pronóstico de la función renal no es tan bueno en dichos pacientes. Entre ellas están:

a) el aumento en la prevalencia de nefroangioesclerosis como una causa de insuficiencia renal terminal en pacientes que inician un tratamiento de diálisis, tanto en Estados Unidos como en Europa (4,5);
b) el descenso progresivo de la función renal en un porcentaje significativo de hipertensos esenciales tratados descrito por diferentes grupos (6-8);
c) la asociación observada entre la presión arterial y la creatinina sérica, consistente con la hipótesis de que las elevaciones de la presión arterial, incluso por debajo del rango hipertensivo, pueden inducir lesión renal de forma precoz (9);
d) la descripción de Pergener y cols. de que, en EEUU, una de cada trece personas hipertensas (7.7 %) puede desarrollar hipercreatininemia (10), y
e) la presencia de proteinuria en porcentajes que oscilan entre el 4 y el 16 % en diferentes series de pacientes hipertensos tratados (11,12). Todos estos argumentos indican que la insuficiencia renal es aún prevalente en la hipertensión esencial, incluso considerando que la determinación de creatinina sérica es un método pobre para estimar la evolución de la función renal, especialmente en los estadios iniciales de la insuficiencia renal crónica.

FACTORES METABOLICOS ASOCIADOS

La nefroangioesclerosis se acompaña de niveles inicialmente más elevados tanto de presión arterial sistólica y diastólica, predominio de sexo masculino, niveles inicialmente superiores de ácido úrico sérico y triglicéridos, y niveles más bajos de HDL-colesterol.

Un análisis de regresión logística múltiple identificó las presiones diastólica y sistólica, el ácido úrico sérico y los triglicéridos como factores predictores independientes del desarrollo de nefroangioesclerosis. Adicionalmente, en pacientes con nefroangioesclerosis y glucemia en ayunas normal, un test de tolerancia oral de glucosa permitió el diagnóstico de diabetes tipo 2 en un 52% de los casos (13).

EVOLUCION Y PRONOSTICO

El incremento en la prevalencia de nefroangioesclerosis y el aumento en el riesgo cardiovascular que acompaña la existencia de insuficiencia renal crónica ha conducido a la búsqueda de factores predictores de mal pronóstico.

En ese sentido, el control de la glucemia y de la presión arterial sistólica, particularmente en el sexo masculino, disminuye la frecuencia de función renal deteriorada (14). Se ha descrito un alto grado de lesión en vasos renales en aquellos pacientes hipertensos que presentan hiperuricemia en presencia de una tasa de filtración glomerular normal (15). Incluso, la presencia de hiperuricemia parece ligada a un peor pronóstico renal para los mismos niveles de control de la presión arterial (16).

TRATAMIENTO: CIFRAS OPTIMAS DE CONTROL Y FARMACOS

Son dos las cuestiones a tener en cuenta a la hora de mejorar el pronóstico renal de los pacientes con nefroangioesclerosis: los valores de presión arterial más apropiados en que el paciente debe mantenerse, y la utilidad de los distintos grupos de fármacos antihipertensivos en cuanto a protección renal.

Es sabido que un control estricto de la presión arterial retarda la pérdida de función renal en pacientes con insuficiencia renal crónica y proteinuria superior a los 3 g/día (17). Por tanto, el objetivo de presión arterial en pacientes con insuficiencia renal crónica y proteinuria superior a 1 g/día debe ser de 125/75 mmHg (18).

En este sentido, el estudio HOT ha demostrado que la presencia de insuficiencia renal leve no impide la consecución de un adecuado control de la presión arterial, pero dicha insuficiencia renal se acompaña de un incremento significativo del riesgo cardiovascular. El adecuado control de la presión arterial protege la función renal en la mayoría de los pacientes, pero no impide el deterioro de la función renal en un pequeño porcentaje de dichos pacientes (19).

Los inhibidores de la enzima de conversión de la angiotensina II (IECA) constituyen el grupo farmacológico que ha demostrado un mayor beneficio en la evolución de distintas nefropatías, tanto diabética como no diabéticas (18,20). En la hipertensión esencial, los IECA han demostrado ser más eficaces que los diuréticos, los betabloqueantes y los calcioantagonistas en la reducción de la excreción urinaria de albúmina (21). Además, estos fármacos han mostrado que facilitan la regresión del remodelado vascular (22) y que mejoran la función endotelial en arteriolas de resistencia (23) en pacientes hipertensos.

TOMADO DE CASOS CLINICOS SOCIEDAD ESPAÑOLA DE NEFROLOGIA

APRENDIZAJE BASADO EN UN CASO CLINICO

ANAMNESIS

Varón de 71 años con antecedentes personales de: HTA de larga evolución tratada con dos fármacos, miocardiopatía hipertensiva con hipoquinesia generalizada, fibrilación auricular crónica en tratamiento con digoxina y anticoagulación oral.

Ha presentado varios episodios de insuficiencia cardiaca congestiva. Además, presenta una hipercolesterolemia moderada, hiperuricemia con varios episodios de artritis gotosa, y un síndrome prostático en seguimiento por su urólogo de zona desde hace 6 años. No presenta diabetes. No refiere hábitos tóxicos ni alergias conocidas.

Motivo de consulta: es remitido a la consulta de Nefrología por su médico de familia por presentar en una analítica rutinaria unas cifras de creatinina plasmática de 1.7 mg/dl y una proteinuria de 150 mg/dl.

En su situación basal presenta una disnea de pequeños esfuerzos, sin ortopnea, ni angina, con claudicación intermitente a los 300 metros.

Antecedentes familiares: madre hipertensa, padre fallecido por cardiopatía, un hermano y un hijo hipertensos.

Antecedentes nefrourológicos: No ha presentado hematuria ni litiasis. Tampoco refiere infecciones urinarias.

Tratamiento habitual: Amiodarona 200 mg/d, Nifedipina retard 30 mg/12h, Digital 0.25 mg/d, Sintron según controles, Alopurinol 100mg/d, Torasemida 10 mg/d.

2) EXPLORACIÓN FÍSICA:

Peso 84 kgs. Talla 170 cms. IMC 29. TA 170/100 mmHg. FC 84 lpm.

Consciente, orientado, obeso, bien hidratado y perfundido. Rubicundez facial. Eupneico, tolera decúbito.

Cabeza y cuello: Carótidas arrítmicas, simétricas, con soplo carotídeo derecho. No ingurgitación yugular.

Tórax: AC: Arrítmico a 84 lpm, sin soplos. AP: murmullo vesicular conservado.

Abdomen: Blando, depresible, no doloroso, no masas ni megalias, no soplos, peristaltismo conservado.

Extremidades: Leves edemas maleolares, pulsos femorales palpables. Soplo en ambas femorales. Soplos dístales débiles.

Fondo de ojo: algún signo de cruce. No presenta exudados, hemorragias ni papiledema.

3) DATOS COMPLEMENTARIOS

• Hemograma: Hem: 6.120.000/mm3, Hto: 60 %, Hb: 17.6 g/dl, Leucocitos: 7.080/mm3 con fórmula normal, Plaquetas: 181.000/mm3.
  
  
• Coagulación: Protrombina: 26 %, Cefalina 28''.
  
  
• Bioquímica: Na: 145 mEq/l, K: 4.4 mEq/l, Creat: 1.8 mg/dl, Urea: 68 mg/dl, Urico: 9.7 mg/dl, Glucosa: 96 mg/dl, Calcio: 9.7 mg/dl, Fosforo: 4.1 mg/dl, Fosfatasa alcalina: 237 U, Proteinas totales: 7.2 g/dl, Albúmina: 4.5 g/dl.
  
  
• GOT: 27 U/l, GPT: 29 U/l, GGT: 75 U/l, LDH: 232 U/ml, BIL: 0.98 mg/dl, Colesterol: 247 mg/dl, TG: 266 mg/dl.
  
  
• Orina: Aclaramiento de creatinina: 49 ml/min, Proteinuria: 3.1 g/día, Hematuria 64x106 hematíes/día, Leucocituria: 2x106 leucos/día. Sedimento: cilindros hialinos. Uricosuria: 415 mg/día, Fosfaturia: 700 mg/día, Calciuria: 1.2 mg/kg/día.
  
  
• Urocultivo: estéril.
  
  
• Serologías virales: AgHBs:neg, Anti HBs:neg, Anti HBc:neg, Anti-HVC: negativo. AntiVIH: negativo.
  
  
• Inmunología: IgG: 910 mg/dl, IgA: 242 mg/dl, IgM: 53 mg/dl, C3: 139 mg/dl, C4: 27.6 mg/dl, FR <20 UI/ml, Criglobulinas negativas, ANA negativo, AntiDNA negativo.
  
  
• Rx Tórax: Cardiomegalia, elongación aórtica y calcificación del cayado aórtico. Cifosis dorsal y dosartrosis.
  
  
• E.C.G.: Fibrilación auricular a 76 lpm. Criterios de hipertrofia ventricular izquierda.
  
  
• Ecografía abdominal: Discreta hepatomegalia con ecogenicidad aumentada. Vía biliar y páncreas normales. Riñón izquierdo de 11x6 cms, sin alteraciones. Riñón derecho de 11x5 cms, con varios quistes corticales. Cálices, pelvis y uréteres de calibre normal.
  
  
• Doppler renal: Arterias renales principales no visualizadas. Flujo arterial intrarrenal de aspecto normal, no evidenciándose signos indirectos de estenosis.
  
  
• Gammagrafía renal: Captación normal en ambos riñones. No hay cambios postcaptopril.
  

COMENTARIOS AL CASO CLINICO...

APRENDIZAJE BASADO EN PROBLEMAS

History
A 63 year old man had been admitted to hospital there and was transferred in a stable condition with a diagnosis of "left lower lobe pneumonia, exacerbation of chronic obstructive airways disease & probable pulmonary embolus". Treatment prior to arrival here was with antibiotics, salbutamol, frusemide, prednisone and warfarin.

Past history was of 'bullous emphysema' with several admissions in recent years to our hospital with acute infective exacerations of his chronic respiratory disease. His previous admission here 9 months previously was complicated by pulmonary embolism and he had been ventilated via a tracheostomy in the Intensive Care Unit. He had been on daily prednisone for the previous few years.

On admission, he was febrile and in severe respiratory distress. A small amount of purulent sputum was noted. Crackles were heard throughout his lungfields. Heart sounds were normal. Initial coagulation testing showed an INR of >7.0. Mild abdominal pain was present.

He was initially managed in a General Medical Ward but developed severe abdominal pain 3 days after admission. An erect xray showed a large amount of gas under each hemidiaphragm. He was transferred to Intensive Care for assessment, insertion of lines and stabilisation prior to theatre for laparotomy. He received fresh frozen plasma (FFP) to rapidly correct his coagulopathy.

Preop Investigations
Na 132, K 3.8, Cl 106, bicarbonate 25, urea 7.3 & creatinine 0.07 (all in mmol/l). Haemoglobin 135 g/l. INR 3.1 (prior to FFP).

On arrival in theatre
He was mildly febrile and tachypnoeic. He was able to talk and was not confused. Saturation was noted to be 85% (SpO₂) on room air and blood gases were collected from the arterial line in theatre prior to Anaesthetic induction.

Blood gases
The results (while breathing room air) were:

pH	7.506
pCO2	35.6	mmHg
HCO3	28	mmol/l
pO2	45.6	mmHg
BE	+5.1
SO2	85%
Hb	114	g/l
Na	139	mmol/l
K	3.7	mmol/l
Ionised Ca	1.11	mmol/l

Questions

[1] How would you analyse these results?
[2] What is the most serious abnormality present?
[3] What would you do about it?