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IOS 9 Exam 4
Diabetes Complications
| Question | Answer |
|---|---|
| What are the 2 components of hypoglycemic symptoms | Neutrogenic Symptoms and Neuroglycopenic symptoms |
| What are the Neuroglycopenic symptoms of hypoglycemia | Glucose deprivation, confusion, dizziness, uncoordination, slurred speech |
| What are the Neutrogenic symptoms of hypoglycemia | Sympathetic palpitations, tremor, sweating |
| What are risk factors for hypoglycemia | Medications (insulin, sulfonyureas, segretalogs, Alcohol (Blocks gluconeogenesis), B-blockers, Decreased food intake, meal/insuline mismatch, exercise |
| Diabetic Ketoacidosis Pathogenesis occurs by | Relative or absolute insulin deficiency coupled with an in stress hormones –Glucagon, cortisol, CCA’s Leads to catabolic state that leads to hyperglycemia and ketonemia (Ketones and Acidemia). Lack of insulin stimulates Liver to uptake FA’s and glycerol |
| Ketone bodies produced during ketoacidosis are | Beta hydroxyl buterate, acetoacetate and acetone-neutral cleared through respiration-fruity |
| Risk Factors for DKA | Type 1 DM, Type 2 –periods of stress or trauma and those with long-standing disease, Acute illiness (MI, surgery), Stress, stopping therapy |
| Clinical Presentation of DKA | Hyperglycemia->250, pH<7.35, ketonemia, Fluid losses and dehydration |
| Treatment of DKA | Correct fluid losses, correct electrolyte abnormalities (Na, K) , insulin administration to decrease glucose levels |
| Hyperglycemic Hyperosmolar State Pathogenesis is | Simular to DKA but occurs more often in Type 2 DM. Relative insulin deficiency (less severe than DKA) & inadequate fluid intake. Small amounts of insulin decreases ketosis bit still hyperglycemia >600mg/dL & dehydration and loss of consciousness. |
| Clinical Presentation of Hyperglycemic Hyperosmolar State | Mild ketosis, Arterial pH >7.3, Older Type 2 patients |
| Treatment of Hyperglycemic Hyperosmolar State | Aggressive correction of fluids and electrolyte abnormalities and insulin infusion |
| What are the 3 theories of diabetic microvascular disease | 1. Aldose Reductase Pathyway, 2. Advanced Glycation End-Products, 3. Protein Kinase C (PKC) |
| How do Aldose Reductase, PKA, Advanced Glycation End-Products contribute to the development of retinopathy, neuropathy, and nephropathy. | Vascular endothelial cells of the retina, kidney, and nerves are insulin independent. In hyperglycemic states vascular endothelial cells are “overloaded” |
| Explain the Aldose Reductase Pathyway | Excess gluose is converted by enzyme aldose reductase into sorbital (with high affinity) which requires NADPH. Loss of NADPH caused loss of reduced Glutathione causing increased ROS, decreased NOand loss of NA/K ATPase activity. Sorbital =cell swelling |
| Explain the Advanced Glycation End-Products | Glucose forms covalent bonds with non-soluble proteins. The Glucose + proteins or Advanced glycation End productios bind receptors called Receptors for Advanced Glycation End Products (RAGEs) which releases cytokines & Growth factors, NO inactivated |
| Explain the Protein Kinase C | Diacylgylcerol (DAG activates PKC ) are critical intracellular signaling molecules which regulate vascular permeability (increased), vasodilator release (decreased) , endothelian-1 (increased constriction), GF signaling. |
| clinical stages of diabetic retinopathy are | Chronic hyperglycemia causes functional changes in retinal cells and retinal vasculatrure which cause 4 progressions- Mild- Nonproliferative, Moderate-Nonproliferative, Severe-Nonproliferative, Proliferative Retinopathy |
| All forms of retinopathy have | All stages present with macular edema. Excessive fluid in retinal center leads to vision impairment |
| Prevention of Retinopathy by | Yearly Eye exams, Good glycemic control, laser therapy, HTN control, Lipid control, smoking cessation |
| Symptoms of Mild- Nonproliferative are | Microaneurysm formation (Pouches) and death of pericytes caused by protein and lipids that leak and precipitate (harden). |
| Symptoms of Moderate-Nonproliferative are | – Progressive retinal ischemia & abundant hemorrahages and microaneurysms (pouches) and “cotton wool spots” |
| Symptoms of Severe-Nonproliferative are | Extensive hemorrhages and microaneiursms (pouches) & widesoread retinal ischemia and poor perfusion as well infarcts. |
| Symptoms of Proliferative Retinopathy are | Neovascularization on retina (growth of new vessels), hemorrhages, scar tissue around ruptured vessels and retinal detachment. |
| Treatment if patient is suspected of producing excessive Advanced Glycation End-Products | Aminoguanidine |
| Treatment if patient suspected of producing excessive Protein Kinase C (PKC) | Ruboxistaurin |
| Peripheral Neuropathy | Involves sensory and motor nerves of the appendages. Symptoms: Patesthesi, pain, numbness leads to ulcers. |
| Autonomic Neuropathy | Involves involuntary control pathyways-Gastroparesis, bladder function, sexual function, cardiovascular (postural HypoTN |
| Risk Factors for Neuropathy are | Age, duration of DM, Poor glycemic control, Dyslipidema, HTN, smoking, Other microvascular complications |
| Pathophysiology oc diabetic neuropathy is | Glucose uptake in the peripheral nerves is NOT dependant on insulin. A high levels causes Increased sorbital levels(Aldose), Deposits and thickening on retina(AGE), alteration of vasculuture (NO, endothelian-1) |
| Treatment of Diabetic Neuropathy | Good glycemic control, appropiate foot care, antidepressants (TCA, SNRI, Anticonvulsants) |
| Pathophysiology diabetic nephropathy is | Hyperglycemia and increased glomerular filtration causes cells in glomerulus to expand causing Increase in growth factos, Thickening, increase in glomerular cell permibility |
| Steps in renal damage | Glomerular hyperfiltration, glomerular lesions, microalbuminuria, Albuminuria, ESKD |
| Glomerular Hyperfiltration is | Dialation in the afferent causes increase in glomerular hydrostatic pressure |
| Glomerular lesion is | After Glomerular hyperfiltration the basement membrane thicken and form lesions |
| Microalbuminuria is | First indication the kidney has damage, reduced fitering capacity>30mg of albumib excreted per 24 hours |
| Albuminuria is | The filtering of the glomerulus is highly reduced >300mg of albumin excreted in 24 hours |
| Prevention and Treatment of diabetic nephropathy | Good glycemia control, BP control, ACEi or ARB which cause efferent dialation and decrease intra-glomerular pressure |
| Macrovascular disease involves | Hyperglycemia is important but not must important, (Lipids, HTN, obesity, PTL activation & aggregation), insulin resistance = atherosclerosis |
| DM alters function of | endothelial cells, vascular smooth muscle, PTL, plaque stability |
| Endothelial cells are | The inter face between blood and the vessel tissue. The modulate blood flow and nutrient deliveru and coagulation. Endothelium synthesize NO,(inhibits PAF), and prevents leukocyte adhesion |
| Hyperglycemia leads to endothelial dysfunction in DM what is/are the dysfunction? | Decrease NO, decreased prostacylin, increased ATII, and endothelian -1result= Vascoconstriction, inflammation, Thrombosis=ATherosclerosis |
| Cardiovascular damage of AGE pathway | Attack of cytokines and GF leads to vascular smooth muscle proliferation and inflammation, decrease in collogen, loss of strength, plaque rupture, increase in procoagulant |
| PKC cardiovascular damage is | Vascular smooth muscle proliferation, and inflammation, leads to decrease in NO, causing increase in PAF and thrombos formation |
| How dyslipidemia affects DM | Increase in lipids and oxidation products contributes to atherosclerotic plaques |
| How obesity affects DM Cardiovascular | Increase release of Pro-inflammatory & pro-thrombotic cytokines from adipose tissue |
| PVD is | Also called PAD, atherosclerosis in lower extremeties and feet, causing impaired wound healing, nocturnal and resting pain, absent pulses, abscent hair growth on feet and toes |
| RISK for PVD (PAD) | Hyperglycemia, HTN, dyslipidemia, smoking |
| Cerebrovascular Disease is | Atherosclerosis causes impaired arterial circulation or narrowing of the cartid artery (3x CVA risk) |
| Actions of nitric oxide | Vasodialation, promotes vessel dialation, inhibits PAF, prevents leukocyte adhesion to vessel walls |
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liza001
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