Uploaded by Muran Mujahed

case 1- nikol

Nikol is a 16 year old female that presents to the emergency department with deep breathing,
nausea and vomiting. She also has frequent urination but no hematuria nor ​dysruia. She is
disoriented and holds a can for vomiting, and has acetone smell.
What is metabolic acidosis?
Metabolic acidosis​:​ clinical disturbance characterized by an increase in plasma acidity; due to
increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete
excess acids
When you have ​diabetes​ and don't get enough insulin and get dehydrated, your body burns fat
instead of carbs as fuel. Breaking down fatty acids produces ketones, which can make your
blood acidic. (​diabetic​ ketoacidosis/ DKA)
How does the body respond to metabolic acidosis?
*As blood pH drops (becomes more acidic), the parts of the brain that regulate breathing are
stimulated to produce​ faster and deeper breathing​ (​respiratory compensation​). Breathing
faster and deeper increases the amount of carbon dioxide exhaled.
*Respiratory compensation for metabolic acidosis increases the respiratory rate to ​drive off
CO2​ and readjust the bicarbonate to carbonic acid ratio to the 20:1 level.
*The kidneys also try to compensate by ​excreting more acid in the urine, ​ which in turn
facilitates the excretion of acid and partially ​restore systemic acid-base balance.
Elevated levels of blood glucose and ketone bodies ​are the hallmarks of ​untreated T1D.
Hyperglycemia is caused by increased hepatic production of glucose via gluconeogenesis,
combined with diminished peripheral utilization,
Diabetic ketoacidosis (DKA)​,​ a type of metabolic acidosis, occurs in T1D. DKA is treated by
replacing fluid and electrolytes and administering short-acting insulin to gradually correct
hyperglycemia without precipitating hypoglycemia
Signs and symptoms of diabetic ketoacidosis include:
*Nausea *Vomiting *Abdominal pain *A sweet, fruity smell on your breath *Weight loss.
The pancreas
the pancreas ​has 2 systems:
the exocrine gland and the
endocrine gland
*​endocrine function​; releases
juices (enzymes) directly into
the bloodstream.
*​exocrine function;​ releases juices into ducts.
The pancreatic juice has a ​pH of 8.0- 8.3,​ and the pH of liver bile is 7.8
pancreatic islets — the islets of Langerhans— secrete the hormones glucagon, insulin,
somatostatin, and pancreatic polypeptide (PP)
Pancreas endocrine​ function involves the secretion of insulin, and glucagon; that regulate the
rate of glucose metabolism in the body.
*​The alpha cell ​produces the hormone ​glucagon​ and makes up approximately 20 percent of
each islet. ​Low blood glucose levels stimulate the release of glucagon.
*​The beta cell ​produces the hormone ​insulin​ and makes up approximately 75 percent of each
islet. ​Elevated blood glucose levels stimulate the release of insulin.
*​The delta cell ​accounts for four percent of the islet cells and secretes the peptide hormone
somatostatin​. Which is also released by the hypothalamus, stomach and intestines. An
inhibiting hormone that ​inhibits the release of both glucagon and insulin.
*​The pancreatic polypeptide cell​ (PP cell) accounts for about one percent of islet cells and
secretes the ​pancreatic polypeptide hormone.​ It plays a role in appetite, and in the regulation
of pancreatic exocrine and endocrine secretions.
The pancreas is divided into ​lobules by
connective tissue septae. ​Lobules are
composed largely of grape-like clusters
of exocrine cells called ​acini​, which
secrete ​digestive enzymes​. Exocrine
secretions from acini flow through
intercalated ducts, intralobular ducts,
interlobular ducts​ and finally into the
duodenum​ through the main
pancreatic​ ​duct​.
Vomiting​: the forceful expulsion of stomach contents via the
mouth or sometimes the nose, also known as ​emesis.​ The
causes of vomiting are as wide ranging as those for nausea
and include anything from food poisoning or gastritis to head
injuries and brain cancer. ​Nausea​ is the discomfort that is felt
before vomiting but not all nausea actually results in
Vomiting​ is the means by which the ​upper gastrointestinal
tract​ rids itself of its contents when almost any part of the
upper tract becomes excessively ​irritated​, ​overdistended​, or even ​overexcitable​. Excessive
distention or irritation of the duodenum provides an especially strong stimulus for vomiting.
The ​sensory signals​ that initiate vomiting originate mainly from the ​pharynx, esophagus,
stomach, and upper portions of the small intestines.​ And the nerve impulses are transmitted by
both ​vagal and sympathetic afferent nerve fibers ​ to the vomiting center. From here, ​motor
impulses ​that cause the actual vomiting are transmitted from the vomiting center by way of
1. fifth, seventh, ninth, tenth, and twelfth cranial nerves to the upper gastrointestinal
2. vagal and sympathetic nerves to the lower tract,
​ ​spinal nerves to the diaphragm and abdominal muscles​.
In the early stages of excessive gastrointestinal irritation or overdistention, ​antiperistalsis
begins to occur often many minutes before vomiting appears. (Antiperistalsis: peristalsis up
the digestive tract rather than downward)
Vomiting Act​.
Once the vomiting center has been sufficiently stimulated and the vomiting act instituted, the
first effects are
1. a deep breath,
raising of the hyoid bone and larynx to pull the upper esophageal sphincter open,
3. closing of the glottis to prevent vomitus flow into the lungs, and
4. lifting of the soft palate to close the posterior nares. Next comes a strong downward
contraction of the diaphragm along with simultaneous contraction of all the abdominal
wall muscles. This squeezes the stomach between the diaphragm and the abdominal
muscles, building the intragastric pressure to a high level.
5. Finally, the lower esophageal sphincter relaxes completely, allowing expulsion of the
gastric contents upward through the esophagus
Thus, the vomiting act results from a ​squeezing action​ of the ​muscles of the abdomen
associated with simultaneous​ contraction of the stomach wall ​and ​opening of the esophageal
sphincters ​so that the gastric contents can be expelled.
​leading cause of adult ​blindness​ and ​amputation​ and a major cause of ​renal failure​, ​nerve
damage,​ ​heart attacks​, and ​strokes​.
Most cases of diabetes mellitus can be separated into two groups:
1. type 1 [T1D] formerly called insulin-dependent diabetes mellitus
2. type 2 [T2D] formerly called noninsulin-dependent diabetes mellitus
Other types of diabetes include:
-​Gestational diabetes​ is a condition in which blood sugar levels become high during pregnancy
-​Diabetes insipidus (DI)​ is a condition characterized by large amounts of dilute urine and
increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of
fluid has little effect on the concentration of the urine. ​Complications may include dehydration
or seizures.
Type 1 diabetes:
The disease is characterized by ​deficiency of insulin​ caused by an ​autoimmune attack on the β
cells of the pancreas​. In T1D, the islets of Langerhans become infiltrated with ​activated T
lymphocytes​, leading to a condition called ​insulitis​. Over a period of years, this autoimmune
attack on the β cells leads to gradual depletion of the β-cell population, symptoms appear
abruptly when 80%– 90% of the β cells have been destroyed. At this point, the ​pancreas fails to
respond adequately to ingestion of glucose​, and insulin therapy is required to restore
metabolic control and prevent life-threatening ​ketoacidosis​.
The onset of T1D is typically during childhood or puberty, and symptoms ​develop suddenly.
Patients with T1D can usually be recognized by the abrupt appearance of ​polyuria​ (frequent
urination), ​polydipsia​ (excessive thirst), and ​polyphagia​ (excessive hunger). These symptoms
are usually accompanied by ​fatigue and weight loss.
The diagnosis ​ is confirmed by
1. glycosylated hemoglobin concentration ≥ 6.5 mg/dl ​(normal is less than ​5.7​)
2. fasting blood glucose ≥ 126 mg/dl ​(normal is 70–99)
3. nonfasting (random) blood glucose level ≥200 mg/dl​ in an individual with symptoms of
When blood glucose is ​greater than 180 mg/dl,​ the ability of the kidneys to reclaim glucose is
impaired. This results in glucose ​spilling into the urine​. The loss of glucose is accompanied by
the ​loss of water​, resulting in the characteristic ​polyuria​ (and dehydration) and ​polydipsia​ in
The metabolic abnormalities ​of T1D mellitus result from a deficiency of insulin that profoundly
affects metabolism in three tissues: liver, muscle, and adipose tissues.
Treatment of type 1 diabetes; ​periodic injection or continuous pump-assisted infusion to
control the hyperglycemia and ketoacidosis
Contraindications for tight control​: Children are not put on a program of tight control of blood
glucose before age 8 years because of the risk that episodes of ​hypoglycemia ​may adversely
affect​ brain development​. Elderly people
typically do not go on tight control
because ​hypoglycemia​ can cause ​strokes
and heart attacks​ in this population.
Type 2 Diabetes:
Patients with T2D have a combination of
insulin resistance and dysfunctional β
cells. ​but do ​not require insulin​ to sustain
life, although insulin eventually will be
required to control hyperglycemia.
T2D is characterized by ​hyperglycemia;
insulin resistance; impaired insulin
secretion; and, ultimately, β-cell failure.
insulin resistance is characterized by
increased hepatic glucose production,
decreased glucose uptake by muscle and
adipose tissue, and increased adipose
lipolysis with production of free fatty
Obesity is the most common cause of insulin resistance and T2D, ​ Insulin resistance increases
with weight gain and decreases with weight loss,​ and excess adipose tissue is key in the
development of insulin resistance, With obesity, there are changes in adipose secretions that
result in insulin resistance. ​In the long-term, FFAs suppress glucose-induced insulin release.
With time β cell becomes increasingly dysfunctional and ​fails to secrete enough insulin to
correct the prevailing hyperglycemia.
is caused by i​ncreased hepatic production of glucose​, ​diminished peripheral use​. ​Ketosis​ is
usually minimal or absent in patients with T2D because the ​presence of insulin​, even in the
presence of insulin resistance, restrains hepatic ketogenesis
Because lipoprotein degradation catalyzed by lipoprotein lipase in adipose tissue is low in
diabetics, the plasma ​chylomicron and VLDL levels ​are elevated, resulting in
treating T2D is to maintain blood glucose concentrations within normal limits and to prevent
the development of long-term complications
Alpha-glucosidase inhibitors
These medications help your body break down starchy foods and table sugar. This effect
lowers your blood sugar levels; ​acarbose (Precose), miglitol (Glyset)
Biguanides decrease how much sugar your liver makes. The most common biguanide is
glucose uptake into muscle cells and adipocytes:
Glucose cannot diffuse directly into cells but enters by one of two transport mechanisms: a
Na+-independent​, ​facilitated diffusion ​transport system or an ATP-dependent Na+monosaccharide cotransport system.
Sodium-independent facilitated diffusion transport system
This system is mediated by a family of 14 glucose transporters
found in cell membranes. They are designated ​GLUT-1 to GLUT-14
Sodium–monosaccharide cotransport system
This is an energy-requiring process that transports glucose “against” a concentration gradient,
Glycogen is synthesized from molecules of​ α-D-glucose​. The
process occurs in the ​cytosol​ and ​requires energy​ supplied by
ATP (for the phosphorylation of glucose) and uridine
triphosphate (UTP).
1. Synthesis of uridine diphosphate glucose
2. Synthesis of a primer to initiate glycogen synthesis
3. ElongFormation of branches in glycogen
4. elongation of glycogen chains by glycogen synthase
1. Shortening of chains
2. Removal of branches
3. Conversion of glucose 1-phosphate to glucose 6-phosphate
4. Lysosomal degradation of glycogen
1. Phosphorylation of glucose
2. Isomerization of glucose 6-phosphate enzyme
phosphoglucose isomerase
3. Phosphorylation of fructose 6-phosphate
4. Cleavage of fructose 1,6-bisphosphate
5. isomerization of dihydroxyacetone phosphate
6. Oxidation of glyceraldehyde 3-phosphate
7. Synthesis of 3-phosphoglycerate, producing ATP
8. Dehydration of 2-phosphoglycerat
Formation of pyruvate, producing ATP
1. Pyruvate carboxylase converts pyruvate
to oxaloacetate in the mitochondrion.
2. Oxaloacetate is converted to malate or
aspartate, which travels to the cytosol
and is reconverted to oxaloacetate.
3. Phosphoenolpyruvate carboxykinase
converts oxaloacetate to
4. Phosphoenolpyruvate forms fructose
1,6-bisphosphate by reversal of the steps
of glycolysis.
5. Fructose 1,6-bisphosphatase converts
fructose 1,6-bisphosphate to
fructose-6-phosphate, which is converted
to glucose-6-phosphate.
6. Glucose-6-phosphatase converts
glucose-6-phosphate to free glucose,
which is released into the blood.
Fatty acid synthesis;
In adult humans, fatty acid
synthesis occurs primarily in
the ​liver ​and ​lactating
mammary glands​ and, to a
lesser extent, in ​adipose tissue
catabolic process by which ​fatty acid ​molecules are
broken down​ in the cytosol in prokaryotes and in
the mitochondria in eukaryotes to generate
amino acids synthesis and breakdown;
The ​liver​ is the only tissue that has all the
pathways of​ amino acid synthesis and
degradation​. During fasting, the carbon
skeletons of amino acids produce glucose,
ketone bodies, and CO2; in the fed state the
liver can convert intermediates of amino
acid metabolism to triacylglycerols; the fate
of amino acid carbon skeletons, thus,
parallels that of glucose and fatty acids
Ketone bodies​;
produced using ​acetyl-CoA ​derived from ​fatty acid β-oxidation​ in the liver under specific
metabolic conditions. The two ketone bodies are ​acetoacetate and β-hydroxybutyrat
Ketone Body Synthesis
Two molecules of ​acetyl-CoA ​are condensed to form a
​ cetoacetyl-CoA​, which is then conjugated
to another molecule of acetyl-coA to form​ 3-hydroxy-3-methylglutaryl-CoA ​(HMGCoA).
Maintaining blood glucose;
Eating a healthy diet with plenty of fruit and vegetables, maintaining a healthy weight, and
getting regular physical activity can all help maintaining normal levels of blood glucose
1. Keep track of your blood sugar levels to see what makes them go up or down.
2. Eat at regular times, and don’t skip meals.
3. Choose foods lower in calories, saturated fat, trans fat, sugar, and salt.
4. Track your food, drink, and physical activity.
5. Drink water instead of juice or soda.
6. Limit alcoholic drinks.
7. choose fruit, instead of sweets.
8. Control your food portions (for example, use the plate method: fill half your plate with
non-starchy vegetables, a quarter with lean protein, and a quarter with a grain or
starchy food).
Maintaining normal blood sugar levels is a very important part of ​avoiding long-term health
issues​, managing your weight and just feeling good. Health problems related to blood sugar
imbalances are a rapidly growing
To avoid;
1. cardiac or vascular event, such as myocardial infarction (heart attack) or stroke;
2. kidney problems that may require dialysis;
3. eye problems, which may lead to loss of vision (blindness);
4. sexual issues, such as erectile dysfunction;
5. problems with circulation and scarring, which can lead to amputation.
Receptors in the pancreas can sense the ​decline
in blood glucose levels, such as​ during periods
of fasting or during prolonged labor or
exercise​. In response, the ​alpha cells​ of the
pancreas secrete the hormone ​glucagon​, which
has several effects:
1. Glucagon ​stimulates​ the liver to convert its stores of ​glycogen back into glucose.​ This
response is known as ​glycogenolysis​. The glucose is then released into the circulation
for use by cells throughout the body.
2. Glucagon ​stimulates​ the liver to take up ​amino acids​ from the blood and convert them
into glucose. This response is known as ​gluconeogenesis​.
3. Glucagon ​stimulates​ ​lipolysis​, the breakdown of stored​ triglycerides into free fatty
acids and glycerol.​ Some of the free glycerol released into the bloodstream travels to the
liver, which converts the glycerol into glucose. This is also a form of gluconeogenesis.
Taken together, these actions ​increase blood glucose levels​. The activity of glucagon is
regulated through a negative feedback mechanism; rising blood glucose levels inhibit further
glucagon production and secretion.
The primary function of insulin is to ​facilitate the
uptake of glucose into body cells
The presence of food in the intestine triggers the
release of ​gastrointestinal tract hormones ​such as
glucose-dependent insulinotropic peptide​ (known
as gastric inhibitory peptide). This is the initial
trigger for ​insulin production and secretion by the
beta cells of the pancreas.​ Once nutrient
absorption occurs, the resulting surge in blood glucose levels further stimulates insulin
Insulin is composed of 51 amino acids​ arranged in two polypeptide chains, designated A (21
amino acids) and B (30 amino acids), which are linked together by ​two disulfide bridges​. The
insulin molecule also contains an intramolecular disulfide bridge between amino acid residues
of the A chain.
Insulin is degraded by ​insulin-degrading enzyme, ​which is present in the ​liver​ and, ​kidneys​.
Insulin has a plasma half- life of approximately 6 minutes. This short duration of action
permits rapid changes in circulating levels of the hormone.
Regulation of insulin secretion;
Insulin secretion by the pancreatic β cells is closely coordinated with the release of glucagon
by pancreatic α cells. The relative amounts of insulin and glucagon released by the pancreas
are regulated so that ​the rate of hepatic glucose production is kept equal to the use of glucose
by peripheral tissues
In particular, ​insulin​ secretion is increased by ​glucose​, ​amino acids, and gastrointestinal
peptide hormones
1. Glucose​: Ingestion of a carbohydrate-rich meal leads to a rise in blood glucose, the
primary stimulus for insulin secretion
​Inhibition of insulin secretion​: The synthesis and release of insulin are decreased when
there is a scarcity of dietary fuels and also during periods of physiologic stress (for
example, infection, hypoxia, and vigorous exercise).
3. Secretion is largely controlled by the​ nervous system.
other tissues have ​insulin-insensitive systems ​for glucose transport. For example, ​hepatocytes;
erythrocytes; and cells of the nervous system, intestinal mucosa, renal tubules, and cornea​ do
not require insulin for glucose uptake
A buffer is a system of molecules and ions that acts to ​prevent changes in H + concentration
and thus ​serves to stabilize the pH of a solution.​ In blood plasma, the pH is stabilized by
reversible reaction involving the bicarbonate ion (HCO 3 – ) and carbonic acid (H 2 CO 3 ):
………………… …………… ……………....​HC O 3 – + H + →← H 2 C O 3
The double arrows indicate that the reaction could go either to the right or to the left; the net
direction depends on the concentration of molecules and ions on each side. If an acid (such as
lactic acid) should release H + into the solution, the increased concentration of H + would drive
the equilibrium to the right and the following reaction would be promoted:
...................................... ............ ...........​HC O 3 – + H+ → H 2 C O 3
Notice that in this reaction, H + is taken out of solution. Thus, the H + concentration is
prevented from rising (and the pH prevented from falling) by the action of bicarbonate buffer.
osmotic diuresis;
osmotic diuresis is ​increased urination​ due to the presence of certain substances in the fluid
filtered by the kidneys. This fluid eventually becomes urine. These substances cause additional
water to come into the urine, increasing its amount.
Osmotic diuresis ​can be caused by:
1. High blood sugar (glucose)
2. Use of certain medicines, such as Mannitol (used in the treatment of DM)
Transport maximum​ for glucose is expressed by the maximum transporting capacity of the
SGLT transportation system. Excessive glucose is ​not reabsorbed and consequently passes into
urine​. Transport maximum for glucose tubular transport system in adult humans is about ​375
Na + and K + levels in plasma;
In ​hypokalemia​, the level of potassium in blood is too low. A low potassium level usually results
from ​vomiting, diarrhea, adrenal gland disorders, or use of diuretics. ​A ​low potassium​ level
can make muscles ​feel weak, cramp, twitch, or even become paralyzed, and abnormal heart
rhythms may develop​.
Potassium affects the way the heart's muscles work. When there is ​hyperkalemia​; ​too much
potassium​, the ​heart may beat irregularly, which may cause heart attacks.
hyponatremia​ can include altered personality, lethargy and confusion, seizures, coma and
even death.
Hyponatremia treatments may include
1. changing a medication that affects your sodium level, treating the underlying disease,
changing the amount of water you drink or changing the amount of salt in your diet.
2. Intravenous fluids, IV sodium solution to slowly raise the sodium levels in your blood.
3. Medications, to manage the complications of hyponatremia, such as headaches, nausea
and seizures
People with diabetes are advised to ​limit sodium,​ to prevent or control​ high blood pressure
Hyponatremia​ can result from multiple diseases that affect the ​lungs​, ​liver​, ​brain​, or ​heart
problems like congestive heart failure. the amount of sodium you consume can worsen your
condition by causing ​hypertension​ (high blood pressure).
Vascular diseases that are associated with diabetes;
Diabetes mellitus increases the risk of developing
coronary, cerebrovascular, and peripheral arterial
disease​. The pathophysiology of vascular disease in
diabetes involves abnormalities in ​endothelial,
vascular smooth muscle cell, and platelet function.
The metabolic abnormalities that characterize
diabetes, eg; ​hyperglycemia, increased free fatty
acids, and insulin resistanc​e​, each provoke molecular
mechanisms that contribute to ​vascular dysfunction. ​These abnormalities contribute to the
cellular events that cause ​atherosclerosis​ and increase the risk of the adverse cardiovascular
events that occur in patients with diabetes and atherosclerosis.
Expression of both ​glycoprotein Ib and IIb/IIIa​ is increased, augmenting both platelet–von
Willebrand factor and platelet–fibrin interaction. ​Hyperglycemia​ further changes platelet
function by ​impairing calcium homeostasis​ and thereby alters aspects of ​platelet activation
and aggregation​, including platelet conformation and release of mediators.
Vascular complications in diabetics;
1. Peripheral artery disease,​ known as PAD, occurs when plaque builds up in the arteries
and reduces blood flow to the feet and legs
2. Diabetic eye disease​. Diabetes' effect on the vascular system is what causes diabetic eye
disease. The tiny blood vessels in the retina become swollen, which blocks the oxygen
supply to the retina. If the condition becomes severe, it can cause blindness.
The endocrine system;
series of glands that ​produce and secrete hormones ​that the body uses for a wide range of
functions. These control many different bodily functions, including:
1. Respiration
2. Metabolism
3. Reproduction
4. Sensory perception
5. Movement
6. Sexual development
7. Growth
Hormone- producing glands are;
1. Hypothalamus​: responsible for​ body temperature, hunger, moods​ and the ​release of
hormones from other glands​; also c​ontrols thirst, sleep and sex drive​. Hormones of the
*Thyrotropin-releasing hormone (TRH) *Gonadotropin-releasing hormone (GnRH) *Growth
hormone-releasing hormone (GHRH) *Corticotropin-releasing hormone (CRH) *Somatostatin
2. Pituitary​: master control gland, the pituitary gland ​controls other glands and makes
the hormones that trigger growth​. Hormones produced by the pituitary gland
*Adrenocorticotrophic hormone (ACTH) *Thyroid-stimulating hormone (TSH) *Luteinising
hormone (LH) *Follicle-stimulating hormone (FSH) *Prolactin (PRL) *Growth hormone (GH)
*Melanocyte-stimulating hormone (MSH)
3. Parathyroid​: controls the amount of ​calcium​ in the body. produces the *parathyroid
hormone, which plays a role in regulating your body's levels of the minerals calcium
and phosphorus. ​Hyperparathyroidism​ is when your parathyroid glands create too
much parathyroid hormone in the bloodstream
4. Pancreas​: This gland produces the insulin that helps control blood sugar levels.
*insulin, *somatostatin, *gastrin, and *glucagon, play an important role in maintaining
sugar and salt balance in our bodies
5. Thyroid​ : The thyroid produces hormones associated with calorie burning and heart
rate. *triiodothyronine (T3) and *thyroxine (T4). It also​ stores these thyroid hormones
and releases them as they are needed​.
6. Adrenal​ : produce the hormones that ​control sex drive and cortisol, the stress hormone​.
* Cortisol *Aldosterone *DHEA *Androgenic Steroids *epinephrine (adrenaline)
*norepinephrine (noradrenaline)
7. Pineal​: This gland produces *melatonin which affects sleep.
8. Ovaries​: Only in women, the ovaries secrete *estrogen, *testosterone and
*progesterone, the female sex hormones.
9. Testes​:Only in men, the testes produce the male sex hormone, *testosterone, and
produce *sperm.
Laboratory findings explanaition;
helps keep the water and electrolyte balance of the body
Complications of ​hyponatremia​ include ​altered personality, lethargy and confusion. Severe
hyponatremia can cause seizures, coma and even death​.
Hypernatrenia​ can lead to high ​blood pressure, heart disease, and stroke. It can also cause
calcium loss​.
helps the nerves to function and muscles to contract and helps the heartbeat stay regular.
If left untreated, both severe ​hypokalemia and severe hyperkalemia​ can lead to ​paralysis,
cardiac arrhythmias, and cardiac arrest​.
mild cases of ​hyperkalemia​ may not produce symptoms and may be easy to treat, but severe
cases that are left untreated can lead to​ fatal cardiac arrhythmias​.
​Hyperkalemia​, hads a higher risk of morbidity and mortality if left untreated. Severe
hypokalemia may also cause ​respiratory failure, constipation and ileus​( lack of movement
somewhere in the intestines that leads to a buildup and potential blockage of food material.)
helps keep the amount of fluid inside and outside of the cells in balance. It also helps maintain
proper blood volume, blood pressure, and pH of body fluids.
Hypochloremia​ is an electrolyte imbalance that occurs when there's a low amount of chloride
in your body. Symptoms include:​ fluid loss. Dehydration. weakness or fatigue. difficulty
breathing. diarrhea or vomiting, caused by fluid loss.
Hyperchloremia​ complications include:​ ​ excessive fatigue, muscle weakness, breathing
problems, frequent vomiting, prolonged diarrhea, excessive thirst, high blood pressure.
Bicarbonate​ :
help maintain the acid-base balance (pH) and to work with sodium, potassium, and chloride to
maintain electrical neutrality at the cellular level.
A low CO2 level can be a sign of several conditions, including: ​Kidney disease. Diabetic
Low bicarbonate​ levels in the blood are a sign of metabolic acidosis.
1. Long and deep breaths.
2. Fast heartbeat.
3. Headache and/or confusion.
4. Weakness.
5. Feeling very tired.
6. Vomiting and/or feeling sick to your stomach (nausea)
7. Loss of appetite.
High bicarbonate​ levels may cause:
1. Confusion (can progress to stupor or coma)
2. Hand tremor.
3. Lightheadedness.
4. Muscle twitching.
5. Nausea, vomiting.
6. Numbness or tingling in the face, hands, or feet.
7. Prolonged muscle spasms (tetany)
Urea​ :
Urea is made when protein is broken down in your body. Urea is made in the liver and passed
out of your body in the urine, high urea in the blood indicates kidney dysfunction.
Uremia​ may cause (high urea)
1. extreme tiredness or fatigue.
2. cramping in your legs.
3. little or no appetite.
4. headache.
5. nausea.
6. vomiting.
7. trouble concentrating.
Low urea levels​ are not common and are not usually a cause for concern. They can be seen in
severe liver disease
creatinine​ :
High levels of creatinine in the blood can be caused by several conditions;
1. Chronic kidney disease
2. Kidney obstruction
3. Dehydration
4. Increased consumption of protein
5. Intense exercise
6. Certain medications
High creatinine ​levels in the blood cause several complications;
1. Nausea.
2. Chest Pain.
3. Muscle Cramps.
4. Vomiting.
5. Fatigue.
6. Changes in urination frequency and appearance.
7. High blood pressure.
8. Swelling or fluid retention
low creatinine ​complications;
Low muscle mass: Lack of strength, difficulty exercising, a thin or frail body. Liver disease:
Inflamed liver, which may cause pain in the upper right-side of the abdomen, fatigue or
nausea. Diet-related: Feeling faint or dizzy, losing weight.
Hyperglycemia​ can damage the vessels that supply blood to vital organs, which can increase
the risk of ​heart disease and stroke, kidney disease, vision problems, and nerve problems.
Hypoglycemia​ may cause other complications;
1. An irregular or fast heartbeat
6. sweating
2. Fatigue
7. Hunger
3. Pale skin
8. Irritability
4. Shakiness
5. Tingling or numbness of the lips, tongue or cheek