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    Pa Tho Physiology of Diabetes Mellitus

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    Pong's Teodoro Salvador
    This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

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    Pa Tho Physiology of Diabetes Mellitus

    Uploaded by

    Pong's Teodoro Salvador
    101 views3 pages
    This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

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    This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as DOCX, PDF, TXT or read online from Scribd
    Download as docx, pdf, or txt
    101 views3 pages

    Pa Tho Physiology of Diabetes Mellitus

    Uploaded by

    Pong's Teodoro Salvador
    This document describes the pathophysiology of diabetes mellitus and benign prostatic hyperplasia in an 80-year-old male patient with a family history of diabetes. Precipitating factors included a diet high in sugar, carbs and fats, smoking, alcohol use, and non-compliance with diabetes medications. This led to exhaustion of beta cells, altered pancreatic function, hyperglycemia, tissue damage, infections, and various complications affecting the heart, kidneys, nerves and other organs. Similarly, increasing age, smoking, diabetes and other conditions contributed to benign prostatic hyperplasia through enlarged prostate size, decreased bladder emptying, and lower urinary tract symptoms.

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    PREDISPOSING FACTOR AGE: 80 yrs.

    Old Family History of DIABETES Hereditary

    PRECIPITATING FACTORS DIET: eating foods rich in sugar, carbs, and fats LIFESTYLE: smoking, drinking alcohol Compliance: no maintenance of meds. for DM

    Exhaustion of beta cells occurs

    Altered pancreatic insulin production Decreased insulin production Decreased absorption of glucose by the cells Glucose is unable to enter the cells Glucose remains in the blood stream Increased serum glucose level
    HYPERGLYCEMIA (304 mg/dl, 13.2 mg/dl)

    Sluggish flow of blood Impaired delivery of blood components Inadequate inflammatory response Microorganism would enter the body at any route

    Serum osmolarity
    Blood viscosity

    Tissue perfusion of kidney


    Impaired removal of waste Failure to initiate erythropoietin

    Osmotic pressure in blood H20 from cell towards the blood

    Glucose concentration in urine Reabsorption of glucose in renal tubule

    Glucose intake of cells ATP production Energy for normal cells functions Cells starvation occurs Stimulation of the hunger mechanism Hunger occurs
    POLYPHAGIA

    Blood flow to the organs and extremities Tissue perfusion in nerves Nerve hypoxia Segmental demyelization Nerve damaged Excessive glucose is converted into SORBITOL w/c accumulate in nerves Sorbitol impairs motor nerve conduction

    Impaired removal of waste from blood Glucose level exceeds renal threshold Impaired renal Fnx Permeability of the renal cell wall Filtration of macro cells & particles

    Stimulation of the bone marrow fails RBC production decreased

    Dehydration Stimulation of osmoreceptors thirst

    Osmotic pressure H20 reabsorption Urine output

    Infection occurs
    WBC (14.4), eusinophils (7%)

    POLYDIPSIA RBC (4.5) POLYURIA

    Fatigue

    Inadequate nutritional support

    Poor wound healing

    Paresthesia, numbness

    Decreased PR (60 bpm)

    Sugar+2, protein+2, blood+5, RBC >100/hpf

    DIABETES MELLITUS
    Pathophysiology of BPH

    Thickening of the cardiac blood vessels wall Plaque formation begins

    Occlusion of the blood vessels occurs

    Blockage of blood flow

    Myocardial ischemia occurs Decreased myocardial O2 supply

    + TROPONIN T ST-T abnormality

    Half of the bundle of his loss its function Left fascicular block occurs

    Increased cellular hypoxia


    Mild left axis deviation

    Increased lactic acid production release of metabolites Altered cell membrane functions

    CHEST PAIN

    MYOCARDIAL INFARCTION (ACS)

    Ineffective right ventricular contractility

    Reduced right ventricular pumping ability

    Decreased cardiac output

    Backflow of blood into the right atrium and peripheral circulation

    Shifting of fluids into interstitial spaces

    Grade 2 edema @ lower extremities

    SINUS BRADYCARDIA

    DOB, fatigue, with rales upon auscultation

    Ineffective left ventricular contractility

    Reduced left ventricular pumping ability

    Decreased cardiac output

    Backflow of blood into the left atrium and lungs

    Pulmonary congestion

    Pulmonary edema

    HEART FAILURE

    PREDISPOSING FACTORS AGE: 80 yrs. Old FAMILY HISTORY OF BPH NORMAL BODY CHANGES

    PRECIPITATING FACTORS SMOKING WITH DM, HF, AND MI

    As mans age increased prostate gland increased Androgen Testosterone Dihydrosterone Binds to nuclear androgen receptors

    Deterioration of the blood vessel in the prostate Blood flow becomes abnormal and 02 supply impaired

    Signals growth factors

    Stimulation of cell growth

    HYPERPLASIA
    Encroaches upon the bladder neck occurs

    Increased size of prostate

    Reduced ability to funnel in response to micturition

    Overwhelms the detrusor muscles ability to ensure effective bladder evacuation by micturition

    UTI (1-2 PUS CELLS), HEMATURIA

    Obstruction occurs

    Increase urethral resistance

    LUTS

    Dribbling of urine

    Feeling of incomplete emptying of the bladder

    Increased daytime voiding frequency


    POLYURIA

    URGENCY

    NOCTURIA

    BENIGN PROSTATIC HYPERPLASIA

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