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DMCS : 07/10/2010
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Pathophysiology of Diabetes Mellitus Type II
Precipitating factors:
1. development of glucose intolerance during drug therapy
2. GDM3. sedentary lifestyle4. stress5. obesity6. decrease serum potassium7. Toxin/Virus
Predisposing factors:
1. family history of DM/Genetic2. Age above 403. Race4. Gender
Idiopathic
Insufficient insulin-receptor on the insulin-dependent cells (liver
cells, muscles and fats)
Impaired beta cell function and insulin secretion
Reduced hepatic insulin sensitivity
Body does not respond to the action of insulin (Insulin
Resistance)
Decreased insulin production
Reduced tissue uptake of glucose
Liver senses low glucose level
Liver converts Glycogen to glucose
and releasing it to the Blood
A B
Acidity of urine Urethral flora
UTI VaginitisTreatment:
Medications:-Metronidazole-Azithromycin-Diflucan-Doxycycline
Treatment:
Medications:
-Amoxicillin
-Nitrofurantoin
-Ciprofloxacin
-Quinolones
C
Decreased transportation and use of glucose
↑ Insulin demand
Insulin response by beta cells declines d/t exhaustion
Blood glucose level rise: Initial Stage
S/Sx:
Hyperglycemia (>120 mg/dl)
Blood glucose > renal threshold
↓reabsorbtion capacity of the renal tubules
Excess glucose spills into the urine
High blood glucose draw water
from the cell
S/Sx:glucosuria
↑ Osmotic pressure in the filtrate
S/Sx:PolyuriaElectrolyte imbalance
Large volume of urine to be excreted
Fluid loss
Dehydration
S/Sx:polydipsia
Treatment:
Insulin Administration
Fluid & electrolytes
Continuous Decreased transportation of glucose and
nutrients into the cells
Stimulation of hunger mechanism via hypothalamus
Stimulation of appetite
S/Sx:polyphagia
If Treated:
Insulin therapy or Hypoglycemic agent
Exercise Reduction of
stress Diet
FAIR PROGNOSIS
A
B
C
D E
Severe hypoglycemia
If insulin rise due to many factors
Excess insulin transports glucose into cells
Increase gluconeogensis
SNS stimulation
Decreased CNS function
Glucose intake Insulin stores excess glucose in
the Blood
Blood glucose decrease
Return to stable state
Relative insulin deficit
Hyperosmotic plasma
Severe dehydration of cells
Hyperosmolar Hyperglycemic Nonnketotic
Syndrome(HHNS)
Coma
Death
Cells convert fats into glycerol and fatty acids for energy
Fatty Acids accumulate in the Liver
Fatty Acids are converted to Ketones: hydroxybutyric
acid, acetoacetic acid, acetone
Glucose available for brain drops
Some ketoacids excreted in the urine
ketoacidosis
S/Sx:
ketonuria
Ketone acids associate to yield hydrogen ions
Decrease in pH
Metabolic acidosis
S/Sx: Acetone Breath
F
I
J
If poor compliance
Insulin deficit severe/prolonged:
Damage of small blood vessels
Development of microaneurysms in the
capillary walls
Development of microaneurysms in the
capillary walls
Shifting of fluid in the interstitial spaces
Hard exudate formation
Tearing, partial or complete retinal
detachment
Atrophy of new vessels and contractions
Transitory lens change
Opacity of the lens
Neovascularization
New vessels formed are fragile causing hemorrhage and
contractures of the vitreous and pulling of
retina
S/Sx:
Blurring of vision
Decrease color perception
S/Sx:
Dark red circular spots
Sorbitol accumulation in the nerve cells
Damage on the Schwann cells
Diabetic Neuropathy
Impaired peripheral and central vision
Blindness
D E
F
G
KO
Increased blood viscosity
Sluggish circulationBlood pooling at left ventricle
Left ventricle hypertrophy
Imitation of endothelial lining of the blood
vessels
Blood Stasis
Shunting of glucose in polyol pathway
Enzyme system converts glucose to sorbitol and slowly to
fructose in an attempt to normalize the glucose level
Accumulation of sorbitol in the basement membrane of the cell and between that uses sorbitol
pathway
Basement membrane thickening
Poorly controlled glucose
Ischemia
myocardial infarction
Thrombus Formation
Heart
Cerebrovascular Accident(Stroke)
Brain
Decrease blood flow to the periphery(big vessels)
Delayed wound healing
ischemia
necrosis
gangrene
The cell receives inadequate oxygen and nutrition and retained waste products
Decreased blood flow in small vessels S/Sx:
Ulceration Diabetic
foot
Treatment:
debridementamputation
G
K
L
Neurons unable to store glucose
Energy Crisis
Hypoglycemic shock
Neurons cannot function
DEATH
coma
Lung exhaustion
Failure of respiratory buffer system
Rise in carbonic acid
Further decrease in the pH level, hyperosmolality, hypotension, tissue damage, depression of
central function
Coma
Death
pH compensation; Kussmaul respirationABG: Decreased PaCO2
I
J
Associated Complications
as a result
of DM together with CRF
Accumulation of fats and toxic substances in the liver as a result of DM and CRF
Liver necrosis
Fibrosis and scarring
glucose
Liver inflammation
Bile saltLipoprotein cholesterol
Hyper bilirubenemia
Steroid hormones
bilirubnDrug interaction/t
oxicities
Amino acidsproteins bilirubin
hypoalbuminemia Decreased coagulation factors
Dec. cholesterol
Impaired fat absorption
Impaired conver-sion of ammonia to urea
Hepatic encephalo-pathy
Increased aldosterone
Disorders of synthesis and storage functions
Disorders of metabolic and excretory functions
Increased androgen, estrogen
S/Sx:
Hypoglyce-mic
S/Sx:Edema/ascites
S/Sx:bleeding
S/SDef. of fat-soluble vitamins
S/Sx:Fatty stools
S/Sx:Asterixis, confusion, coma
S/Sx:edema, ascite
S/Sx:Menstrual irregularities
S/SxJaundice, ictieric sclera, clay-colored
stool
drugs
Decreased renal blood
flow
Nodular glomerulosclerosis
(inter-capillary glumerulosclerosis
Diffuse glomerular sclerosis (mesangial
matrix)
Progressive loss of kidney function
Acute Renal Failure
Initiation Stage
Maintenance Stage
Slow progress characterized by irreversible reduction in
GFR
Loss of nephrons
S/S:
Oliguria Scanty
output Hematuria Decrease
urine
Management:
Maintenance of body fluids
Hemodialysis Peritoneal
Dialysis Medicatrtions Nutritional
Therapy
Nephropathy
L
M
Fibrosis and scarring
Portal hypertension
Inc. pressure in peritoneal cavities
Portosystemic shunting of blood
splenomegaly
Shunting of ammonia and toxins into circulation
Development of collateral channels
S/Sx:
ascites
S/Sx:HemorrhoidsEsophageal varices
Hepatic encephalopathy
S/Sx:
asterixis
S/Sx:Anemia, thrombocytopenia
Stage 1
Decreased Renal Reserve
No symptoms:
Residual Reserve 40%
Further loss of nephron function
Stage 2
Renal Insufficiency
S/S:
Mild azotemia Mild anemia GFR decrease to 20
mL/min Residual renal function
15-20%
No homeostasis;
symptomatic in many systems;
5 % residual renal function
Loss of excretory renal function
Stage 3Renal Failure
Decreased excretion of nitrogenous waste
Uremia
Stage 4End Stage Renal Disease (ESRD)
Chronic Kidney Disease
S/S:
Severe azotemia
Severe anemia Nocturia 5-15% residual
renal function
M
N
Excess pronucleating factor
(Mucin and Non-mucin glycoprotein)
Deficiency of antinucleating factor (apolipoproteins AI &
AII)
Cholesterol monohydrate crystal nucleation and crystal growth within mucin gel layer
Unstable cholesterol-rich vesicle remain
Vesicle fusion
Liquid Crystals
Continued growth of the crystals by direct nucleation of cholesterol molecules from supersaturated unilamellar or multilamellar biliary vesicles
Biliary sludge
SUPERSATURATION OF BILE WITH CHOLESTEROLSupersaturation of
cholesterol is a necessary but not
sufficient condition for the formation of
gallstone
Gallstone formation:
CHOLECYSTOLITHIASIS
Silent/ Asymptomatic gallstones
If Treated:
• Nutritional and supportive Therapy
•Pharmacologic Therapy
• T-tube Tract
•Extracorporeal Shockwave Lithotripsy
•Intracorporeal Lithotripsy
•Cholecystectomy
FAIR
R
O
G
N
O
S
I
If not treated
Small Stones pass into CBD
<5mm
Obstruction of Bile Flow on
CBD
Larger stones obstruct bile flow
on the Gallbladder
CHOLEDOCHOLITHIASIS
Gallbladder Distention
Migrate in the extra hepatic biliary tree through cystic duct
MIZZIRI’S SYNDROME
Increase Intraluminal pressure
(Mechanical inflammation)
Release of lysolecithin and other tissue local
factors(Chemical inflammation)
Bacterial Inflammation
Erodes lining of Gallbladder
Erodes lining of CBD
S/S:
• Asymptomatic gallstonesOr
• Follows acute cholecystitis
If Treated:
Hemodialysis Peritoneal
Dialysis Pharmacologic
Therapy Nutritional
Therapy Kidney
Transplant
Fair prognosis
If Not Treated
Hematologic:
Anemia Bleeding Infection
Musculoskeletal:
Retarded growth Renal
osteodystrophy
Cardiovascular:
Increase Blood Pressure
Congestive Heart Failure
Pericarditis
Neurologic:
Peripheral neuropathy
Uremic encephalopathy
Neurologic:
Peripheral neuropathy
Uremic encephalopathy
Multi-system Failure
Death
N
O
PHERIPHERAL NEUROPATHY
AUTONOMIC NEUROPATHY
PROXIMAL NEUROPATHY
FOCAL NEUROPATHY
numbness or insensitivity to pain or temperature
a tingling, burning, or prickling sensation
sharp pains or cramps extreme sensitivity to
touch, even light touch loss of balance and
coordination
HEART GASTRO-INTESTINAL
Urinary Tract & Sex Organs
Sweat Glands
EYES
Sharp Decrease in Blood Pressure
Increased Heart rate Constipation
Gastroparesis Nausea and
Vomiting Loss of Apetite
GASTROPATHY Urine retention Impotence
Profuse sweating at night or during eating
Sluggish pupils Cannot see well
when there is sudden change in light
Pain in thighs, hips, buttocks, or legs
Weakness of legs
Inability to focus the eye
Double vision Aching behind
one eye Paralysis on one
side of Face( Bell’s Palsy)
Severe pain on lower back
Pain in chest, abdomen, foot