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Endocrine Sensory

DM

-Group of disorders
-Glucose intolerance
-Chronic hyperglycemia
-Disturbances in carb, AA, fat metabolism

DM Type

Type I: Total insulin deficiency
Type II: Insulin resistance w/ insulin secrection deficit
Gestational: During pregnancy
Other: Conditions influence DM

DM- Type I

-Absolute insulin deficiency
-Primary B cell defect or failure
-Prone to ketoacidosis

DM- Type II

-Insulin Resistance w/ insulin sectetory deficiency
-Not ketosis prone (but may develop under stress)

Other types of DM

Associated w/ other conditions--
pancreatic dz, hormonal disease, drugs & chm agents

Gestational DM

Gluc intolerance 1st recognized during prego (~3rd trimst)
After prego-norm, impared OR become DM

DM Labs

-Fasting plasma glucose
-Glucose tolerance test (oral glucose)
-Clinical Manifestations
-Glycosated hemoglobin (elev. HbA1C)- not dx test, life rbc 120 day
glucose + Hb=glycosylated hemoglobin...inc=hypergly
glucose cell is exposed to, shows results of therapy
LT glucose regulation
-Impaired fasting glucose (Inc. hepatic glucose output)
>100&<126 mg/dL (fasting plasma gluc)
-Impaired glucose tolerance (d/t dec insulin secretion)
>140&<200 mg/dL (2 hr after oral gluc tol test)

Diabetes S/S

3 P's
-Polyuria (Inc urination)
-Polyphagia (Inc hunger)
-Polydipsia (Inc thirst)
-Wt loss
-Glucose conc >200 mg/dL
-Inc. UTI (bacteria love glucose)
-Fatigue

DM- Goals of Txt

Maintain euglycemia
Avoid hypoglycemia
Prevent severe CV & Neuro complications

Type I DM Cause

-auto-immune destruction of beta cells (gene-environ interaction?)
-Loss of islet cells/beta cells=genetic, a-immune, envir
-Gen. Risk marker: Human leukocyte antigen of chrom 6
-Most common: Type IA, beta cell autoantib, insulin antibodies to glutamic acid decarboxylase which participate in damage to islet cells
-Environmental factors-***Box 18-12
-Nonimmune type I: Secondary to dz, ex. pancreatitis
-B/c hyperglyc occurs, 80-90% of insulin secreting beta cells of the islet of Langerhans must be destroyed
-Beta cell abnorm, dec insulin prod, prod of amylin (beta cell hormone co-secreted w/ insulin, funct: supress glucagon release from alpha cells) fails

DM

-Disequilibrium of hormones produced by Iselet of Langerhans occurs. Both beta cell function & alpha cell functions are abnormal, w/ lack of insulin & an excess of glucagon (prod by alpha cells)
-Insulin deficiency=hyperglycemia, ketonemia
-Excess glucagon
-Elevated blood glucose levels fail to suppress the production of glucagon.
-Both hormones cause the full metabolic syndrome

Type I DM S/S

-Affects metab of fats, AA, carbs
-Glucose accumulates in blood, spills into the urine, renal threshold for glucose is exceeded
-Protein & fats break down d/t lack of insulin, result: wt loss
-Initial S/S (acute): 3 P's, wt loss, fluctuations in blood gluc levels
-Ketoacidosis: dec metab of fats & AA->high level of circulating ketones->pH drops (met acid)->Acetone (volatile form of ketones) is blown off (breath: sweet fruity odor)
-Sometimes diabetic coma first S/S

Type I Treatment

-Goal: avoid high & low levels of gluc & insulin
-Indiv planning: age, type of dz, activity level
-Combo of insulin, meal planning, exercise
-HBA1C: dx, monitor effect of txt, prev complications
-Islet cell transplantation
-Pancreas transplant (w/ end stage renal failure)

Type II DM

Risk: Gender (F), Age (40), Race (NA, Blk, Hsp), Metabolic syndrome, genetics (beta, insulin), environmental factors, Family Hx, Obesity/BMI
Cause: unknown
*MODY: autosomal dominant, 6 types (specific mutation in critical enzyme involved in beta cell fxn or insulin axn)
*Cellular resistance: Insulin resistance inc w/ obesity
Dec. beta cell responsiveness to plasma glucose levels (islet dysfunction)
Abnorm glucagon secretion
Alt in insulin receptor
Amyloid deposits=islet cell destruction (age, degree of dz)
Fat in nonadipose tissue (ectopic fat)
Fatty infiltration of liver (nonalcoholic steatohepatisis) can result in hepatic failure & cirrhosis d/t overnutrition

Amylin

Hormone co-secreted w/ insulin by beta cells
Deficiency in Type I diabetes

S/S of Type II DM

Nonspecific
Overweight, hyper lipidemic
Onset: slow, insidious
Pruritus, recurrent infxn, visual changes, paresthesias

Txt of Type II DM

-Goal: restore euglycemia (norm blood glucose levels), correct metabolic disorders
-Diet (Dec caloric intake, sat fat, high fiber diet
-Dec wt=dec in insulin resistance & improve gluc tolerance
-Oral hyperglycemic agents
-Exercise
-Insulin therapy (when other meds fail to restore b.s.)

Gestational DM

glucose intolerance during pregnancy
Risk: family hx DH, race, adv maternal age (>25), prior hx, polycystic ovary syndrom, overwt,
-Aggressive txt

Acute Complications of DM-Hypoglycemia

*** Hypoglycemia (insulin shock, insulin rxn)
-d/t dec b.g. (45-60) & neurogenic rxns
-S/s: pallor, tremor, anxiety, tachycardia, palpatations, diaphoresis, HA, dizziness, irritability, gatigue, poor judgement, confusion, visual disturb., hunger, seizures, coma
-Txt: replace glucose
-Prevention: Indv txt, b.g. monitor, education
*** Diabetic ketoacidosis
-d/t dec insulin & inc counterreg hormones (catecholamines, glucagon, GH)/ Hepatic glucose production increases & periferal usage decreases/Fat is mobilized/ Stimulated Ketogenesis
-Freq peaks in adolescence

Dawn phenomenon

Acute Complications of DM- HHNKS

** Hyperosmolar hyperglycemic nonketotic syndrome
-uncommon, High mortality rate
-elderly w/ comorbities (infxn, CV, Renal dz)
-poor glucose control->high serum glucose (>500mg/dL) & high serum osmotic pressure (dehydration, low blood V, low perfusion rates
-Txt: fluid & electrolyte resuscitation & strict control of serum glucose levels

Acute Complications of DM-Somogyi phenomenon

Somogyi phenomenon
-Hypoglycemia followed by rebound hyerglycemia
-Rise in b.g. d/t counterregulatory hormone (epi, GH, corticosteroids) stimulated by hypoglycemia (produce gluconeogenesis).
-Excess carb intake may result in rebound hypoglycemia

Acute Complications of DM-Dawn Phenomenon

-Early morning rise in b.g. w/ no hypoglycemia @ night
-r/t nocturnal elevations of GH , dec metabolism of glucose by muscle & fat
~Inc clearance of plasma insulin
-Txt: managmt of time & dose of insulin admin

Chronic Complications of DM-

1.) Diabetic Neuropathies
2.) Microvascular dz (retinopathy, nephropathy)
3.) Macrovascular dz (coronary artery dz, stroke, peripheral vascular dz
4.) Infection
Metabolic alterations (hyperglycemia)
Txt: strict control of blood glucose
-Shunting of glucose into the polyol pathway, activation of protein kinase C, overproduction of reactive oxygen species (oxidative stress), production of advance glycation end products or nonenzymatic glycosylation of proteins

Nonenzymatic glycosylation

reversible attachmt of glucose to AA, lipid, NA w/o enzyme

Advanced glycosylation endproducts (AGE's)

result from attachmt of glucose + proteins=tissue injury?

Hyperglycemia & the polyol pathway

Polyol pathway-metabolic pathway for glucose metabolism (vs insulin glucose transport) ex. kidneys, RBCs, blood vessels, eyelense, nerves
-W/ Hyperglycemia, glucose is shunted to this pathway & converted to Sorbitol (a polyol) by aldose reductase/ then Fructose by sorbitol dehydrogenase=accumulation of sorbitol=Increase Intracellular osmotic pressure, attracts H2O->Cell injury
-Ex. Lens of eye, swellling w/ visual changes & cataracts
-Ex. Nerves, interfers w/ ion pumps, damages, Schwann cells, disrupts nerve conduxn
-Ex. RBCs become swollen & stiff & interfere w/ perfusion

Protein kinase C

PKC
intrecellular signaling proteins that inappropriately activate in different tissues d/t hyperglycemia
-Lead to: insulin resistance, production of extracellular matrix & cytokines, vascular cell proliferation, Inc contractility, & Inc. Permeability
-Can cause: microvasc, macrovasc, & neurologic complications
-Txt?=Ruboxistaurin, selective PKCB inhibitor

Diabetic neuropathies

Cause: metabolic & vascular issues r/t hyperglycemia
-Nerve degeneration & delayed conduxn d/t glycosylation end products & Increased polyols
=damage to somatic & periph cells=neuropathies

Microvascular dz

thickened basemt membrane, endothelial hyperplasia, thrombosis, & pericyte degeneration
-Dec tissue perfusion & hypoxia

Diabetic retinopathy

Cause: retinal ischemia d/t vessel changes & RBC aggregation, GH, Activation of PKC
-Severity related to age & duration
-Macular edema, hard exudates, microaneurysms, hyperglycemia, sorbitol accumulation, dehydration of the lens

Diabetic nephropathy

-Leads to end stage renal dz
-Cause: AGE's, polyol pathway, glucose toxicity, PKC
HTN, proteins,
-nephrons thicken and slowly become scarred over time
-Microalbuminuria: proteinuria, decreased plasma oncotic pressure, fluid overload, anasarca (general body edema), HTN

Macrovascular disease

proliferation of fibrous plaques in the arterial wall & elevated lipid levels
Due to AGE attaching to blood vessel walls, leading to atherosclerosis

CAD

High LDL & triglycerides, low HDL, platlet abnorm's, endothelial cell dysfunction
Inc platelet adhesion & dec fibrinolysis promote thrombus formation

Peripheral vascular dz

+ osteomyelitis or gangrene & amputation

Inc Risk for Infection

1.)The senses: Dec vision d/t retinal changes & Dec touch d/t neuropathy
2.)Hypoxia: glycosated hemoglobin in RBCs blocks release of O2 to tissues
3.) Pathogens: bacteria love glucose (energy to grow)
4.) Blood Supply: Vascular changes=dec blood supply=Dec WBCs
5.) White cells: Impaired function (abnorm chemotaxis & defective phagocytosis)

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