Pa Tho Physiology of Diabetes Mellitus

8/2/2019 Pa Tho Physiology of Diabetes Mellitus

1/3

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- Com liance: 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

Serum osmolarity

Blood viscosity

Blood flow to theorgans and extremities

Tissue perfusion innerves

Nerve hypoxia

Segmentaldemyelization

Nerve damaged

Excessive glucose isconverted into SORBITOLw/c accumulate in nerves

Sorbitol impairsmotor nerveconduction

Sluggish flow of blood

Impaired deliveryof blood

components

Inadequateinflammatory

response

Microorganismwould enter the

body at any route

Infection occurs

Tissue perfusionof kidney

Impairedremoval of

waste

Failure toinitiate

erythropoietin

Stimulation of the bone

marrow fails

Impairedremoval of

waste fromblood

Glucose levelexceeds renal

threshold

Impaired renalFnx

Permeabilityof the renal

cell wall

Filtration of macro cells &

particles

Inadequatenutritional

support

Osmoticpressure in

blood

H20 from celltowards the

blood

Dehydration

Stimulation of osmoreceptors

thirst

Glucoseconcentration

in urine

Reabsorptionof glucose inrenal tubule

Osmoticressure

H20reabsorption

Urine output

Glucose intakof cells

ATProduction

Energy fornormal cell

functions

Cells

starvationoccurs

Stimulation othe hungermechanism

Hunger occu

WBC (14.4),eusinophils

(7%)

Sugar+2,protein+2,

blood+5, RBC>100/hpf

RBCproductiondecreased

RBC(4.5)

POLYDIPSIA

POLYURIA

POLYPHAG

Paresthesia,numbness

Poorwoundhealing

DecreasedPR (60 bpm)

Fatigue

DIABETES MELLITUS

HYPERGLYCEMIA (304mg/dl, 13.2 mg/dl)

Pathophysiology of BPH


2/3

Thickening of the cardiac blood vessels

Plaque formation begins

Occlusion of the blood vessels occurs

Blockage of blood flow

Myocardial ischemia occurs

Decreased myocardial O2 supply

Increased cellular hypoxia

Increased lactic acid production releaseof metabolites

Altered cell membrane functions

MYOCARDIAL INFARCTION(ACS)

+ TROPONIN TST-T

abnormality

CHEST PAIN

Half of the bundle of hisloss its function

Left fascicular block occurs

Mild left

axisdeviation

Ineffectiveright

ventricularcontractilit

Reduced rightventricularpumping

abilit

Decreasedcardiacoutput

Backflow of blood into the

right atrium andperipheral

Shifting of fluids intointerstitial

spaces

Ineffectiveleft

ventricularcontractilit

Reduced leftventricularpumping

abilit

Decreasedcardiacoutput

Backflow of blood into theleft atrium and

lungs

Pulmonarycongestion

Pulmonaryedema

SINUSBRADYCARDIA

Grade 2edema @

lowerextremities

DOB,fatigue, withrales upon

auscultation

HEART FAILURE


3/3

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

PRECIPITATING FACTORS- SMOKING- WITH DM, HF, AND MI

Deterioration of the blood vessel in theprostate

Blood flow becomes abnormal and 02supply impaired

Stimulation of cell growth

As mans age increasedprostate gland increased

Androgen

Testosterone

Dihydrosterone

Binds to nuclearandrogen receptors

Signals growth factors

HYPERPLASIA

Encroaches upon thebladder neck occurs

Increased size of prostate

Reduced ability to funnelin response to micturition

Obstruction occurs

Overwhelms the detrusormuscles ability to ensure

effective bladderevacuation by micturition

Increase urethralresistance

LUTS

UTI (1-2 PUSCELLS),

HEMATURIA

Dribbling of urine

Feeling of incompleteemptying of the bladder

POLYURIA

Increased daytimevoiding frequency

URGENCY NOCTURIA

BENIGN PROSTATIC HYPERPLASIA

Documents

Pa Tho Physiology of Diabetes Mellitus