NIFEDIPINEDRUG
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Nifedipine is a calcium channel blocker used to treat hypertension and angina. It works by relaxing blood vessels and increasing blood flow to the heart. It comes as tablets and capsules in doses from 10-90mg taken twice daily. Nurses monitor patients for reductions in blood pressure and potential side effects like headache, flushing, and leg cramps. They also educate patients to take nifedipine consistently with food and avoid activities like driving until its effects are known.
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3) The nursing role includes ongoing assessment, accurate monitoring, treatment, education, and psychological support of patients experiencing acute diabetic complications.
DIABETIC KETOACIDOSIS IN CHILDREN by Dr.Gobinda
This document discusses the pathophysiology, diagnosis, and management of diabetic ketoacidosis (DKA). It begins by providing background on diabetes and the prevalence of type 1 diabetes. It then discusses the causes and presentation of DKA, describing the biochemical criteria for diagnosis. The document outlines the pathogenesis of DKA in terms of dehydration, dyselectrolytemia, and cerebral edema. It provides guidelines on evaluation and management, including fluid resuscitation and insulin administration. Complications like cerebral edema are also reviewed. Management of specific cases and guidelines from leading organizations are presented.
Drug presentation on diamox
Diamox (acetazolamide) is a carbonic anhydrase inhibitor used to treat glaucoma and seizures by lowering intraocular pressure and abnormal neuronal firing. It works by inhibiting carbonic anhydrase in the eye, kidneys, and central nervous system. Common side effects include fatigue, nausea, and hypokalemia. Nursing responsibilities involve monitoring for side effects and assessing response to treatment by checking intraocular pressure, seizure activity, and edema. Patients should be advised to use sun protection and report any adverse reactions or symptoms.
Acute metabolic complications of diabetes mellitus
This document provides information on acute metabolic complications of diabetes mellitus, including diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state, hypoglycemia, and lactic acidosis. It defines DKA as hyperglycemia, ketosis, and acidemia and describes the pathogenesis involving unchecked ketogenesis in insulin deficiency. Precipitating factors, symptoms, signs, investigations, and treatment of DKA are outlined. Treatment involves fluid replacement, insulin administration, monitoring of electrolytes like potassium and phosphate, and ongoing monitoring of the patient. Complications of DKA include shock, cerebral edema, pulmonary edema, hypoglycemia, and electrolyte imbalances. Hyperosmolar hyperglycemic
dkadrsyed2584-190602083813 (1).pdf
Diabetes is a condition where the body does not properly process glucose due to lack of insulin or insulin resistance. Diabetic ketoacidosis (DKA) occurs when a lack of insulin causes the body to break down fat and produce ketones, leading to hyperglycemia, ketosis and acidosis. DKA treatment involves rehydration, insulin therapy to lower blood glucose and ketone levels, electrolyte replacement, and identifying/treating the precipitating cause. Complications can include infection, shock, cerebral edema and death if not properly managed. Prevention relies on education about sick day management to avoid DKA during illness.
Diabetic Ketoacidosis
Diabetes is a condition where the body does not properly process glucose due to lack of insulin or insulin resistance. Diabetic ketoacidosis (DKA) occurs when a lack of insulin causes the body to break down fat and produce ketones, leading to hyperglycemia, ketosis and acidosis. DKA treatment involves rehydration, insulin therapy to lower blood glucose and ketone levels, electrolyte replacement, and identifying/treating the precipitating cause. Complications can include infection, shock, thrombosis, pulmonary edema and cerebral edema. Prevention relies on education about sick day management to avoid DKA during illness.
DKA Discussion Paediatrics.pptx
This document summarizes diabetic ketoacidosis (DKA), including its diagnosis, pathophysiology, clinical manifestations, treatment goals, and management. DKA is characterized by severe dehydration and electrolyte depletion due to insulin deficiency and increased counterregulatory hormones. Its treatment involves intravenous fluid resuscitation and insulin therapy to correct dehydration, acidosis, and ketosis. Careful monitoring is required to watch for complications like cerebral edema. Recent studies have found subcutaneous insulin and lower-dose intravenous insulin to be effective alternatives to standard intravenous insulin therapy for mild-moderate DKA.
dkadrsyed2584-190602083813 (1).pptx
Diabetes mellitus, often referred to simply as DIABETES.
Diabetes is a condition in which the body:
Does not produce enough insulin, and/or
Does not properly respond to insulin
Insulin is a hormone produced in the pancreas. Insulin enables cells to absorb glucose in order to turn it into energy.
Type 1 diabetes:
Diagnosed in children and young adults
Previously known as Juvenile Diabetes
Type 2 diabetes:
Typically diagnosed in adulthood
Also found in overweight children
Complications of blood glucose alterations
Hypoglycemia
Hyperglycemia
Ketosis
Acidosis
DKA (Hyperglycemia + Ketosis + Acidosis)
Normal fasting blood glucose level 4-6 mmol/L
definition:
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.
Can occur in both Type I Diabetes and Type II Diabetes
– In type II diabetics with insulin deficiency/dependence
The presenting symptom for ~ 25% of Type I Diabetics.
160,000 Admissions to private hospitals/year
Cost = over 1 billion $ annually
65% = <19 years old
Main cause of death in children with diabetes (approximately 85%)
Cerebral edema in 69%
Hyperosmolar Hyperglycemic State (HHS):
An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia.
Occurs predominately in Type II Diabetics
– A few reports of cases in type I diabetics.
The presenting symptom for 30-40% of Type II diabetics.
Not commonly associated with ketonaemia and acidosis
The biochemical criteria for the diagnosis of DKA3,4
Hyperglycemia - blood glucose greater than 11.1 mmol/L
Ketosis - ketones present in blood and/or urine
Acidosis - pH less than 7.3 and/or
bicarbonate less than 15 mmol/L
DKA is generally categorized by the severity of the acidosis.
MILD – Venous pH less than 7.3 and/or
bicarbonate concentration less than 15 mmol/L
MODERATE – Venous pH less than 7.2 and/or
bicarbonate concentration less than 10 mmol/L
SEVERE – Venous pH less than 7.1 and/or
bicarbonate concentration less than 5 mmol/L
Risk factors:
Age <12 yrs
No first degree diabetic relative
Lower socioeconomic status
High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs
Poor access to medical care
Uninsured
Usage of SGLT-2 inhibitor – euglycaemic DKA
SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism
AETIOLOGY:
No carbohydrate intake
fasting
gastroenteritis
Atkins diet, neonates fed high-fat milk
Prolonged exercise, pregnancy
Lack of insulin activity
onset of diabetes (insufficient secretion)
interruption of insulin delivery in established pt
Increase in insulin resistance
infection, illness, surgery, stress
Alcohol, salicylate ingestion, inborn metabolic errors
Causes:
Stressful precipitating event that results in increased cate
DKA by Dr. A. Mandour.pptx
DIABETIC KETOACIDOSIS (DKA):
A state of absolute or relative insulin deficiency aggravated by ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary metabolism, including production of serum acetone.
Can occur in both Type I Diabetes and Type II Diabetes
– In type II diabetics with insulin deficiency/dependence
The presenting symptom for ~ 25% of Type I Diabetics.
Hyperosmolar Hyperglycemic State (HHS): An acute metabolic complication of diabetes mellitus characterized by impaired mental status and elevated plasma osmolality in a patient with hyperglycemia.
Occurs predominately in Type II Diabetics
– A few reports of cases in type I diabetics.
The presenting symptom for 30-40% of Type II diabetics.
Not commonly associated with ketonaemia and acidosis
Classic Triad of DKA:
Hyperglycemia - blood glucose greater than 11.1 mmol/L
Ketosis - ketones present in blood and/or urine
Acidosis - pH less than 7.3 and/or
bicarbonate less than 15 mmol/L
DKA is generally categorized by the severity of the acidosis.
MILD – Venous pH less than 7.3 and/or
bicarbonate concentration less than 15 mmol/L
MODERATE – Venous pH less than 7.2 and/or
bicarbonate concentration less than 10 mmol/L
SEVERE – Venous pH less than 7.1 and/or
bicarbonate concentration less than 5 mmol/L
Risk factors for DKA at onset:
Age <12 yrs
No first degree diabetic relative
Lower socioeconomic status
High dose glucocorticoids, atypical antipsychotics, diazoxide and some immunosuppresive drugs
Poor access to medical care
Uninsured
Usage of SGLT-2 inhibitor – euglycaemic DKA
SGLT2 inhibitors blunt insulin production in the face of stress hormones leading to increased ketotic metabolism
Why do ketones develop?
No carbohydrate intake
fasting
gastroenteritis
Atkins diet, neonates fed high-fat milk
Prolonged exercise, pregnancy
Lack of insulin activity
onset of diabetes (insufficient secretion)
interruption of insulin delivery in established pt
Increase in insulin resistance
infection, illness, surgery, stress
Alcohol, salicylate ingestion, inborn metabolic errors
Causes of DKA/HHS: Stressful precipitating event that results in increased catecholamines, cortisol, glucagon.
Infection (pneumonia, UTI)
Alcohol, drugs
Stroke
Myocardial Infarction
Pancreatitis
Trauma
Medications (steroids, thiazide diuretics)
Non-compliance with insulin
DKA is a complex metabolic state of: hyperglycemia, ketosis, and acidosis
Symptoms include:
Deep, rapid breathing
Fruity breath odor
Very dry mouth
Nausea and vomiting
Lethargy/drowsiness
DKA is life-threatening and needs immediate treatment
Symptoms of DKA/HHS
Polyuria
Polydypsia
Blurred vision
Nausea/Vomiting
Abdominal Pain
Fatigue
Confusion
Obtundation
Physical Examination in DKA/HHS: Hypotension, tachycardia
Kussmaul breathing (deep, labored breaths)
Fruity odor to breath (due to acetone)
Dry mucus membranes
Confusion
Abdominal tenderness
Treatment of DKA:
Fluids and Electrolytes
Fluid replacement
–Restores perfu
Sargent noon conference 072618
This document provides an overview of diabetic ketoacidosis (DKA) presented by Dr. Jonathon Sargent at a noon conference. It discusses the clinical presentation of DKA, including symptoms like polyuria and abdominal pain. The pathophysiology of DKA is described as reduced insulin leading to increased gluconeogenesis, glycogenolysis, and ketone production. Precipitants, diagnostic testing, treatment including IV fluids, insulin and electrolyte repletion, and tips for management are reviewed. The goals of treatment are to rehydrate the patient and lower their blood glucose levels by 10% per hour with intravenous insulin.
HTN IN PREGNANCY.pptx
This document discusses hypertensive disorders in pregnancy, including their classification, symptoms, pathogenesis, predictors, and management. It classifies hypertensive disorders into gestational hypertension, preeclampsia, eclampsia, preeclampsia superimposed on chronic hypertension, and chronic hypertension. It describes the symptoms and criteria for diagnosing each condition. It discusses the risk factors, preventive measures, pathological alterations, maternal and neonatal complications, and medical management for preeclampsia. The medical management involves monitoring, controlling blood pressure below certain thresholds, and delivering early if certain severe conditions develop.
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NIFEDIPINEDRUG
- 1. B.Sahithya 2nd year bsc (N) ACONC NIFEDIPINE
- 2. OBJECTIVES • Classification • Introduction • Doses • Available forms of drugs • Indications • Contra indications
- 3. CONT • Mechanism of action • Pharmacokinetics • Therapeutic effects • Adverse effects • Nurses responsibilities
- 4. CLASSIFICATION •Nifedipine belongs to the class calcium channel blockers
- 5. INTRODUCTION •Calcium channel blocker •Prescribed to treat hypotension •Affects the way calcium moves into the cells of the heart and blood vessels
- 6. CONT •Results in the relaxation of blood vessels •Increases the oxygen to the heart and reduce the work load of the heart
- 7. DOSAGES HYPERTENSION •ADULT : 30 – 60 mg ,po,BD •CHILD : 0.25 – 0.5 mg /kg /day ANGINA •ADULT /CHILD : 10mg ,po,BD
- 8. AVAILABLE FORMS OF DRUG ROUTE : ORAL AVAILABLE FORMS •TABLETS : 20mg ,30mg ,60 mg ,90 mg •CAPSULES : 10mg , 20mg
- 9. TABLET
- 10. CAPSULE
- 12. CONTRA INDICATIONS •Acute MI •Cardiogenic shock •Acute unstable angina •Severe GI narrowing
- 13. MECHANISM OF ACTION HYPER TENSION Highly specific to vascular smooth muscle Inhibits the calcium channel found on smooth muscle Increases the intracellular concentration of calcium
- 14. CONT Leads to smooth muscle cell relaxation Causes vasodilation Increased blood pressure
- 15. PHARMACOKINETICS ABSORPTION •Nifedipine is almost completely absorbed from the gastrointestinal tract •Oral bioavailability ranges from 45 to 68% because of first pass metabolism
- 16. CONT DISTRIBUTION •The steady state volume of distrubtion of nifedipine is 0.062- 0.77L/kg •Volume of distrubtion of the central compartment is 0.25 – 0.29L/kg
- 17. CONT METABOLISM • It is metabolized in the liver by cypac • Po: onset 20 min , duration 6 – 8 hrs EXCRETION • 60-80 % excreted through the urine • 20- 40 % excreted through the urine
- 18. THERAPEUTIC EFFECTS •Maintains blood pressure •Reduces angina •Inbits calcium ion exchange across cell membrane •Dilates coronary arteries •Increases myocardial oxygen delivery
- 20. CONT • Drowsiness • Constipation • Insomnia • Rash • Frequent urination • Warm feeling of the skinn • Peripheral edema • Hypotension
- 21. NURSES RESPONSIBILITIES • Monitor patient closely • Monitor the patients BP and for any adverse reactions • Vital signs should be monitored q 4 hours • Educate patient on potential side effects /adverse reactions • Encourage patient to avoid hazardous activities
- 22. CONT •Allergy to nifedipine •Preganancy •Lactation •Product drug from light and moisture •Ensure that patients do not chew or divide sustained – release tablets
- 23. CONT • Watch for symptoms for the heart failure • Advise patient to avoid taking this drug with grape fruit juice PATIENT TEACHING • Nifedipine can be taken with or without food • Take the drug at the same time everyday • If patient miss a dose of this medication take it as soon as possible
- 24. CONT •Do not double the dose •Limit caffine consumption •Avoid alcohol