Carbohydrate Disorders – Situational Questions and Clinical Tasks

Some situational questions or Clinical task on carbohydrate disorders

Here we provide you some Situational Questions or we can say Clinical Questions on Carbohydrate Disorders pathology. Situational Questions on Carbohydrate Disorders are mainly created for understanding the questions which are mainly come in exams or sometimes in real life. These Situational Questions which is mainly are on Carbohydrate Disorders, tell us that how’s these situations can affect our life, how we can diagnose these cases. Which physiology will work in these Situational Questions on Carbohydrate Disorders? So enjoy your cases.

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Situational Questions on Carbohydrate Disorders - Clinical Tasks

 

  1. The patient is 33 years old and has been suffering from diabetes since she was 23. Not having had dinner, I made an insulin injection in the evening in the usual dose. I woke up suddenly in the night in a state of great anxiety and fear. The patient has. confused consCIousness, profuse sweating, weakness, palpitation, tremor of the limbs. Blood sugar – 2,8 mmol /1. what complication of diabetes should I think about? Explain the mechanism of development of this pathology? (Carbohydrate Disorders Questions)
Hypoglycemia: is a clinical syndrome with diverse causes in which low plasma glucose concentrations lead to symptoms and signs, and there is a resolution of the symptoms/signs when the plasma glucose concentration is raised. In patients with diabetes, hypoglycemia is defined as All episodes of an abnormally low plasma glucose concentration (with or without symptoms) that expose the individual to harm. The human brain depends on glucose as its primary source of energy It is unable to synthesize or store glucose (accounting for the common manifestation of hypoglycemia as altered mental status).
1.       Symptoms consistent with the diagnosis.
2.       Symptoms associated with a low glucose level, usually <50 mg/dL (<2.7 mmol/L).
3.       Symptoms resolve with glucose administration It is clinically defined as follows: WHIPPLE TRIAD.
·         Normal: – 70-99mg/dL , PP: 140mg/dL
·         Plasma glucose is normally maintained at 3.6-5.8mmol/L
·         Cognitive deteriorates at levels <3.0mmol/L
·         Symptoms are uncommon >2.5mmol/L
The precise mechanism(s) of the key feature of HAAF (Hypoglycemia-Associated Autonomic Failure), the attenuated sympathoadrenal response to falling plasma glucose concentrations, is unknown. 1) One hypothesis is that hypoglycemic episodes lead to up-regulation of glucose transport in the brain, resulting in the maintenance of glucose uptake and therefore the prevention of warning symptoms of hypoglycemia. 2) Another is that an increase in cortisol during hypoglycemia causes a reduced sympathoadrenal response to subsequent hypoglycemia. 3) A third is that hypoglycemia-induced alterations in hypothalamic functions, or even a cerebral network, reduce the sympathoadrenal response to subsequent hypoglycemia.
Normal physiological responses to hypoglycemia The human brain primarily uses glucose as its source of energy. Under normal conditions, the brain is unable to synthesize or store glucose and is exquisitely vulnerable to glucose deprivation. To protect the integrity of the brain, several physiological mechanisms have evolved to respond to and limit the effects of hypoglycemia. In humans, the initial response to a decline in blood glucose is the suppression of endogenous insulin secretion followed by the release of counterregulatory hormones, of which glucagon and epinephrine (adrenaline) are the most potent. When blood glucose falls in a nondiabetic adult, the secretion of counterregulatory hormones and the onset of cognitive, physiological, and symptomatic changes occur at reproducible blood glucose thresholds within a defined hierarchy. Subjective recognition of the symptoms of hypoglycemia is fundamental to effective self-management and to prevent progression in severity. Symptoms are generated at arterialized blood glucose concentrations around 2.8–3.2 mmol/l (50–58 mg/dl) and in young adults have been classified as neuroglycopenic, autonomic, and malaise. Hypoglycemic symptoms are idiosyncratic and age-specific.
 
 
  1. Child N., 12 years old, makes complaints about the separation of a large amount of urine, strong thirst, dry mouth, weight loss. Ill for about a month. Recently, these symptoms have been joined by nighttime urinary incontinence. It is known that it is born with large fruit. There are cases of diabetes in the family. Objectively-a child of low nutrition. What pathology can be assumed in this patient? Explain the mechanism of development of this pathology? (Carbohydrate Disorders Task)
Type 2 DM
àBegins with insulin resistance, a condition in which cells fail to respond to insulin properly.
àThis form was previously referred to as “noninsulin-dependent diabetes mellitus” (NIDDM) or “adult-onset diabetes”.
àThe primary cause is excessive body weight and not enough exercise.
GENERAL
1) Insulin is the principal hormone that regulates the uptake of glucose from the blood into cells of the body, especially the liver, adipose tissue, and muscle, except smooth muscle, in which insulin acts via the IGF-1 (Insulin-like growth factor – 1).
2) Therefore, deficiency of insulin or the insensitivity of its receptors plays a central role in all forms of diabetes mellitus.
3) The body obtains glucose from three main places: 1) the intestinal absorption of food, 2) the breakdown of glycogen, the storage form of glucose found in the liver, and 3) Gluconeogenesis, the generation of glucose from non-carbohydrate substrates in the body.
4) Insulin plays a critical role in balancing glucose levels in the body: a) it can inhibit the breakdown of glycogen or the process of gluconeogenesis. b) It can stimulate the transport of glucose into fat and muscle cells. c) It can stimulate the storage of glucose in the form of glycogen.
5)  Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating.
6) Lower glucose levels result in decreased insulin release from the beta cells and results in the breakdown of glycogen to glucose.
7) This process is mainly controlled by the hormone glucagon, which acts oppositely to insulin.
8) If the amount of insulin available is insufficient ¢ If cells respond poorly to the effects of insulin ¢If the insulin itself is defective ¢à Then glucose will not be absorbed properly by the body cells ¢à The net effect is persistently high levels of blood glucose, poor protein synthesis, and break down of fat storage ¢ à Acidosis.
9) When the glucose concentration in the blood remains high over time, the kidneys will reach a threshold of reabsorption à Glycosuria. ¢à This increases the osmotic pressure of the urineàpolyuria àincreased fluid loss ¢à Lost blood volume will be replaced osmotically from water held in body cells and other body compartments à dehydration à polydipsia
10) Type 2 DM is characterized by insulin resistance.
The defective responsiveness of body tissues to insulin is believed to involve the insulin receptor.
In the early stage of type 2, the predominant abnormality is reduced insulin sensitivity.
Type 2 DM is due primarily to lifestyle factors and genetics.
Many lifestyle factors are known to be important to the development of type 2 DM, including
1.       Obesity
2.       lack of physical activity
3.       poor diet
4.       Stress
Dietary factors also influence the risk of developing type 2 DM such as
1.       sugar-sweetened drinks
2.       Type of fats in the diet
a.       saturated fats and trans fatty acids increasing the risk
b.      polyunsaturated and monounsaturated fat decreasing the risk
3.       Eating lots of white rice also may increase the risk of diabetes.
4.       A lack of exercise is believed to cause 7% of cases
  1. A Situational Questions on Carbohydrate Disorders, Patient L., 52 years old, an employee of a confectionery factory, turned to a dermatologist with complaints of skin itching and the appearance of pustules Considers himself sick for 2 years Patient with high nutrition Additional complaints include increased fatigue and dry mouth. The doctor prescribed local treatment, which was ineffective Blood glucose -84 mmol / What disease should I think about in this case? Explain the mechanism of the development of this disease.
Defective insulin secretion is central to the pathophysiology of type 2 diabetes. To maintain normal glucose levels, insulin secretion varies over a wide range in response to insulin sensitivity. The relationship between insulin secretion and insulin sensitivity is curvilinear and is expressed as the disposition index. People with type 2 diabetes cannot adequately increase insulin secretion to overcome insulin resistance and have a low disposition index. Consequently, while absolute insulin levels may be higher in obese subjects with type 2 diabetes who are insulin resistant than they are in lean control subjects who are insulin sensitive, they are lower than appropriate for their degree of insulin resistance. First-phase insulin secretion, especially in response to stimulation by glucose, is markedly impaired or lost. Maximal insulin secretion and potentiation by hyperglycemia of insulin responses to nonglucose stimuli are severely reduced, and the ratio of proinsulin to insulin (C-peptide) is high in type 2 diabetes. Over time, hyperglycemia tends to become more severe and more difficult to treat. This progressive nature of type 2 diabetes is usually due to ongoing deterioration of β-cell function.
There are many agents now available to treat hyperglycemia in type 2 diabetes, with varying mechanisms of action and targeting different pathophysiological components of the disease. Many agents are not always able to achieve adequate control unless they are started earlier in disease progression or are used in combinations (metformin, SGLT2 inhibitors, DPP-4 inhibitors, GLP-1 receptor agonists, peroxisome proliferator-activated receptor γ agonists). This limitation in efficacy may be due in part to the fact that these agents are often initiated after β-cell function or mass has deteriorated beyond a critical level or to their limited effects on insulin secretion. Many people with type 2 diabetes ultimately require insulin therapy, which reflects long-standing type 2 diabetes and greatly diminished β-cell function but also likely includes individuals who have slowly progressing autoimmune diabetes with adult-onset (LADA) or other ambiguous forms of diabetes.
The paths to β-cell demise and dysfunction are less well defined, but deficient β-cell insulin secretion in the face of hyperglycemia appears to be the common denominator. Future classification schemes for diabetes will likely focus on the pathophysiology of the underlying β-cell dysfunction and the stage of disease as indicated by glucose status (normal, impaired, or diabetes).
  1. In an animal with an experimental pathology of the endocrine system, a deficiency of glucose 6- phosphate: hypoglycemia, and an increase in the blood content of free fatty acids, lipoproteins, phospholipids, and triglycerides were detected in the study of metabolism What type of metabolic disorder is medicated by these biochemical indicators? What disease should I think about in this case? Explain the mechanism of development. (Clinical Task on Carbohydrate Disorders)
    1. The dog has hyperglycemia-11 mmol /1. Glucosuria30 g/1 and polyuria-up to 4 days. Insulin therapy was ineffective. What can be associated with insulin resistance in a dog?
    2. The dog’s blood glucose level is 4 mmol 1. m the urine -25 g/l. What is the pathogenesis of glycosuria in this animal?
a. Insulin therapy which is given to the dog. It can be beef insulin. Because It can be release and production of anti-insulin antibodies, which are unable to control glucose level due to antigen-antibody reaction.
b. Differential diagnosis for glucosuria with normoglycaemia
·         Pyelonephritis
·         Leptospirosis
·         Lilies toxicity (cats)
·         Idiopathic / hereditary / congenital
o   Fanconi syndrome (with no other diseases or with renal dysplasia)
o   Primary renal glucosuria
·         Acquired (Fanconi-like syndrome) associated with
o   Gentamicin, ethylene glycol, lead, or grapes/raisins toxicity
o   Ingestion of dry meat treats
o   Copper storage hepatopathy
o   Chemotherapy with chlorambucil (cats)
o   Hypoparathyroidism
o   Expired tetracycline exposure
·         False-positive urine dipstick reaction
o   Associated with amoxicillin, cefalexin, or enrofloxacin exposure
Glucosuria (or glycosuria) is the excretion of glucose into the urine. Normally, the kidneys can reclaim all of the filtered glucose from the urine into the bloodstream. Glucosuria, therefore, is nearly always due to kidney disorders, such as diabetes mellitus.
3. Situational Questions on Carbohydrate Disorders:
Task 1: The child of 8 months was constantly capricious, had a sickly appearance, quickly tired, fell into drowsiness, he often had digestive disorders.  Laboratory analysis blood Glucose (1 hour after feeding) 3.5 mmol /1, 5 mmol /1 After 4 hours after feeding, the glucose level was 2 mmol/1 against the background of signs of a painful condition with a pulse of 110 in 1 min. the Symptoms were removed after eating. Liver biopsy showed massive deposits of glycogen in the cytoplasm of hepatocytes.
QUESTION
What pathological condition can be assumed? Explain the mechanism of development.
 
Glycogenic hepatopathy results from the pathologic accumulation of excess glycogen within the liver and is most commonly associated with poorly controlled type I diabetes mellitus. Additional patient groups that can be affected by glycogenic hepatopathy include those with type II diabetes mellitus, urea cycle defects, and drug effects. The clinical presentation typically includes varying degrees of hepatomegaly, abdominal pain, and elevated transaminases. Occasionally, the transaminase elevations can be dramatic and reach levels greater than 10 times the upper limit of normal. The liver shows diffusely pale staining hepatocytes on routine H&E stains and excessive glycogen accumulation on PAS stains. Abundant glycogenated nuclei and megamitochondria can be seen, but there should be little or no inflammation, mild or absent fatty change, and no significant fibrosis. Other clinical and histologic lesions associated with abnormal glycogen accumulation include genetic glycogen storage disease, glycogen storing foci, and pseudo-ground glass change.
Elevated serum transaminases in type 1, as well as type 2 diabetes mellitus (DM), are most frequently caused by non-alcoholic fatty liver disease (NAFLD), with possible progression to liver cirrhosis. Glycogenic hepatopathy (GH) is a rare cause of elevated serum transaminases, mostly confined to type 1 diabetics. We present a case of GH in a patient with poorly controlled type 1 DM. The recovery of severe transaminase elevations in this patient illustrates the more benign course of GH as compared with NAFLD.
An essential element in the pathophysiology of GH is wide fluctuations in both glucose and insulin levels. High serum glucose levels cause an insulin-independent inflow of glucose in hepatocytes where it is rapidly phosphorylated, trapping it in the cell. Subsequent treatment of high glucose levels with insulin causes the trapped glucose to polymerize to glycogen. Glycogen production persists for some time after insulin levels have declined. The alternation of high glucose and insulin levels in poorly controlled DM causes glycogen accumulation.
It is unclear why only a small subset of patients develops GH. It could be speculated that defects exist in genes that encode regulatory proteins, such as laforin, causing mild or no abnormalities in normal individuals, but marked glycogen storage under certain conditions such as glucose and insulin fluctuations. These proteins could regulate the activity of glycogen synthase and/or glucose-6-phosphatase.
Task# 2:- A large girl (about 5.3 kg) was born to a mother with diabetes. She quickly screamed, but 1 hour after birth, She developed symptoms of hypoglycemia. There was a sign of distress syndrome, including palpitation and shortness of Breathing. The glucose level was 3.5 mmol/l at birth and 1.5 mmol/l after 1 hour, at which point they fell into a comatose state. With glucose infusion and subsequent nutrition with added carbohydrates, the child’s conditions quickly improved. After 2 weeks, he was discharged from the hospital in normal conditions.
Questions: –
1.       What pathological conditions can be assumed?
Ans #1): -Small or premature infants often have low glycogen stores and become hypoglycemic until they are fed early and often. Hyperinsulinemia occurs due to high maternal glucose levels in infants of diabetic mothers; They may develop transient hypoglycemia after birth when maternal glucose is withdrawn.  If the Mother having diabetic patients then it may cause Respiratory Distress Syndrome (RDS) in Neonatal In which can Rapid or shortness of breathing. All were born with a risk of hypoglycemia, mainly because the mother had diabetes, can be born with low or very high birth weight.

 

Deficiency of glycogen stores at birth is common in very-low-birth-weight preterm infants, infants who are small for gestational age because of placental insufficiency, and infants who have perinatal asphyxia. Anaerobic glycolysis consumes glycogen stores in these infants, and hypoglycemia may develop at any time in the first few hours or days, especially if there is a prolonged interval between feedings or if nutritional intake is poor. A sustained input of exogenous glucose is therefore important to prevent hypoglycemia.

 

2.       Explain the mechanism of its development in a newborn.
Ans #2)·         Brain-to-body weight ratio of newborns -> high glucose demand.
·         Impaired establishment of normal glucose homeostasis during the transition from intrauterine to extravascular life -> hypoglycemia.
·         Normal glucose homeostasis requires a supply to meet demands.
·         The supply is dependent on adequate reserves of glycogen, gluconeogenesis precursors, working liver enzymes, and a functioning endocrine system.
·         The demands depend on the metabolic rate of the infant, which can be increased during times of stress (ie sepsis, asphyxia).
There are many types of hypoglycemia, including transient and reoccurring. Each is associated with different risk factors and may have many underlying causes. Neonatal hypoglycemia occurs because an infant’s brain is dependent on a healthy supply of glucose. During the last trimester of pregnancy, glucose is stored in the liver, heart, and skeletal muscles. All newborns experience a physiological and transient fall in blood glucose, reaching a nadir at 2–3 hours of age before slowly rising over the next 24 hours. Newborns do have the ability to use an alternative form of energy, especially if breastfed. However, some newborns are only able to compensate for this glucose deficiency up to a certain limit. Infants who have hyperinsulinism may increase the risk to develop hypoglycemia. Other conditions can increase the risk of an infant becoming hypoglycaemic.

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