ASSIGNMENT 1

SECTION
BSMT 3-A BSMT 3-A SCORE
GROUP
Group 5 7 DATE March 07, 2022

Members:

O Ramos, Rezzel – Answered ACP, LDH, CK, Troponin and case 3

O Regala, Earl Joval – Answered sodium, potassium, lactate, chloride and case 1

O Reyes, Angela – Answered AST, ALT, GGT, ACP, cholinesterase and cases 3 & 4 number 1

O Rodil, Nicole – Answered bicarbonate, calcium, phosphorus, magnesium and case 4

O Salve, Aezel - Answered Myoglobin, AML, Lipase, G6PD and case 2

I. In a Table form, give the enzymes we have studied and indicate

1. Tissue sources
2. Clinical significance
3. Methods used for its determination and the principle involved
4. Reference value/s

METHODS USED FOR ITS

 ENZYMES TISSUE SOURCES CLINICAL SIGNIFICANCE DETERMINATION AND THE REFERENCE
PRINICPLE INVOLVED VALUE
Transferases
 In the diagnosis of myocardial
infarction, hepatocellular diseases, and
involvement of skeletal muscle.
 Following an acute myocardial
infarction (AMI), AST levels start rising  Applying coupled enzyme
Aspartate
six to eight hours, peak at 24 hours, and kinetic reactions based on the 5-37 U/L
Transferase  Cardiac tissue return to normal within five days. Karmen method.
 Kidney  It is released to a greater degree in  The aspartate and oxoglutarate
(AST)
 Liver chronic disorders of the liver with in the AST sample react to
 Pancreas progressive damage. create oxaloacetate and NADH.
 Red blood cells  AST is used to monitor therapy with ALT and AST both use the
 Skeletal muscles potentially hepatotoxic drugs; a result Reitman and Frankel method.
greater than three times the upper
limit of normal should indicate that
therapy should be cancelled.
 Significant in the evaluation of hepatic
disorders
 Heart - markedly increased concentration  Following Karmen method, ALT
Alanine  Liver in acute inflammatory conditions is measured using lactate
 Lungs than AST. dehydrogenase as indicator 6-37 U/L
Aminotransferas
 Kidney  It also monitors the course of enzyme. LD catalyzes the
e  Pancreas hepatitis treatment and the effects of conversion of pyruvate to
 Red blood cell drug therapy. lactate with the subsequent
(ALT)
 Skeletal muscles  ALT measurement is a more sensitive oxidation of NADH to NAD+
and specific screening test for post-  Reitman and Frankel method
transfusion hepatitis or occupational
toxic exposure.
 ALT levels are also used to screen
blood donors.
 Hydrolases
 Alkaline Phosphate is
characterized using a variety of
methods, including
electrophoresis, heat
 When total ALP levels are increased, it fractionation or the stability
is the major liver fraction that is most test, chemical inhibition, and
frequently elevated – obstructive the Bowers and Mc Comb
jaundice. method.
 ALP is increased in obstructive jaundice  Bodansky, Shinowara, Jones,
 Liver due to greater rate of secretion. Reinhart method Adult
Alkaline  Bone  For bone disorders, highest elevations - End product : Inorganic male:
 Spleen occur in Paget’s disease (osteitis phosphorus glycerol 0 to 50
phosphatase
 Kidney deformans).  King and Armstrong method IU/L
(ALP)  Placenta  ALP levels increase with healing bone - End product: Phenol
 Intestine fractures.  Bessy, Lowry & Brock and Adult
 Renal  ALP levels are normally higher in Bowers and Mc Comb method female:
children than adults because of bone - End product: P-nitrophenol or 0 to 30
growth yellow nitrophenoxide ion IU/L
 ALP levels are normally higher in  Huggins and Talalay method
women during pregnancy because the - End product: Phenolphthalein
placenta is a source of ALP. red
 Low levels of ALP may also be due to  Moss method
deficiency of zinc or malnutrition. - End product: Alpha-naphtol
 Klein, Babson & Read method
- End product: Free
phenolphthalein
 Total ACP:

 For the detection of prostatic  Naphthyl phosphate is Male – 2.5

adenocarcinoma preferred for continuous -11.7 IU/L
 After surgical treatment of prostate methods
 Prostate gland cancer, ACP levels falls faster than PSA,  Gutman and Gutman method Female –
Acid and plasma levels are expected to be - End product: Inorganic 0.3 – 9.2
 Bone
IU/L
Phosphatase  Liver undetectable following complete phosphate
 Spleen removal of tumor.  Shinowara method
(ACP)  It is also useful in forensic clinical - End product: P-nitrophenol Prostatic
 Erythrocyctes
 Platelets chemistry, in the investigation of rap  Babson, Read and Phillips ACP:
cases – vaginal method
Male – 0.2
washings are examined for seminal - End product: Alpha-napthol
– 5.0 IU/L
fluid-ACP activity, which can persists for  Roy and Hillman (best method)
up to 4 days. - End product: Free Female –
thymolphthalein 0.0 – 0.8
IU/L
OTHER ENZYMES

 In the presence of GGT, the

 Increased levels in hepatobiliary gamma glutamyl residue L-y-
 Liver (canaliculi of diseases, with levels increasing to 2-5 glutamyl-3- carboxy-4
hepatic cells and times the upper reference limit; very nitroanilide is converted to Male - up
Gamma- epithelial cells sensitive indicator for these conditions. glycylglycine. The production to 55 U/L
lining biliary  Higher levels observed in intra- and and measurement of a at 37°C
Glutamyl
ductules) posthepatic biliary tract obstruction, chromogenic product at 405
Transpeptidase  Kidneys with levels increasing 5-30 times the nm is associated with GGT Female -
 Pancreas upper reference limit; increases before activity and concentration. up to 38
(GGT)
 Intestine and remains elevated longer than ALP,  Methods: U/L at 37°
AST and ALT. - Szass
 GGT activity induced by drugs (e.g. - Rosalki & Tarrow
phenobarbital and phenytoin) and by - Orlowski
 alcohol consumption.
 GGT levels are normal in the presence
of bone disease and during pregnancy
in contrast to alkaline phosphatase,
where levels would be elevated
 It affects the cell membrane and
microsomal fractions
- elevated among individuals
undergoing warfarin, phenobarbital
and phenytoin therapies.

 LD catalyzes the oxidation of

 Highest LD level is detected in cases of
lactate to pyruvate with the Forward
pernicious anemia and hemolytic
mediation of NAD. The reaction:
 Liver disorders.
pyruvate-to- lactate reaction
 Heart  Other diseases that may be associated (L -> P):
proceeds at about twice the
Lactate  Skeletal muscle with LD elevations are hepatic 100 - 225
rate as the forward reaction.
Dehydrogenase  Kidney disorders, acute myocardial infarction, U/L
 Using NADH as enzyme, LD
 Brain pulmonary infarct and acute
(LDH) catalyzes the conversion of
 Erythrocytes lymphoblastic leukemia.
pyruvate to lactate (reverse
 In AMI, LD levels rise within 8-12 hours. Reverse
reaction). The rate of
Peak at 24-48 hours, and return to reaction:
conversion of pyruvate to
normal in 7-10 days.
lactate and of reduced (P -> L): 80
 Although LD and LD isoenzymes are not
nicotinamide adenine – 280 U/L
used to diagnose AMI, knowledge of
dinucleotide (NADH) to
their pattern may be useful when
oxidized NAD is monitored at
assessing concurrent liver damage.
340 nm.
 Modified LDH Assay
  Elevations of total CK in serum are
associated with cardiac disorders, such
as AMI and skeletal muscle disorders,
such as muscular dystrophy  Tanzer-Gilbarg Assay Male: 15 –
(Duchenne’s) (forward/ direct method) – pH 160 U/L
 Brain tissue
Creatinine  Occasionally, elevations are due to 9.0, 340nm
 Smooth-skeletal
disorders of the CNS, including seizures Female: 15
Kinase muscles
and cerebral vascular accidents  Oliver-Rosalki – 130 U/L
(CK)  Heart muscles  Demonstration of elevated levels of CK- (reverse/indirect method) –
MB, ≥ 6% of the total CK is considered most commonly used method, CK-MB: <
to be the most specific indicator of faster reaction, pH 6.8; 340nm 6% of total
myocardial damage, particularly AMI CK
 The most specific indicator of
myocardial damage particularly AMI
 Used as an AMI indicator because of
specificity and early rise in serum
concentration following MAI. cTnT
 In cases of AMI, cTnT increases in 3-4 - 0.3
TROPONIN hours following infarction, peaks in 10- ng/m
 Skeletal muscle Quantified by immunoassay L
24 hours, and returns to normal in 10-
 Cardiac muscle 14 days. cTnI increases in 3-6 hours cTnI
following infarction, peaks in 14-20 - <
hours and remains elevated 5-10 days 0.40
ng/m
L

 Increased in skeletal muscle injuries,

Male – 30-
muscular dystrophy and AMI.
MYOGLOBIN 90 ng/mL
 Skeletal muscle  Myoglobin is released early in cases of Quantified by immunoassay
 Cardiac muscle AMI, rising in 1-3 hours and peaking in Female -
5-12 hours, and returns to normal in
 18-30 hours <50 ng/mL

 Saccharogenic – measures the

 Acinar cells of the  Increased AMS blood levels are
AMYLASE pancreas and the
salivary glands
(AML)  Adipose tissue  In acute pancreatitis (AP), AMS levels
 Fallopian tubes
 Small intestine
 Skeletal muscles
accompanied by increased urinary
excretion – acute pancreatitis.
rise 2-12 hours after onset of attack,
peak at 24 hours, and normalize within
3-5 days.
amount of reducing sugars
produced by the hydrolysis of
starch by the usual glucose
methods. it is the classic
reference method expressed in Somogyo
Somogyi units. units: 60-
 Amyloclastic – it measures 180 SU/dL
amylase activity by following
the decreases  in substrate
concentration (degradation of 95-290 U/L
starch).
 Chromogenic – it measures
amylase activity by the increase
in color intensity of the soluble
dye-substrate solution
produced in the reaction.
 Coupled-enzyme – it measures
amylase activity by a
continuous-  monitoring
technique.

 Cherry-Crandal using
 In acute pancreatitis (AP), LPS levels phenolphthalein as indicator,
 Pancreas
rise 6 hours after onset of attack, principle of most lipase
 Gastric mucosa peak at 24 hours, remains elevated procedure – titration liberated
LIPASE  Intestinal mucosa for 7 days, and normalize in 8-14 fatty acids. Substrate used is 0-1.0 U/mL
 Adipose tissue days. olive oil.
 In chronic AP, acinar cell  Teitz and Flereck involves
 degradation occurs resulting in loss hydrolysis of triglycerides in
of amylase and lipase production. olive oil into fatty acid and
diglyceride
 Peroxidase coupling – most
commonly used, doesn’t use
50% olive oil

 True
cholinesterase
- RBC
- Lungs  Pseudocholinesterase found in serum
- Spleen in decreased amount in hepatocellular
Male – 40-
- Nerve endings, disease due to decreased synthesis
78 U/L at
(e.g., hepatitis, cirrhosis)
CHOLINESTERAS - Gray matter of Butyrylcholine to thiocholine 37°C
E  Decreased PChE occurs in insecticide
the brain
poisonings Female –
 Pseudocholinester
as
 PChE testing identifies individuals with 33-76 U/L
atypical forms who are at risk of at 37°C
- Liver
prolonged response to muscle relaxants
- Pancreas
used in surgery
- Heart
- White matter of
the brain
- Serum

 Quantitative evaluation. G6PD

Glucose-6- activity is measured by its
 Clinical significance G6PD is remarkable
ability to reduce NADP to
Phospahte for its genetic diversity.
 Adrenal cortex NADPH in erythrocytes. 8-14U/g
 Many variants of G6PD, mostly
Dehydrogenase  The fluorescent spot test, HgB
produced from missense mutations,
 (G6PD)  Spleen have been described with wide-ranging which allows for direct
 RBC levels of enzyme activity and associated visualization of a fluorescently
 Lymph node clinical symptoms. tagged NADPH, is the most
commonly employed testing
method.

II. In a table form, give the electrolytes we have studied and indicate
1. Tissue sources
2. Clinical significance
3. Methods used for its determination and the principle involved
4. Reference value/s

METHODS USED FOR ITS

ELECTROLYTES TISSUE SOURCES CLINICAL SIGNIFICANCE DETERMINATION AND THE REFERENCE VALUE
PRINICPLE INVOLVED
 Low levels of Sodium in serum  Chemical Methods
 Sodium is the or plasma, particularly below - Flame Emission
most abundant 135 mmol/L or 130 mmol/L Spectrophotometry
cation in the respectively, indicates - Atomic Absorption
extracellular Hyponatremia.  Spectrophotometry
fluid  Decreased values may be due - ISE
 Sodium to increased water retention  ISE  Serum/Plasma:
concentration (retail failure, nephrotic - This uses a semipermeable 135-145
is largely seen syndrome, hepatic cirrhosis, membrane, which most mmol/L
SODIUM inside the cells. congestive heart failure), uses glas ion-exchange  Urine (24h): 40-
 Kidneys water imbalance, or sodium membrane, with different 220 mmol/L;
 Blood plasma loss in cases of low ion concentrations on both and varies with
and serum aldosterone, diuretics, salt- sides to create a potential. diet
 Lymph fluid losing nephropathy, or One electrode side is the  CSF: 135-
 Sodium levels Potassium deficiency. reference electrode with a 150mmol/L
 are partly  Increased Sodium in serum constant potential, while
controlled by experiencing Hypernatremia the other is the measuring
the aldosterone due to excessive water loss electrode. And the  ion
from adrenal (Nephrogenic or Central activity is measured either
glands. Diabetes insipidus), low water directly or indirectly. Direct
intake, or increased sodium measure uses an undiluted
intake or retention. sample, while indirect uses
dilute sample. 
- VITROS analyzers by Ortho-
Clinical Diagnostics use a
single-use direct ISA
potentiometric system.

 Increased plasma potassium

decreases cell’s Resting
Membrane Potential, thus
decreasing net difference of
 Major resting potential and
intracellular threshold 
cation  Tubular reabsorption and
 Found inside secretion regulates
the cells, potassium   Serum: 3.5-
mostly 20 times  Loss of potassium happens  ISE 5.1 mmol/L
more than when N, K -  ATPase pump is - the method uses a  Male Plasma:
outside inhibited by conditions like valinomycin membrane to 3.5-4.5
POTASSIUM  Skeletal and hypoxia, hypomagnesemia, or selectively bind potassium, mmol/L
cardiac muscles digoxin. that can cause an  Female
 Subcutaneous  Increases Na, K - apATPase impedance change Plasma: 3.4-
tissues pump upon usage of insulin to correlating as the K 4.4 mmol/L
 Red blood cells enter Potassium into skeletal concentration.  Urine (24h):
 Bones muscles and liver 25-125
 Kidneys  Diet may also affect  mmol/d
 Potassium is released from
 muscle cells during exercise,
thereby increasing plasma K
 Hyperosmolality in the case of
uncontrolled diabetes
mellitus
 Breakdown of cells due to
trauma, tumor lysis
syndrome, blood transfusion
releases K into extracellular
fluid
 Low plasma K concern e
traction shows Hypokalemia
brought up by GI or urinary
potassium loss, or increased
cellular potassium uptake
 Increased levels of potassium
indicated Hyperkalemia with
underlying conditions such as
decreased renal excretion in
cases of acute or chronic
renal failure,
hypoaldosteronism, Addison’s
disease, and diuretics.
Hyperkalemia is also caused
by cellular shift brought by
acidosis, muscle injury,
chemotherapy, leukemia and
hemolysis, and another is
caused by increased intake
like in  oral or IV Potassium
replacement therapy, and can
be artifactual.
  Major  Disorders relating to chloride  ISEs
extracellular are mostly a result of same - utilization of an ion-
anion causes when Na are disturbed exchange membrane to
 Almost  Excessive HCO3- loss in selectively bind chloride  Serum/Plasma:
completely Hyperchloremia due to GI ions  98-107 mmol/L
CHLORIDE absorbed by losses, RTA, or metabolic  Ampero metric-coulometric  Urine (24h):
intestinal tract acidosis. titration 110-250
 Filtered by  Excessive loss of chloride - utilization of coulemtric mmol/d; and
glomerulus and shows Hypochloremia due to generations of silver ions, varies with die
passive prolonged vomiting, diabetic combining it to chloride,
reabsorption ketoacidosis, aldosterone e and then can be quantitated
with sodium in deficiency, or salt-losing renal for Chloride concentration.
the proximal diseases like pyelonephritis,   Mercurimetric titration
tubules in the  Low serum chloride may also  Colorimetric
kidneys be seen in conditions with
 Blood high serum HCO3-  like during
Compensated respiratory
acidosis or metabolic alkalosis
 Enzymatic
Method
 By-product of - Venous:
an emergency 0.5-2.2
mechanism mmol/L
producing a  Metabolically monitoring (4.5-19.8
small amount critically ill patients  Blood Lactate measurements mg/dL)
of ATP used in  Type A lactic acidosis - hindered because of - Arterial:
severely - associated with hypoxia inefficiency and being 0.5-1.6
diminished conditions such as shock,  laborious mmol/L
oxygen delivery myocardial infarction,  Enzymatic methods (4.5-14.4
 Blood severe CHF, pulmonary - the method utilizes lactate mg/dL)
LACTATE  Red blood cells edema or severe blood oxidase to produce pyruvate - CSF: 1.0-
 Hepatocytes in loss and hydrogen peroxide. 2.9
the liver  Type B lactic acidosis - Pyruvate or hydrogen mmol/L
  Skeletal Metabolic peroxide may be used for (9-26
myocytes of - seen in  diabetes mellitus, the next reactions. mg/dL)
skeletal severe infections, Meanwhile, with hydrogen  Colorimetric
muscles leukemia, liver or renal peroxide, peroxidase can Whole Blood
 Brain disease and toxins like generate a chromogen - Venous:
 Gut or ethanol, methanol, or  Colorimetric Whole Blood 0.9-1.7
intestines with salicylate poisoning Method mmol/L
 Lactate are (8.1-15.3
metabolized in mg/dL)
the liver, - Arterial:
kidneys, and <1.3
heart; thus mmol/L
seeing them (<11.7
there as well mg/dL)

 Low level of bicarbonate may  CO2 measurements may be

cause a condition called
metabolic acidosis or too much
acid in the body
- Wide range of conditions
including diarrhea, kidney
 Bicarbonate is a disease, liver failure, can
byproduct of cause metabolic acidosis
body's - Also associated with
metabolism. diabetic ketoacidosis,
 Blood brings salicylate toxicity
bicarbonate to  High level of bicarbonate can
lungs, and then be from metabolic alkalosis,
exhaled as condition that causes a pH
BICARBONATE carbon dioxide increase in tissue
 Bicarbonate is - Metabolic alkalosis can
excreted and happen from loss of acid
obtained in several ways:
- ISE – for measuring total
CO2 uses an acid reagent to
convert all the forms of CO2-
to-CO2 gas and is measured
by a pco2 electrode
- Enzymatic method –
alkalinizes the sample to
convert all forms of CO2 to
HCO3 −. HCO3 − is used to
carboxylate
phosphoenolpyruvate (PEP)
in the presence of PEP
carboxylase, which catalyzes 22-29 mmol/L
the formation of
oxaloacetate
 reabsorbed by from the body such as
kidneys. through vomiting and
 This regulates dehydration
your body's pH, - It may be also related to
or acid balance. conditions including
anorexia and chronic
obstructive pulmonary
disease, emphysema
 Decreased ctCO2 associated
with metabolic acidosis,
diabetic ketoacidosis, salicylate
toxicity
 Increased ctCO2 associated
with metabolic alkalosis,
emphysema, severe vomiting
 Calcium in blood  Hypercalcemia
is only 1% of the - Caused by primary
total calcium in hyperparathyroidism,
the body; almost other endocrine disorders
99% of calcium is such as hypothyroidism
found in the and acute adrenal
bone insufficiency, malignancy
 Remaining 1% of involving bone and renal
 Bicarbonate reacts with
phosphoenolpyruvate (PEP) in the
presence of PEP Carboxylase to
produce oxaloacetate and
phosphate. This reaction is
coupled with one involving the
transfer of a hydrogen ion from
NADH analog to oxaloacetate
using malate dehydrogenase
(MDH).
 The resultant consumption of
NADH analog causes a decrease
in absorbance, which is
proportional to the concentration
of bicarbonate in the sample
being assayed.
 Spectrophotometric (O-
cresolphthalein complexone,
orzenazo III dye)
- Use metallochromic
indicators that bind calcium
using a color change o Easily
automated
 ISE (ion-specific electrode)
- With ISE analysis, the
specimen must be acidified
to convert protein-bound
and complexed calcium to Total calcium – 8.6-
the free form in order to 10.3 mg/dL
measure total calcium
 CALCIUM Ca is distributed failure  Atomic absorption (reference
in the blood and  Hypocalcemia method)
other - Caused by  Measure free (ionized) serum Free calcium – 4.6-
extracellular fluid hypoparathyroidism, calcium 5.3 mg/dL
and it may be in hypoalbuminemia,  Ion-specific electrode measures
the form of free chronic renal failure, free form
calcium, calcium magnesium deficiency  Measurement is temperature
bound to and vitamin D deficiency sensitive
proteins and  Tetany – a condition associated  Generally, analysis is performed
calcium bound to with decrease in serum calcium at 37°C
anions such as  Calcium ions react with o-cresol-
phosphates, phthalein complexone in an
citrates and alkaline medium to form a
bicarbonates purple-colored complex
 The absorbance of this complex is
proportional to the calcium
concentration in the sample

 Serum or lithium heparin plasma

is acceptable for analysis
 Most of the current methods for
phosphorus determination
involve the formation of an
ammonium phosphomolybdate
complex.
 Hyperphosphatemia  This colorless complex can be
 Bulk of the - Caused by renal failure, measured by ultraviolet
phosphates in hypoparathyroidism, absorption at 340 nm or can be
the body is found neoplastic diseases, reduced to form molybdenum
in the bones and lymphoblastic leukemia blue, a stable blue chromophore,
PHOSPHORUS only a small and intense exercise which is read between 600 and
portion is found  Hypophosphatemia 700 nm.
 in the soft tissues - Diabetic ketoacidosis,  Ammonium molybdate + 2.5-4.5 mg/dL
and in hyperparathyroidism, phosphate ions 
serum/plasma asthma, alcoholism and phosphomolybdate complex
malabsorption syndrome (colorless)
 When aminonaphthol-sulfonic
acid is used to reduce the
complex, a colored product is
formed
 Phosphate reacts with molybdate
in strong acidic medium to form a
complex.
 The absorbance of this complex in
the near UV is directly
proportional to the phosphate
concentration
 Most of  Hypermagnesemia  Colorimetric method:
magnesium is - Caused by renal failure - Calmagite: Mg2+ binds with
found in the (most frequent) and calmagite to form a reddish-
bones, and some excess acidosis violet complex that may be 1.7-2.4 mg/dL
MAGNESIUM are found in the  Hypomagnesemia read at 532 nm
muscles, soft - Caused by gastrointestinal - Formazan dye: Mg2+ binds
tissues serum disorders, renal diseases, with the dye to form a
and red blood hyperparathyroidism colored complex that may
cells (hypercalcemia) be read at 660 nm
- Drugs (e.g. diuretic - Methylthymol blue: Mg2+
therapy, cardiac binds with the chromogen
glycosides, cisplatin, to form a colored complex
cyclosporine)  Atomic absorption
- Diabetes mellitus with  Spectro-photometry (reference
glycosuria method)
- Alcoholism due to dietary  Measure free (ionized) serum
deficiency magnesium; ion-selective
electrode
  Magnesium ions in an alkaline
medium form a colored complex
with xylidyl blue.
 The increase in absorbance is
proportional to the magnesium
concentration in the sample.
Glycotherdiamine— N1N1N’ 1N’
1 tetraacetic acid (GEDTA) is used
as masking agent for calcium ions

III. In all the following cases (below), answer the following questions:
1. Is the blood acidemic or alkalemic?
2. Determine whether the primary disorder is respiratory or metabolic.
3. Calculate the anion gap.
a. Case 1
A 70 year-old smoker presents with an acute onset of shortness of breath with the following results:
 ABG: pH = 7.30; PCO2 = 60 mmHg; PO2 = 60 mmHg
Metabolic panel: Na = 135; Cl = 100; HCO3 = 30
b. Case 2
A 22 year-old woman presents with 4 hours of numbness in both hands typical of previous episodes of anxiety
ABG: pH = 7.48; PCO2 = 30 mmHg; PO2 = 86 mmHg
Metabolic panel: Na = 140; Cl = 110; HCO3 = 22
c. Case 3
A 32 year-old man with depression and alcohol abuse presents with altered status
ABG: pH = 6.9; PCO2 = 29; PO2 = 100
Metabolic panel: Na = 140; Cl = 101; HC3 = 5
d. Case 4
A 68 year-old man who recently took antibiotics for a skin infection presents with 10 episodes of watery diarrhea per
day for the last five (5) days
ABG: pH = 7.34, PCO2 = 34; PO2 = 80
Metabolic panel: Na = 135; Cl = 108; HCO3 = 18

Answers

a. Case 1

A 70 year-old smoker presents with an acute onset of shortness of breath with the following results:
ABG: pH = 7.30; PCO2 = 60 mmHg; PO2 = 60 mmHg
Metabolic panel: Na = 135; Cl = 100; HCO3 = 30
 1. Is the blood acidemic or alkalemic? 
The blood is acidemic because the arterial blood pH is less than 7.35

2. Determine whether the primary disorder is respiratory or metabolic. 

The patient’s primary disorder is related to respiratory problems. Based on the values of ABG and metabolic
panel above, the pCO2 was elevated by 20 units, which should show a 2 units increase in HCO3 if acute and 8 units of
chronic. And because the HCO3 increased from 24 to 30, with 6 units increased, the patient is experiencing acute on
chronic respiratory acidosis

3. Calculate the anion gap.

Reference Value: 8-16 mmol/L
AG = Na+ - (Cl- + HCO3)
AG = 135 - (100 +26)
AG = 135 – 126
AG = 9 mmol/L
b. Case 2
A 22 year-old woman presents with 4 hours of numbness in both hands typical of previous episodes of anxiety
ABG: pH 7.48, pCO230 mmHg, pO286 mmHg
Metabolic panel: Na 140, Cl 110, HCO322
1. Is the blood acidemic or alkalemic
The blood is alkalemic because the arterial blood pH is greater than 7.35

2. Determine whether the primary disorder is repiratory or metabolic

The patient’s primary disorder is related to respiratory problems.
3. Calculate the anion gap
- AG 140-(110+22) = 8mmol/L
c. Case 3
32-year-old man with depression and alcohol abuse presents with altered mental status.
ABG: pH 6.9, pCO2 29, pO2 100
 Metabolic panel: Na 140, Cl 101, HCO3 5
1. Is the blood acidemic or alkalemic?
The blood is acidemic because the arterial blood pH is less than 7.35
2. Determine whether the primary disorder is respiratory or metabolic.
The patient’s primary disorder is related to metabolic problems.
3. Calculate the anion gap.
AG = 140 – (101 + 5) = 34 mmol/L
d. Case 4
A 68-year-old man who recently took antibiotics for a skin infection presents with 10 episodes of watery diarrhea per day
for the last five (5) days
ABG: pH = 7.34, PCO2 = 34; PO2 = 80
Metabolic panel: Na = 135; Cl = 108; HCO 3 = 18
In all the following cases (below), answer the following questions:
1. Is the blood acidemic or alkalemic?
The blood is acidemic because the arterial blood pH is less than 7.35
2. Determine whether the primary disorder is respiratory or metabolic.
The patient’s primary disorder is related to metabolic problems.
3. Calculate the anion gap.
AG = 135 – (108 + 18) = 9 mmol/L