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B. Pathophysiology A) Schematic Diagram (Book - Based) : Wasting Blood Glucose Level

This document provides a schematic diagram outlining the pathophysiology of type 2 diabetes mellitus. It lists both non-modifiable and modifiable risk factors. The key steps in the pathophysiology include insulin resistance leading to impaired insulin production and increased glucagon release. This results in elevated blood glucose levels and wasting. Over time, this chronic hyperglycemia can lead to complications affecting small blood vessels and major organs like the eyes, kidneys, and heart.

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Carl Elexer Cuyugan Ano
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© Attribution Non-Commercial (BY-NC)
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3K views2 pages

B. Pathophysiology A) Schematic Diagram (Book - Based) : Wasting Blood Glucose Level

This document provides a schematic diagram outlining the pathophysiology of type 2 diabetes mellitus. It lists both non-modifiable and modifiable risk factors. The key steps in the pathophysiology include insulin resistance leading to impaired insulin production and increased glucagon release. This results in elevated blood glucose levels and wasting. Over time, this chronic hyperglycemia can lead to complications affecting small blood vessels and major organs like the eyes, kidneys, and heart.

Uploaded by

Carl Elexer Cuyugan Ano
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 DOC, PDF, TXT or read online on Scribd
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B.

Pathophysiology

a) Schematic Diagram (book – based)

Non – modifiable Risk Factors: Modifiable Risk Factors:


-45 y/o and above -Glucokinase mutation -Obesity -Sedentary lifestyle
-African American, Native -Familial history of DM type 2 -Stress -gestational DM
Americans, Asian American -Familial history of hypertension -Previously known Impaired - certain medication such as
Pacific Islander Fasting glucose Thiazides & corticosteroids.
-↑consumption of fatty, salty - Smoking
& sweet food - Alcoholism

Insulin resistance and desensitization

↓insulin production ↑glucagon Fats and Proteins breaks


Release down to glucose

↑blood Impaired glucose Cellular


absorption starvation Wasting
glucose level

Weight loss / fatigue


↑osmolality Polyphagia

Chronic glucose
Fluid shifts from elevation Glycoprotein cell
IC to IV wall deposits

Sluggish blood
Cellular dehydration ↑blood volume
flow Narrowing of
blood vessel
Thirst activation ↑GFR

polydipsia polyuria
Small vessel Accelerated
disease atherosclerosis ↑LDL

Hypertension Coronary Artery Disease


Diabetic Diabetic
retinopathy neuropathy
Plaque rupture

Alteration numbness
in vision/ Exposure of subendohelial matrix
blindness
Foot
ulceration
Platelet activation

Diabetic Change in platelet Platelet ↑ Expression of Platelet


nephropathy shape degranulation GP IIb/IIIa

ESRD Platelet adhesion to Release of Thromboxane A2, Enhanced affinity to


subendothelial matrix Serotonin and other platelet fibrinogen
aggregatory agent

Platelet aggregation

↓ Arterial lumen Plasma Coagulation


System activation

Formation of thrombin

Converts fibrinogen Enhances platelet


to fibrin aggregation

Stabilization of
Nidusfibrin clot
of rethrombosis
Backflow of
Impaired
blood in the
Productive Pulmonary repolarization of the Blood pooling
of on left ↓
Adventitious lungs
myocardium
Release lysosomal
Re-establishment ofventricular
Hardening theofendothelium
the Irregular heart
Myocardial
cough
Breath sounds congestion enzymes
ventricle function ↓cardiac contractility ↑BP, HR, and O needs irritability
beats
Fatigue ↓ oxygenation
DOB Lactic
Anaerobic
ECG changes
acid production
glycolysis
Angina ↑ CKMB
Ischemia
with fibrotic coronary
Vasospasm
Impaired
ofMyocardial
the
Coronary
tissue arteries
dislodges
cardiac
tissue ↓ cell
supplied
occlusion
andCOperfusion
death
thrombus
by the artery
thrombus SNS
vasocontriction
Stimulation
2

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