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who maintain the acid base balance
- complex systems of buffers
princible buffer and the other buffers
- princible buffer is carbonic acid/ bicarbonate system
- other buffers are proteins, phosphate and HB
ph : ???
- ph: 7.36- 7.44
- lower acidemia
- higher alkalemia
- Provides information about the adequacy of lung function
- in excreting CO2. Increase CO2 reflects inadequate ventilation.
PO2 (100 mm hg)
has to relate the result ot the oxygen-hgb dissociation curve
this reflect bicarbonate so it is a measure of a base
reflects alteration in fluid status or acid- base balance.
is a byproduct of anaerobic metabolism of glucose. in patients with inadequate tissue perfusion or increased tissue metabolic rates anaerobic metabolism predominates. lactate level increases
- low ph, low serum bicarbonate, body compensate by hyperventilation and low PaCo2.
- causes are:
- renal failure
- ketoacidosis (DM, starvation, ethanol)
- lactic acidosis( shock, liver disease)
- intoxication (salicylates)
- drugs( amphotericin, li, carbonic anhydrase inhibitors )
- high PH, high serum bicarbonate, compansate by hypoventilation
- causes :
- mineralcorticoid excess
- alkali administration
- diuretic therapy
- decrease ph, increase PaCO2, increase bicarbonate
- cause is hypoventilation either :
- CNS disorder,
- neuromuscular disorder ( mysthemia gravis)
- lung disorder( airway obstruction, asthma, COPD, pulmonary edema)
- increase ph, decrease CO2, decrease bicarbonate
- lung disease( pneumonia)
- CNS stimulation (CvA, Fever, anxiety)
myocardial dysfunction due to:
- valvular heart disease
- congenital heart disease
- Normal values vary depending on the individual muscle mass. Males tend to have higher
- Levelsrise sharply 6-8 hours after AMI.
They can also increase after trauma, IM injection, surgery, vigorous excercise.
- There are 3 CK isoenzymes. Elevated CK-MB is
- relatively specific for MI.
Lactate dehydrogenase (LDH) & other tests
- High LDH concentration occur in skeletal muscle, liver, RBC, kidneys, & heart.
- After AMI LDH does not increase until 12 hours after chest pain. It peaks at 3-4 days.
- LDH has 5 isoenzymes. In the heart LDH1 & to a lesser extent 2 predominate.
- Other blood tests: AST, Myoglobin(Within 2hours & clear rapidly).
- CRPwill be also elevated in acute MI.
- cardiac troponins I & T This chemical is present in heart muscle cells. Damage to heart muscle cells releases troponin into the bloodstream. with an MI, the blood level of troponin increases within 3-12 hours from the onset of chest
- pain, peaks at 24-48 hours, and returns to a normal level over 5-14 days.
- Very specific to cardiac tissue, 100% of AMI will have elevated levels, considered best marker
- due to high specificity.
Diagnosis of AMI
- •Two biochemical markers should be used for routine diagnosis.
- •With definitive ECG changes no need for markers (T-wave inversion or elevation, ST
- elevation, appearance of Q-waves.
•In the absence of definitive ECG changes do serial tests.
Electrocardiography & other exams
- •ECG: Diagnosis &
- location of MI. Cardiac rhythm.
•Echocardiography:Visualize structural anatomy & assess LV ejection fraction. (Wall thickness & motion).
- •Cardiac angiography. (Diagnose presence of CAD, visualize coronary arteries, estimate cardiac & valvular performance)
- •Myocardial perfusion imaging
•CT scan ,MRI, PET scan.
- •It is the largest solid organ in the body. Weighing between 1200 7 1500 g. It is
- located in the right upper quadrant of the abdomen.
- •It produces bilirubin, a product of Hgb breakdown, excreted via the bile duct.
- •Plays a major role in AA & carbohydrate metabolism. (Coagulation factors & albumin)
- •Most lipids & lipoprotein including cholesterol are synthesized in the liver.
- •The primary location for most drug & hormonal metabolism including barbituates, certain
- tranquilizers, sex hormones, H2-blockers,& many narcotics.
- •It is affected by many systemic diseases, but is capable of regeneration.
Tests of liver synthetic capabilities
- •Total protein is the
- sum of Albumin & globulin.
- •Albumin: 3.5-5 g/dL. Important in maintaining plasma oncotic pressure. Symptoms when it is less than 2. & in cases where the synthetic ability of the liver is affected. Other causes is malabsorption, nephrotic syndrome, malnuitrition.
- •Globulin increase in inflammation.
- •Prothrombin time: Many factors synthesized in the liver.
Cholestatic liver disease
•Alkaline phosphatase: Normal values vary with age, bone disorders can increase its level.
- •5’nucleotide. It is elevated only in liver diseases.
- •Gamma GT: No origin in bone or placenta. Can be elevated in non liver disease, but a
- marked elevation points to liver.
- •Aminotransferases are the most frequent measured indicators of hepatic diseases. Both AST (SCOT), & ALT (SCPT) are very sensitive indicators.
- •Markedly high levels indicate: viral hepatitis, severe drug toxicity, or ischemic hepatitis.
- •Jaundice becomes visible when total bilirubin is 2-4 mg/dL.urine may be dark.
- •Uncojugated/indirect: Increase in hemolytic process. Large hematoma, transfusion of old blood, hemolytic anemia, neonatal jaundice.
- •Conjugated/Direct :reflect liver disease.
- •Amylase, an enzyme, helps break starch into its glucose molecules. Found in pancreas & salivary glands. It is the single most useful biochemical test to diagnose acute pancreatitis. It could be elevated in Alcholism, drugs, gallstone, hypercalcemia, trauma.
- •Lipase increase in acute pancreatitis less sensitive but more specific.
•IT is a Gram-negative, microaerophilic bacterium that can inhabit various areas of the stomach, particularly the antrum. It causes a chronic low-level inflammation of the stomach lining and is strongly linked to the development of duodenal and gastric ulcers, stomach cancer. Over 80 percent ofindividuals infected with the bacterium are asymptomatic.
- •Normal serum Na: 136-145 mEq/L
- •When encounter an asymptomatic patient the clinician should suspect an error.
- •Agitation,anorexia, disorientation, depressed DTR, seizures.
- •Hyponatremia with low body Na: vomiting, diarrhea, pancreatitis, diueritics.
- •With normal body Na: dilutional type,hypothyroidism, glucocorticoid deficiency, increase water adminstration
•High total Na: e.g. Chronic heart failure, cirrhosis,CRF.
•It is less common than hyponateremia
- •Found in those with impaired thirst mechanism(neurohypophyseal lesion), or inability to replace water depleted from skin, respiration, renal, & GI.
- •Manifestation is primarily neurological.
•Normal range: 3.5-5.0 mEq/mL.
- •Intracellular shifting: Alkalosis, insulin.
- •K loss: From kidney or GI
- •GI:vomiting, diarrhea, laxative abuse, intestinal fistula.
- •Decrease intake: e.g. K-free IV fluid.
- •Renal: Corticosteroids, Amphotericin B, Diuretics, Hyperaldosteronism, Cushing syndrome, licorice abuse.
- •Primarily concerned on cardiac rhythm also muscle arreflxia.
- •Extracellular shifting: metabolic acidosis.
- •Increased intake: Hemolysis, rhabdomyolysis, muscle crushinjuries, burns, Salt substitutes.
- •Decrease output: Chronic renal failure, deficiency of adrenal steroids, addison’s disease.
- •Drugs:K-sparing diuretics, NSIDs, heparin,Angiotensin- converting enzyme inhibitor.
- •The main signs & symptoms are cardiological
- •Fictitious Hyperkalemia in hemolyzed sample.
- •Also if sample clotted.
- •Normal range: 1.5-2.2 mEq/L
- •Hypo:more common than hyper, result from GI or kidney loss, poor intestinal absorption, chronic alcohol consumption. Manifestation weakness, tremor, tetany, personality problems & cardiac.
- •Hyper:Increase intake e.g. Antacids, rapid infusion. Neuromuscular signs
- •8.5-10.8 mEq/mL
- •Plays an important role in N-M activity, endocrine functions, blood coagulation, & bone metabolism.
- •Ca is regulated by PTH, serum P, vit.D, & target organ
- •Found as complex bound (6%), Protein bound (40%), Free (54%)
- •Medications: Calcitonin, Clucocorticoids, loop diuretics,
- phosphate salts
- •Hyperphosphatemia, hypoalbuminemia, hypomagnesemia, hypoparathyroid, pancreatitis, renal
- failure, secondary hyperpara. Vit D deficiency.
- •Finger numbness, burning of extremities, tetany.
- •Malignancy, primary hyperparathyroidism.
- •Calcium supplements, immobilization, Excess vit D, Estrogen, progesterone
- •Lethargy, psychosis
- •Factitious results if tourniquet is left too long or if albumin is very high
- •Normal: 2.6-4.5
- •Hypo:Increase renal excretion, intracellular shifting, decrease phosphate or vit. D intake. Neurological irritability occurs when P is less than 2 mEq/mL.
- •Hyper: Decrease renal excretion (CRF), extracellular shifting, Increase vitD or phosphate
- intake.. Symptoms are primarily hypocalcemia
- •They filter about 180L of fluid each day; of this amount they excrete 1.5L as urine. Thus, more than 99% of the glomerular filtrate is absorbed back into the blood
- stream as urine. Many solutes that are not reabsorbed are concentrated in the urine e.g. creatinine, urea.
- •GFRis the volume of water filtered out of plasma per minute through the
- surrounding capillary walls into Bowman’s spaces.
Blood urea nitrogen (BUN)
- •Normal range: 8-20 mg/dL.
- •BUN is the concentration of N in the serum & not blood. It reflects GFR but not ideal. It depends also on urea production in the liver& tubular reabsorption.
- •BUN can be used to assess hydration status, renal function, protein tolerance,& catabolism in numerous clinical settings
- •Azotemia: other than renal failure may be caused by a high protein diet, upper GI bleeding (blood being digested), administration of corticosteroids, tetracycline or any other drug with antianabolic effects.
- •Decreased BUN does not have pathophysiological consequences.
Common causes of BUN elevation
- 1-Prerenal: Decreased renal perfusion secondary to blood loss, dehydration or shock.
- Increase protein breakdown: GI bleed, crash
- injury, burn, excess protein intake, corticosteroid, tetracycline.
- 2- Intrarenal: Acute & chronic renal failure
- 3- Postrenal: Obstruction of ureter or bladder.
- •Normal range: 0.7-1.5 mg/dL.
- •Non protein nitrogenous biochemicals of the blood. After synthesis in the liver , creatinine is taken by muscle
- cells & is stored as creatinine phosphate.
- •A rise in SCr. Almost always indicates worsening renal function.
- •Muscle mass, & some dugs affect Scr. levels
Drugs reported to cause increase serum creatinine
BUN /Cr. ratio
- •Ratio greater than 20/1 suggest prerenal causes.
- •Ratio 10/1 to 20/1 suggest intrinsic renal damage..
- •Both types may occur simultaneously confounding typical interpretations.
- •Crcl provides the best approximation of the GFR.
- •Tests asked to assess kidney function, moniter patients on nephrotoxic drugs, or for dosage adjustment.
- •Crcl= UV/P x 1.73/BSA
- •U: Creatinine in urine
- •V: Urine volume
- •P: Plasma creatinine
- •BSA: Body surface area (Standard normogram).
- •Unadjusted clearance: Ucr. x 0.07 / SCr.