Diabetes Mellitus PDF

Miscellaneous Conditions Diabetes Mellitus Diabetes Mellitus  Most common disorders of carbohydrate metabolism  Chronic hyperglycaemia due to:  Absence of insulin  Decrease in insulin  Normal insulin secretion but inadequate to cope with blood glucose level  Decreased sensitivity of ins...

Miscellaneous Conditions Diabetes Mellitus Diabetes Mellitus  Most common disorders of carbohydrate metabolism  Chronic hyperglycaemia due to:  Absence of insulin  Decrease in insulin  Normal insulin secretion but inadequate to cope with blood glucose level  Decreased sensitivity of insulin receptors Type 1 Diabetes Mellitus  Autoimmune pancreatic beta -cell destruction = little or no insulin production  Possibly triggered in the genetically susceptible by :  Infectious stimulus  Toxic environmental stimulus  Develops in childhood or adolescence  Accounts for < 10 % of all cases of diabetes mellitus Type 2 Diabetes Mellitus  Due to tissue insensitivity to insulin  Generally not evident until later in life  Incidence is increasing in young people  Accounts for 90 -95% of diabetes  Most DM 2 patients are obese – lifestyle related Risk Factors for DM  Ethnicity – American Indians, Hispanics and Asians  Family history of diabetes  > 45 years of age  Overweight/obesity  History of high cholesterol or triglyceride levels  Not physically active  Gestational diabetes or giving birth to large baby Why are we learning about DM?  Only half of diabetic patients are aware of their disorder  Often present with various MSK & neurologic complaints  Link the dots  Numbness, tingling or pain in the lower extremity  MSK origin?  Diabetic etiology?  Significantly affects decision making for management and prognosis Patient Presentation  Early symptoms are related to hyperglycaemia :  Polyuria  Polydipsia  Polyphagia  Later complications :  Vascular disease – microvascular & macrovascular disease  Peripheral neuropathy  Nephropathy  Predisposition to infection Complications of Hyperglycaemia  Acute diabetic ketoacidosis – EMERGENCY!!! Due to macrovascular & microvascular disease:  Increased risk of atherosclerosis -related death  Blindness  Renal failure  Neuropathy  Infection & gangrene of the feet Diabetic Ketoacidosis  Insulin deficiency causes the body to metabolise triglycerides & muscles for energy  Leading to hyperglycaemia, hyperketonaemia & metabolic acidosis  Most common with DM type 1 Symptoms  The 3 P’s  Fruity breath  Nausea  Vomiting  Headaches  Abdominal pain  Lethargy  Hypotensive & tachycardia  Rapid & deep breathing  Loss of consciousness, coma & death Diabetic Ketoacidosis Immediate medical attention to:  Replenish intravascular volume  IV saline  Correction of hyperglycaemia  IV insulin  Correction of acidosis  IV NaHCO3 Patient Presentation  Polydipsia  Polyuria  Polyphagia  Dehydration  Generalised fatigue & weakness  Weight loss  Blurred vision and/or blindness  Numbness & tingling in extremities  Unilateral or bilateral  Overweight/obesity  Fungal/bacterial infection Physical Exam Vitals  BP  Hypertensive  HR  Possibly increased  Respiratory rate  Normal  Temperature  Normal  Weight  Overweight/obese Physical Exam Inspection  Overweight/obese  Fatigued/general weakness  Altered gait  Sensory deficit & loss of proprioception  Missed foot trauma  Charcot’s joint  Signs of sores, cuts, ulcerations, burns, infection, gangrene (esp. lower extremities)  Between the toes Physical Exam Neurological exam  Cranial nerves  Diplopia  Ptosis  Ophthalmoscopic exam  Microaneurysms, exudates & punctate haemorrhage => scarring => retinal detachment => blindness  Macular oedema & neovascularisation  Change in lens shape => fluctuating visual acuity  More prone to cataract formation & glaucoma Physical Exam Neurological exam  Dermatomes  Paraesthesia, dysesthesia or  Painless loss of:  Vibration  Sense of soft & sharp touch  2 point discrimination  Temperature  Proprioception  Most common: symmetric stocking -glove distribution affecting distal feet & hands Physical Exam Neurological exam  Myotomes  Reduced muscle strength  Muscular atrophy  Reflexes  Reduced DTR Physical Exam Cardiovascular  Hypertension  Tachycardia Abdominal  Kidneys: flank pain, Murphy’s punch Physical Exam X -rays  Charcot’s joint  Vascular calcification  Atherosclerosis  Monckeberg’s arteriosclerosis  DISH & OPLL Diagnostic Tools  Fasting plasma glucose  126 mg/ dL (>7 mmol /L) or higher  2 -hour plasma glucose  200 mg/ dL (>11.1 mmol /L) or higher  Symptomatic + random plasma glucose  200 mg/ dL (>11.1 mmol /L) or higher Other tests:  Renal function  Urinalysis: glycosuria, proteinuria, ketonuria, yeast infection  Cholesterol Medical Treatment Type 1:  Must be controlled through insulin injections  Self -monitoring of blood glucose Medical Treatment Type 2:  Screening high -risk patients  Fasting glucose  Pharmaceuticals  Reduce glucose levels  Insulin  Oral antihyperglycemic drugs  Monitoring blood glucose level  HbA1c  Glycemic control & surgery for retinopathy  Surgery for gangrene Chiropractic Management  Recognising acute diabetic ketoacidosis  Monitor patient for complications/clinical indicators for macro/microvascular disease  Neuropathy  Vascular compromise – increased risk for cardiovascular disorders  Absolute contraindication to chiropractic adjustment for Charcot’s joint  Be careful when setting up for side posture  Leg checks – best opportunity to look for foot pathology Chiropractic Management Lifestyle  Dietary program  Nutritionist referral  Low in saturated fat & cholesterol  Moderate amounts of whole grain carbohydrate with high fibre  Exercise program  PT referral Chiropractic Management Lifestyle  Patient education  Prevention of further progression & development in other family members  Feet protection: covered, well -support shoes  Daily checking of feet for skin changes, cuts, sores Nutritional Support for DM From Souza:  Vitamins C & E  Vitamin B6  Biotin  Chromium  Magnesium  Aloe vera juice  Capsaicin  Coenzyme Q10  Evening primrose oil  Alpha -lipoic acid  Inositol  Gymnema  Ginseng Splenic Rupture Spleen  Largest collection of lymphoid tissue in the body  ~12cm long and weighs ~160g  Lies on the lateral curvature of the stomach and extends up to the 9 th rib  Connected to the stomach via the gastrosplenic ligament Splenic Rupture  Usually results from blunt abdominal trauma:  Significant impact: MVA  Penetrating trauma: knife, gunshot  May spontaneously rupture from splenomegaly  Leads to haemorrhage into the peritoneal cavity Patient Presentation  History of blunt force trauma or conditions causing splenomegaly  Abdominal distention and pain  Haemorrhagic shock:  Hypotension  Tachycardia  Decreased urine output  Altered mental status  LUQ may precede rupture Diagnosis  CT  Bedside ultrasonography  Exploratory laparotomy Medical Treatment  Hospital observation and transfusion:  Small lacerations  Stable patients  Preferred option for children if possible  Surgical repair or splenectomy Chiropractic Management  Splenomegaly:  No absolute contraindications  Patient tolerance for any LUQ pain  Avoid high impact sports to reduce the risk of splenic rupture  Splenic rupture and/or haemorrhage:  Immediate referral to A & E  Post -surgical consideration:  Recovery period of 6 -8 weeks post -surgery before putting a force or stress on the area Acute Meningitis Acute Meningitis  Inflammation of the meninges of the brain and/or spinal cord  Brain parenchyma can also be involved  Often infectious:  Bacterial  Viral  Symptoms develop over hours or days  Common organisms:  Group B streptococci  Neisseria meningitides  Streptococcus pneumoniae Patient Presentation  Respiratory illness or sore throat precedes meningitis  Classic triad:  Fever  Headache  Neck stiffness  Photophobia  Phonophobia  Vomiting  Rash  Dehydration  Lethargy  Confusion  Seizures  Focal neurologic deficit  Changes in consciousness  Irritability  Coma Patient Presentation  Vitals:  Fever  Inspection:  Rash  Nuchal rigidity:  Restricted painful neck flexion  Brudzinski’s  Kernig’s  Focal neurologic deficit *Cranial nerves*  Motor  Sensory  Reflexes Diagnosis  Lumbar puncture → CSF analysis  Culture  Gram stain  Bacterial DNA Medical Treatment  Immediate treatment  Corticosteroids  Antibiotics  Supportive care  High mortality with delayed treatment as well as amongst new -borns, elderly & immunocompromised patients  Survivors may have neurologic deficits  Deafness  Eye problems  Cerebral infarction  Recurrent seizures  Intellectual disability Chiropractic Management  Recognise warning signs and make immediate medical referral  Especially in young patients  Post -recovery  No specific contraindications  Special considerations for possible neurologic deficits Hodgkin’s Lymphoma Hodgkin’s Lymphoma  Lymphoreticular proliferation of unknown cause  More common in males  Bimodal age distribution  20 -30’s or over age 50 B cell transforming event(s) Loss of apoptosis RS cell Inflammatory response EBV? cytokines Hodgkin’s Lymphoma Classic Presentation  Constitutional symptoms:  Fever  Weight loss  Night sweats  Fatigue  Chills  Painless swollen lymph nodes  Pruritis  Headache  Facial oedema  Abdominal pain  Mediastinal mass  Shortness of breath  Chronic cough  Hepatosplenomegaly  Easy bruising/bleeding Hodgkin’s Lymphoma Classic Presentation  Osseous changes secondary to systemic lymphoma  Affects the thoracolumbar spine most commonly  Pain is the most common initial symptom  Neurological findings  Pain increases with alcohol consumption Hodgkin’s Lymphoma Evaluation  Reed -Sternberg cells on lymph node biopsy  Staging of disease Medical Treatment  Based on staging  Stage I & II: radiotherapy  10 -year survival = 80%  Stage III & IV: chemotherapy  5 -year survival = 50 -60% Hodgkin’s Lymphoma Long term complications from treatment  Infertility  Sperm banking  Premature menopause  Secondary malignancy  Skin, lung, non -Hodgkin’s, thyroid, breast, etc.  Cardiac disease  Refer out if you identity painless LN enlargement or red flags:  Fever of unknown origin  Weight loss  Night sweats  Fatigue  If bone is involved – absolute contraindication to adjusting that area! Chiropractic Management Non - Hodgkin’s Lymphoma Non - Hodgkin’s Lymphoma Causes  A collection of lymphocytic cancers  Lymphoid neoplasms  More common than Hodgkin’s lymphoma  More common in males  Age range = 20 -40 years  Classification is based on the degree of aggressiveness  HIV +ve patients are prone to non -Hodgkin’s lymphoma Non - Hodgkin’s Lymphoma Risk Factors  Immunosuppression or immunodeficiency  Connective tissue disease  Family history of lymphoma  Infectious agents  Ionizing radiation Non - Hodgkin’s Lymphoma Classic Presentation  Patient has striking wellbeing  Painless lymphadenopathy  Deeper lymph nodes  Local intermittent pain if bone affected  Constitutional symptoms:  Night sweats  Fever  Anorexia/weight loss  Fatigue  Dyspnea Non - Hodgkin’s Lymphoma Evaluation  Regional or disseminated lymph node involvement  Lymph node biopsy Medical Treatment Category Survival of untreated patients Curability To treat or not to treat Non - Hodgkin’s lymphoma Indolent Years Generally incurable Generally, not treated if asymptomatic Aggressive Months Curable in some Treat Very aggressive Weeks Curable in some Treat Hodgkin’s lymphoma All types Variable – months to years Curable in most Treat Chiropractic Management  Be familiar with the risk factors and refer out if you identity painless LN enlargement or red flags  If bone is involved – absolute contraindication to adjusting that area!