Internal medicine - Diabetes mellitus and other metabolic diseases (79) Flashcards
INT - 12.1
What is body mass index?
A) (body height – 100) + 10%
B) body height – 100
C) body weight (kg) divided by the square of body height expressed in meters
D) the body weight of the general population divided by that of the individual
E) none of the listed
ANSWER
C) body weight (kg) divided by the square of body height expressed in meters
EXPLANATION
Obesity is an important risk factor of diseases such as hypertension, diabetes or ischemic heart disease. Assessment of the degree of obesity, however, is difficult. Ideal body weight was determined and is given in a table based on data acquired from life insurance companies. Skinfold thickness measurement is complicated and requires a device. These days, the most often used and easily calculated value is the body mass index, the value of which displays good correlation with the diseases mentioned above. Non-obese muscular individuals, nevertheless, may be considered as being overweight based on their body mass index alone. People with low muscle mass, on the other hand, may display a normal body mass index despite their obesity.
INT - 12.3
Which categories may patient belong to, according the body mass index?
A) underweight – normal weight – overweight – obese – extreme obese
B) obese – thin
C) normal weight – abnormal weight
D) android obese – gynoid obese
E) none of the listed
ANSWER
A) underweight – normal weight – overweight – obese – extreme obese
EXPLANATION
Abdominal, android type obesity is a risk factor of ischemic heart disease. Gynoid type or proportional obesity does not carry such a risk. Body mass index alone cannot distinguish the different types.
INT - 12.4
Complications of extreme obesity include
A) sudden death, sleep apnea, daytime hypoventilation, somnolence, polycythemia, cor pulmonale
B) congestive heart failure
C) renal vein thrombosis
D) immobility that impedes daily activity
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
Extreme obesity (body mass index above 40) has severe medical and psychosocial complications, irrespective of the type of obesity. Extreme obesity associated with hypoventilation is called Pickwick syndrome.
INT - 12.5
Apart from binge eating, bulimia nervosa is characterized by…
A) consuming high-energy food which is easily absorbed
B) binge eating is followed by abdominal pain, sleep and purging by vomiting
C) repeated attempts to lose weight using severe caloric restrictions, self-induced vomiting, and laxative or diuretic abuse
D) body weight fluctuates by more than 4.5 kg
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
Bulimia nervosa is a psychiatric illness characterized by disturbed body image and abnormal eating habits. It is significantly more common in women (90% of all cases), and it typically starts in teens or in early adulthood. Family history of the patients often includes maniac-depressive psychosis. Major features of the disease include binge eating followed by self-induced vomiting, laxative- or diuretic-abuse and severe caloric restriction. Psychiatric treatment is necessary.
INT - 12.7
The normal daily protein requirement of a healthy adult is:
A) 100 g
B) 10 g/body weight kg
C) 1 g/body weight kg
D) 0.8 g/body weight kg
E) none of the listed
ANSWER
D) 0.8 g/body weight kg
EXPLANATION
Patients with chronic kidney disease or diabetes require lower protein intake than healthy humans. Increased protein intake is desired in febrile diseases, after trauma or burn injuries.
INT - 12.8
A patient suffering from hypertension and ischemic heart disease takes thiazide diuretics regularly. One day this patient wakes up with a swollen and extremely painful right knee. His skin is warm and red above the joint. After some shivering, he took his body temperature, which was 37.7°C. What is the most probable diagnosis?
A) deep venous thrombosis of the lower extremity
B) arterial embolisation of the lower extremity
C) acute gout attack
D) septic arthritis
E) none of the listed
ANSWER
C) acute gout attack
EXPLANATION
The most common cause of secondary gout is diuretic treatment (thiazides, furosemide, etacrin acid). These diuretics inhibit the tubular secretion of urate, paving the way for an acute gout attack
Thiazide diuretics are associated with elevated serum uric acid (SUA) levels. They increase direct urate reabsorption in the proximal renal tubules [3]. Elevated SUA is an independent risk factor for gout [2]. These agents increase the levels of SUA and thus may contribute to the risk of gout
INT - 12.9
Secondary gout is most often caused by:
A) cytostatic treatment of a malignant tumor
B) diuretic treatment
C) large dose of acetylsalicylic acid
D) renal failure
E) none of the listed
ANSWER
B)
diuretic treatment
EXPLANATION
See question BGY-12.8.
INT - 12.10
Allopurinol (Milurit) was initiated to treat the hyperuricemia of a patient with gout. He is receiving 3x200mg daily, but hyperuricemia still persists. How would you decrease hyperuricemia further?
A) Urinary acidifiers should be used to prevent kidney stone formation.
B) 24-hour urine urate output should be measured, and a uricosuric medication should be started in case of a low value.
C) A non-steroid anti-inflammatory drug has to be given to relieve symptoms
D) Start colchicine treatment
E) Diuretics should be given to promote the excretion of uric acid.
ANSWER
B) 24-hour urine urate output should be measured, and a uricosuric medication should be started in case of a low value.
EXPLANATION
Treatment of hyperuricemia may require inhibition of urate synthesis (allopurinol) as well as promotion of urate excretion (probenecide, sulfinpyrazone, benzbromarone). Angiotensin-receptor blockers also have some uricosuric effect. If low urate excretion is observed despite high serum urate levels, uricosuric agents are suggested. Urate concentration can reach high values in the urine, therefore, alkalization is required to prevent urate stone formation. It must be noted, that a sudden change in serum urate levels (due to either allopurinol or an uricosuric drug) may provoke an acute gout attack. Therefore, starting treatment with low dose of the drugs is necessary, and the dose has to be titrated up gradually.
INT - 12.11
The most common cause of idiopathic, primary gout:
A) decreased renal elimination of uric acid
B) Lesch–Nyhan syndrome
C) urate overproduction of unknown origin
D) increased activity of the hypoxanthine-guanine phosphoribosyltransferase enzyme
E) none of the listed
ANSWER
A) decreased renal elimination of uric acid
EXPLANATION
In primary gout, urate synthesis is increased in 10%, whereas urate excretion is decreased in 90% of the cases. Increased urate synthesis is caused by known (such as hypoxanthine-guanine phosphoribosyltransferase) or unknown enzyme deficiencies. Decreases urate excretion may be due to decreased glomerular filtration, decreased tubular secretion, increased tubular reabsorption or their combination. The reason for such renal abnormalities is still mostly unknown. Recent studies revealed relationship between mutations in certain tubular anion and urate transporter genes and the degree of urinary urate excretion.
INT - 12.12
Urate crystal formation is promoted by:
A) decreased pH
B) decreased temperature
C) high urate level of the solution
D) all of the listed above
E) none of the listed
ANSWER
D) all of the listed above
EXPLANATION
In a hyperuricemic patient the most favorable conditions for urate precipitation are found in the peripheral joints of the lower extremities and in the kidneys.
INT - 12.13
The most important step in acute gout attack treatment:
A) 0.5mg colchicin administered hourly until symptoms resolve or gastrointestinal toxicity appears, or a large-dose non-steroid anti-inflammatory drug (such as 2x100 mg indomethacin or 2x550 mg naproxen)
B) large-dose allopurinol
C) large-dose uricosuric agent
D) low-dose acetylsalicylic acid
E) low-purine diet
ANSWER
A) 0.5mg colchicin administered hourly until symptoms resolve or gastrointestinal toxicity appears, or a large-dose non-steroid anti-inflammatory drug (such as 2x100 mg indomethacin or 2x550 mg naproxen)
EXPLANATION
Acute gout attack is caused by the phagocytosis of the precipitated, needle-shaped urate crystals, which then results in the destruction of the phagocyte membrane. Substances released from the destroyed phagocyte induce a severe inflammatory reaction. Colchicine reduces inflammation by inhibiting phagocytosis. Non-steroid anti-inflammatory drugs act through a different pathway. Urate synthesis inhibiting allopurinol or uricosuric agents applied in large dose may promote inflammation and provoke an acute gout attack. Acetylsalicylic acid may increase hyperuricemia by inhibiting urate excretion, thus it may provoke or worsen an acute gout attack.
INT - 12.14
Differential diagnosis of an acute gout attack must include:
A) septic arthritis
B) reactive arthritis
C) traumatic arthritis
D) CPPD- (calcium pyrophosphate dihydrate) arthropathy
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
In the disorders listed, asymmetrical mono- or oligoarthritis can be observed. In case of gout, characteristic, needle-shaped urate crystals can be identified under microscope. Using polarized light negative birefringence occurs. The spontaneous occurrence of septic arthritis is extremely rare in patients with normal immune function. In that population the puncture of a joint (iatrogenesis) results in septic arthritis. Fever is present both in acute gout and in septic arthritis. Medical history of patients with reactive arthritis usually includes certain infections (such as Yersinia enterocolitica O3), or serologic demonstration of the infection is feasible. CPPD crystals can be identified under polarized light in a microscope.
INT - 12.15
A potential cause of hypertriglyceridemia:
A) hyperchylomicronemia
B) VLDL-overproduction
C) decreased LPL-activity
D) alcohol consumption
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
Chylomicrons contain large amount of triglyceride, therefore, hyperchylomicronemia of any origin results in hypertriglyceridemia. Triglyceride levels have to be examined in sera taken after fasting for at least 12 hours. VLDL overproduction is typical of metabolic syndrome. Insulin activates lipoprotein lipase and the absolute lack of insulin in diabetic ketoacidosis results in decreased activity of the enzyme and profound hypertriglyceridemia. Enhanced hepatic VLDL production also contributes to hypertriglyceridemia in insulin deficiency. Alcohol influences enzymes of the lipid metabolism and raises triglyceride levels.
INT - 12.16
Apart from diet and alcohol abstinence, the treatment of hypertriglyceridemia may include:
A) nicotinic acid and its derivatives (such as acipimox)
B) fibrates
C) fish oil
D) drug combinations
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
Treatment of hypertriglyceridemia should always be initiated by alcohol abstinence and a low-calorie, low-fat diet. If desired goals are not achieved within some weeks, drug treatment can be initiated (fibrate, nicotinic acid and derivatives, fish oil capsules or statin in case of an associated hypercholesterolemia). Enhanced physical activity reduces triglyceride levels. Extreme hypertriglyceridemia (> 10 mmol/l) requires both dietary restrictions and drug treatment (fibrates) to prevent acute pancreatitis.
INT - 12.17
Apart from diet, the treatment of hypercholesterolemia may include:
A) inhibition of cholesterol absorption by ezetimibe (inhibitor of Niemann-Pick protein in the bowel mucosa)
B) bile acid sequestrant resins
C) statins
D) drug combinations
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
A diet containing low amount of cholesterol and saturated fat may reduce serum cholesterol level by 10%. If larger reduction is desired or the diet is ineffective, hydroxymethylglutaryl- CoA-synthase inhibitors (statins) or fibrates are suggested. Bile acid sequestrant resins cannot be applied in case of a concomitant hypertriglyceridemia. Instead of resins, ezetimibe, a drug that inhibits Niemann-Pick proteins in the bowel mucosa may be given. Nicotinic acid also reduces cholesterol levels, but it is not used in everyday clinical practice. Target lipid levels are determined by the degree of cardiovascular risk, and values are summarized in guidelines. In case of the heterozygous form of familial hypercholesterolemia, drug combination (statin + fibrate + ezetimibe) may be necessary. Homozygous form of familial hypercholesterolemia does not respond to dietary modifications and drug treatment. In this disorder, LDL-apheresis is required, and in severe cases, liver transplantation has to be considered.
INT - 12.18
Marfan-syndrome is characterized by:
A) connective tissue disorder of autosomal dominant inheritance
B) arachnodactyly
C) partial lens dislocation
D) potentially fatal aortic dissection
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
Marfan syndrome is an autosomal dominant disorder that is characterized by the weakness of connective tissue. The molecular background of the disorder is still unknown.
INT - 12.19
Which of the disorders is characterized by dark discoloration of the sclera and the earlobes, darker urine, and accelerated arthrosis?
A) Wilson’s disease
B) porphyria
C) hemochromatosis
D) ochronosis
E) hepatolenticular degeneration
ANSWER
D) ochronosis
EXPLANATION
Ochronosis is a syndrome caused by the accumulation of homogentisic acid and its derivatives in connective tissues. It is caused by the disturbed catabolism of tyrosine (homogentisate oxidase defect, alkaptonuria). The disease results in early appearance of joint degeneration (arthrosis).
INT - 12.21
The following signs and symptoms appear in diabetes mellitus due to the renal threshold of glucose being exceeded:
A) polyuria
B) polydipsia
C) polyphagia
D) weight loss
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
The syndrome that characterizes diabetes mellitus is caused by hyperglycemia. Exceeding renal threshold for glucose results in glucosuria. Glucose is an osmotically active substance, therefore, it retains free water in the urine, causing polyuria and polydipsia. Loss of glucose via the urine means loss of energy, which makes the patient always hungry (polyphagia) and results in weight loss.
INT - 12.24
When does type 1 diabetes mellitus become manifest?
A) once 75% of pancreatic β-cells are lost
B) once 50% of pancreatic β-cells are lost
C) once 25% of pancreatic β-cells are lost
D) once all pancreatic β-cells are lost
E) none of the listed
ANSWER
A) once 75% of pancreatic β-cells are lost
EXPLANATION
In type 1 diabetes mellitus 4 stages can be distinguished. First stage represents genetic predisposition, which is related primarily to major histocompatibility complex (MHC). Carriers of HLA B8, B15, DR3, DR4 and DQ-beta 0302 histocompatibility antigens are more prone to diabetes. Carriers of of HLA DR2 or DQ-beta 0602, on the other hand, display genetic resistance. Second stage represents the influence of a trigger factor. Viral infection (Coxsackie virus), early introduction of cow milk into an infant’s dies (beta-casein) and other, still unknown factors may act as triggers. Third stage is characterized by immunologic abnormalities. In this stage, autoimmune reactions targeting β-cells of the pancreas result in a gradual decline in the number of functioning cells, and abnormal carbohydrate metabolism may be observed. When at least 75% of all β-cells is damaged, absolute insulin deficiency sets in and diabetes becomes manifest.
INT - 12.25
What does Latent Autoimmune Diabetes in Adults (LADA) mean?
A) a latent disorder of the carbohydrate metabolism in adults, which does not manifest as diabetes
B) a disorder the clinical picture of which starts as a non-insulin dependent diabetes, and which becomes later insulin dependent owing to the islet cell damage of autoimmune origin
C) a slowly developing diabetes in adults
D) a slowly developing type 2 diabetes
E) none of the listed
ANSWER
B) a disorder the clinical picture of which starts as a non-insulin dependent diabetes, and which becomes later insulin dependent owing to the islet cell damage of autoimmune origin
EXPLANATION
In childhood diabetes the stage of immunologic abnormalities is shorter, whereas in adulthood it may last for a longer period, even for many years. In the meantime disturbed carbohydrate metabolism may reach the level of diabetes mellitus, without making the patient insulin dependent, mimicking type 2 diabetes mellitus. Antibodies to glutamic acid decarboxylase (GAD) indicate the autoimmune process. Eventually, the patient becomes insulin dependent. This disorder is called latent autoimmune diabetes in adults.
INT - 12.27
Predicting type 1 diabetes mellitus would require the analysis of the following factors:
A) genetic factors (primarily identifying MHC genes that make someone resistant to diabetes)
B) immunologic abnormalities (mainly islet-cell antibodies (ICA), antibodies to glutamic acid decarboxylase (GAD), ICA 512)
C) first-phase insulin secretion during iv. glucose load
D) all of the listed
E) none of the listed
ANSWER
D) all of the listed
EXPLANATION
The first steps in predicting type 1 diabetes include the investigation of immunologic abnormalities that target islet cells, such as antibodies against islet cell cytoplasm, glutamic acid decarboxylase (GAD), tyrosin phosphatase (IA2, ICA 512) or insulin. Then, genetic predisposition or resistance can be studied. Finally, carbohydrate metabolism is assessed by intravenous, frequently sampled glucose tolerance test. This test may identify the loss of first phase insulin secretion. There is a significant chance of becoming diabetic in a short time, if various autoantibodies are detected, diabetes-susceptible HLA-antigens are present, resistance HLA epitopes are absent and the first phase of insulin secretion lacks.
INT - 12.28
Type 2 diabetes mellitus is characterized by:
A) high plasma glucose and insulin levels
B) impaired pancreatic β-cell function, lack of first phase insulin secretion, and increased and prolonged second phase insulin release
C) insulin cannot properly increase the glucose uptake of skeletal muscle cells and decrease the hepatic glucose production
D) insulin cannot increase hepatic glucose uptake
E) all of the listed
ANSWER
E)
all of the listed
EXPLANATION
See question BGY-12.32.
INT - 12.29
Aims of oral antidiabetic therapy in type 2 diabetes mellitus, except:
A) increase in insulin sensitivity (metformin)
B) increase in insulin secretion (GLP1 effect promoters, sulfonylureas)
C) increase in peripheral glucose use (metformin, insulin)
D) retardation of carbohydrate absorption (α-glucosidase inhibitors), promotion of glucose elimination through the kidneys (SGLT2-inhibitors)
E) inhibition of carbohydrate absorption (α-glucosidase inhibitors)
ANSWER
E) inhibition of carbohydrate absorption (α-glucosidase inhibitors)
EXPLANATION
The following oral antidiabetic agents are available currently. Sulfonylureas increase the insulin secretion of β-cells, and they may cause hypoglycemia. Metformin (a biguanide derivative) decreases appetite and enhances glucose uptake by peripheral tissues, without causing hypoglycemia. α-glucosidase inhibitors retard the digestion and absorption of complex carbohydrates and decrease hyperglycemia after meals. They do not cause hypoglycemia, and they do not inhibit the absorption of carbohydrates, only retard it! Glitasones are agonists of the peroxysome proliferator-activated receptor, which decrease insulin resistance, but currently available agents (pioglitazone) may have severe side effects. In the recent years, drugs that enhance glucagon-like peptide 1 (GLP-1) effect became available, these drugs modify insulin and glucagon secretion according to the blood glucose level without increasing the risk of hypoglycemia. Dipeptidyl peptidase 4 (DPP4) inhibitors and GLP1 agonists belong to this group of drugs. The newest drugs are the SGLT2-inhibitors, which inhibit glucose transporters in the renal tubuli. They inhibit the reabsorption of glucose from the ultrafiltrate, promote urinary glucose excretion, and decrease blood glucose levels.
INT - 12.30
Which is the first step in providing an optimal diet for a diabetic individual?
A) determine energy need
B) determine lipid need
C) determine protein need
D) determine vitamin need
E) determine carbohydrate need
ANSWER
A) determine energy need
EXPLANATION
Setting up an optimal diet for a diabetic individual should start with the determination of energy requirements. Calorie need depend on physical activity, height and current body weight. Once it is set, the distribution of the main nutrients has to be prescribed. 50-60% of the total energy should come from carbohydrates, 10-20% from proteins and 20-30% from lipids. At least 2/3 of lipids should be unsaturated fat. Finally, carbohydrate has to be distributed between meals.
INT - 12.31
How energy intake should be distributed between nutrients in the optimal diet for a diabetic individual?
A) 50-60% carbohydrates, 10-20% proteins and 20-30% lipids (with less than 1/3 saturated fat)
B) 40% carbohydrates, 30% proteins, 30% lipids
C) 30% carbohydrates, 30% proteins, 40% lipids
D) 20% carbohydrates, 30% proteins, 50% lipids
E) 10% carbohydrates, 30% proteins, 60% lipids
ANSWER
A) 50-60% carbohydrates, 10-20% proteins and 20-30% lipids (with less than 1/3 saturated fat)
EXPLANATION
See question BGY-12.30.
INT - 12.32
Which is the optimal approach to start treating type 2 diabetes mellitus?
A) Start with and adhere to a diet that has optimal distribution of nutrients and provides adequate energy intake, increase physical activity and take metformin. In case of suboptimal carbohydrate metabolism, drugs that promote GLP1 effects, sulfonylureas, drugs that retard carbohydrate absorption, drugs that promote renal elimination of glucose or insulin can be added to the therapy.
B) Start with appropriate diet and intensive conservative insulin treatment
C) Start with appropriate diet and sulfonylurea in maximal dose, then, in case of suboptimal carbohydrate metabolism, add biguanide in maximal dose, and lastly, switch quickly to insulin
D) Start with the combination of appropriate diet, oral antidiabetic agents and insulin
E) Start with appropriate diet and low-dose sulfonylurea, then apply maximal dose sulfonylurea, then maximal dose biguanide, and lastly, a long-acting insulin once a day.
ANSWER
A) Start with and adhere to a diet that has optimal distribution of nutrients and provides adequate energy intake, increase physical activity and take metformin. In case of suboptimal carbohydrate metabolism, drugs that promote GLP1 effects, sulfonylureas, drugs that retard carbohydrate absorption, drugs that promote renal elimination of glucose or insulin can be added to the therapy.
EXPLANATION
The main feature of type 2 diabetes mellitus is insulin resistance: insulin is present in the plasma, but it has no adequate effect, therefore, hyperglycemia occurs. Insulin secretion is also disturbed, the first phase is absent whereas the second phase is high and retarded. Insulin resistance manifests as an inadequate decrease in hepatic glucose production and as an impaired hepatic and muscular glucose uptake. Most (90%) of the patients are obese. Insulin resistance is ameliorated by weight loss and physical activity, therefore calorie restriction and exercise represent the first steps of therapy (lifestyle modification). Due to the lack of first phase insulin secretion, rapidly absorbed carbohydrates induce profound prandial hyperglycemia. Such carbohydrates should be avoided in the diet. Metformin therapy may be initiated together with dietary modifications. Therapy should be intensified when fasting glucose or HbA1c are higher than desired despite dietary adherence and regular exercise. Then, therapy may include DPP4-inhibitors, GLP1-agonists, sulfonylureas, α-glucosidase inhibitors, SGLT2 inhibitors or insulin.
INT - 12.33
How large is the daily insulin secretion of a healthy adult?
A) 20–40 U
B) 10–20 U
C) 40–60 U
D) over 100 U
ANSWER
A) 20–40 U
EXPLANATION
The average daily insulin secretion of a healthy adult is 20-40 U. Endogenous insulin is produced by β-cells and secreted to the portal circulation from which it reaches the liver. 50% of all insulin is bound by the liver and exerts its effects, whereas the remaining 50% reaches peripheral tissues. Exogenous insulin treatment provides a completely different route. From the subcutaneous tissues insulin reaches the pulmonary and the systemic circulation, and then it reaches the liver through the hepatic artery. This results in peripheral hyperinsulinism and hepatic hypoinsulinism. As compared to the physiologic secretion, larger doses of insulin are required to achieve adequate insulin effect. Exogenous insulin need may be smaller if the patient still has endogenous insulin secretion.
INT - 12.34
What is the distribution of prandial and basal insulin need?
A) 60% prandial, 40% basal
B) 40% prandial, 60% basal
C) 50% prandial, 50% basal
D) none of the listed
ANSWER
A) 60% prandial, 40% basal
EXPLANATION
In healthy individuals insulin secretion is composed of two parts: basal secretion between meals and during the night and prandial secretion after meals. Prandial secretion can be divided to a very rapid and large first phase and a slower and smaller second phase. Basal insulin secretion is responsible for 40%, whereas prandial secretion for the 60% of all insulin secretion. During intensive conservative insulin treatment, administration of short-acting insulin before meals compensates prandial insulin secretion, whereas bedtime intermediate-acting insulin substitutes nighttime basal insulin secretion. Basal insulin secretion between meals derives from the rather prolonged absorption of short-acting insulin. It must be noted, that due to the insulin resistance in the morning hours, morning insulin need is the largest.
INT - 12.35
What does the term “intensive conservative insulin treatment” stand for?
A) basal insulin need is supplemented by intermediate-acting insulin once or twice a day or by ultra-long-acting insulin analogue, whereas prandial need is covered by short-acting insulin or by ultra-short-acting insulin analogue administered before meals
B) measurement of blood glucose hourly and adjusting short-acting insulin dose accordingly
C) administration of short-acting insulin every 6 hours (starting from 8:00 AM) in the ratio of 4:2:3:1
D) intravenous insulin treatment
ANSWER
A) basal insulin need is supplemented by intermediate-acting insulin once or twice a day or by ultra-long-acting insulin analogue, whereas prandial need is covered by short-acting insulin or by ultra-short-acting insulin analogue administered before meals
EXPLANATION
See question BGY-12.34.
INT - 12.36
What are the principal aims of the treatment in diabetic ketoacidosis?
A) administration of insulin because of absolute insulin deficiency
B) infusion of physiologic saline because of the absolute water and electrolyte deficiency
C) potassium supplementation because of potassium deficiency
D) glucose administration to replenish glycogene stores
E) all of the listed
ANSWER
E) all of the listed
EXPLANATION
The reason for diabetic ketoacidosis is absolute insulin deficiency. Hyperglycemia causes glycosuria, and the osmotically active glucose retains water and electrolytes in the urine, providing absolute water and electrolyte deficiencies. In case of insulin deficiency, glycogen stores are depleted, resulting in potassium loss, therefore, absolute deficiency of potassium develops besides absolute cellular glucose deficiency. Treatment of diabetic ketoacidosis aims at the replenishment of the substances depleted.
INT - 12.37
How should be administered insulin in diabetic ketoacidosis?
A) intravenously
B) intramuscularly
C) subcutaneously
D) intraportally
ANSWER
A) intravenously
EXPLANATION
Due to poor peripheral circulation, treatment of diabetic ketoacidosis has to be performed using intravenous insulin
