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Pa Tho Physiology - Type 1 Diabetes (Hanieyah Guro)

This document summarizes the pathophysiology of type 1 diabetes mellitus. Key points include: - Type 1 diabetes is an autoimmune disease where the immune system attacks the beta cells in the pancreas that produce insulin, resulting in absolute insulin deficiency. - Without insulin to regulate blood glucose, complications arise like hyperglycemia, ketoacidosis, and long-term microvascular and macrovascular complications affecting organs like the eyes, kidneys, nerves and blood vessels. - Treatment involves insulin replacement therapy and managing blood glucose levels to prevent acute complications and reduce risk of chronic complications.

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Hanya Bint Potawan
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126 views1 page

Pa Tho Physiology - Type 1 Diabetes (Hanieyah Guro)

This document summarizes the pathophysiology of type 1 diabetes mellitus. Key points include: - Type 1 diabetes is an autoimmune disease where the immune system attacks the beta cells in the pancreas that produce insulin, resulting in absolute insulin deficiency. - Without insulin to regulate blood glucose, complications arise like hyperglycemia, ketoacidosis, and long-term microvascular and macrovascular complications affecting organs like the eyes, kidneys, nerves and blood vessels. - Treatment involves insulin replacement therapy and managing blood glucose levels to prevent acute complications and reduce risk of chronic complications.

Uploaded by

Hanya Bint Potawan
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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CNS Symptoms: (Moderate) Inability to concentrate Headache, Lightheadedness Confusion Memory lapses, Numbness of the lips and tongue,

Slurred speech, Impaired coordination, Emotional changes Irrational or combative behavior Double vision Drowsiness CNS Symptoms: (Severe) Disoriented behavior Seizures Difficulty arousing from Sleep Loss of consciousness

Idiopathic

Genetic: HLA DR3 and DR4

Age: <30 years old

TYPE 1 DIABETES MELLITUS


Metabolic demand is increased Virus/Toxins Adrenergic Symptoms: (Mild) Sweating Tremor Tachycardia, Palpitation, Nervousness Hunger Autoimmune disorder Pathogenesis Serum Islet Cell Antibdies Immune system attacks self Manifestations Acute Complication Destruction of -cells of the Islet of Langerhans Serum C-peptide Levels Absolute Insulin Deficiency
`

LEGEND
Etiologic Factors Drug Therapy Surgical Management Diagnostic Test Nursing Diagnosis

Whole Pancreas Transplant Islet Cell Transplants Decreased Insulin Production

Chronic Complications

Pramlintide (Symlin)

Hypoglycemia (Glucose: < 60 mg/dl)

Insulin Therapy Decreased utilization of glucose by muscle, fat and liver Fatigue r/t decreased metabolic energy production

HbA1c Test (>8%) FBG Test (>126 mg/dl) OGT Test (>200 mg/dl)

Polyphagia

Cell Starvation

Hyperglycemia

Increased Lipolysis

Slow wound healing Weight loss

Proteolysis

Increased Gluconeogenesis

Increased Glycolysis

Glucose above threshold of renal tubules (>200mg/dl)

Formation of sugar-containing plasma proteins (fibrinogen, clotting factors, etc)

Glucose binds to HbA

Glucose reduced to Sorbitol (in cells with aldosereductase)

Increased Fatty Acids in circulation

Increased Amino Acids in circulation

Glucose production Glucosuria Urinalysis Ketone: (+) Glucose: (+5) Yeast Infections Increased susceptibility to infection Osmotic Diuresis Increased clotting tendency

HbA1c formation

Increased VLDL

Increased production of ketone bodies

Formation of Advanced Glycation End (AGE) products

O2 is less readily released to the periphery Thrombosis Polyuria Hyponatremia Hypokalemia Hypochloremia Dry mucous membrane Poor skin turgor Dry, scaly skin Thin, brittle hair & nails Polydipsia Fatigue Increase Temperature

Accumulates in the lens of the eye

Accumulates in schwann cells and neurons

Acidosis

AGEs binds to call membrane receptors


DIABETIC KETOACIDOSIS

Increased loss of water and electrolytes

Fluid and electrolyte imbalance r/t increased urine output

Impaired lenticular transparency

Reduced nerve conduction

Increased H+ and CO2

Deposition of collagen in blood vessels Serum Test Glucose: >300 mg/dl Ketones: (+) pH: >7.35 HCO3: <15mEq/L Na+: low K+ : low BUN: >20 mg/dl Creatinine: >1.5 mg/dl Urine Ketones: (+)

Water shifts from the ICF space to the ECF space

Impaired sin integrity r/t dehydration Hyperthermia r/t decreased body fluids Decreased cardiac output r/t decreased blood volume

Cataract

Polyneuropathy

Increased rate and depth of respiration

Reduced permeability and luminal narrowing

Sodium Bicarbonate Dehydration

Blurred Vision

Numbness tingling sensation

Kussmaul Respiration Metabolic Acidosis

MICROANGIOPATHY Ischemia of small blood vessels

Hyperosmolarity/Hyperviscosity

Hypovolemia

Weak, thready peripheral pulse

Risk for injury r/t altered sensory perceptions

Cell shrinkage Retinopathy Nephropathy Neuropathy

Slow blood flow

Ischemia

RAAS Mechanism

Hypertension

ABG pH: <7.35 PaCo2: >35 HCO3: <22

Impairement of cell lymphocytes Blindness Loss of glomerulos Increased susceptibility to infection Ris for infection r/t decreased leukocyte function

Cyanosis Nail Clubbing

Hypoxia

Ineffective tissue perfusion r/t decreased arterial flow/ less readily release of O2 to the periphery

Anaerobic metabolism

cell necrosis

Lactic Acid production Acute pain r/t increased lactic acid production

gangrene MACROANGIOPATHY

ESRD

Muscle Spasm Headache

Debridement Renal Artery Stenosis Cerebrovascular Disease Coronary Artery Disease Peripheral Vascular Disease

COMA Impaired tissue integrity r/t hypoxia

Cerebral Infarction Altered LOC Brain Damage

Myocardial Infarction

Congestive Heart Failure

DEATH
Presented by: HANIEYAH GRANDE GURO

Multiple Organ Failure

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