Post on 06-Apr-2018
8/2/2019 Pa Tho Physiology of Diabetes Mellitus
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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- 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
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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
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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