MF: NMF:

-environment - Age
-low socioeconomic

Inhalation of pathogen

Failure of the airway defensive

mechanism in preventing the Inflammatory of pulmonary
descent of pathogens due to capilliaries
lack of cilia in mucociliary

Osmosis pressure that will

Pathogen agent adhere to increased capilliary
mucus membrane and permeability
epithelial cells of the airway
and begin cellular invasion
Larger spaces allows more
fluid, immune cells and large
Uncontrolled proliferation of pressure leak into interstitial
the bacteria occurs in alveoli space

Immune response, release od Decreased IVF osmotic Increased interstitial

T-cell and inflammatory Pressure osmotic pressure
cytokines in the blood stream

This will go from IF to

Increased capilliary interstitial space
permeability

Excess fluid get caught/

Allows passage of released accumulate between visceral
immune response to reach the an parietal cell
alveoli are cause fluid
accumulation
Surrounds the lungs and
increased pleural pressure
Obstruction of alveoli causes
difficulty in lung gas exchange
Leads to compression of lung
tissue.

Decreased oxygenation Impaires ability to breath

Increased oxygen saturation in

tissue Pleural effusion

Tachypnea
 UNIVERSITY OF THE EAST

RAMON MAGSAYSAY MEMORIAL MEDICAL CENTER INC.

#64 Barangay Dona Imelda Aurora Boulevard Quezon City 1113

NCM 103 Concept Map on:

DIABETIC FOOT

Submitted b: Venturillo, Julienne Diana D.

Vision 2020
I.NTRODUCTION
Diabetes Mellitus is a chronic disorder of carbohydrate, protein, and fat metabolism which there is
a discrepancy between the amount of insulin required by the body and the amount of insulin available.
Diabetes is increasing at an alarming rate in Asian countries including the Philippines. Both the prevalence
and incidence of type 2 diabetes (T2D) continue to increase with a commensurate upward trend in the
prevalence of prediabetes.

The prevalence of diabetes in the Philippines is increasing. Rapid urbanization with increasing
dependence on electronic gadgets and sedentary lifestyle contribute significantly to this epidemic. Diabetes
care in the Philippines is disadvantaged and challenged with respect to resources, government support, and
economics. The national insurance system does not cover comprehensive diabetes care in a preventive
model and private insurance companies only offer limited diabetes coverage. Thus, most patients rely on
“out-of-pocket” expenses, namely, laboratory procedures and daily medications. Consequently, poor
pharmacotherapy adherence impairs prevention of complications. Moreover, behavioral modifications are
difficult due to cultural preferences for a traditional diet of refined sugar, including white rice and bread.

Type 2 Diabetes, also known as Non-Insulin-Dependent (NIDDM) are patients who are not
dependent on insulin. They either have insulin resistance or have an impaired insulin secretions and
accounts to 80-90% of DM Patients. Beta cells have no insulitis, and resistance to insulin occurs in the
target cells. Insulin resistance is associated with increased levels of free fatty acids in the blood, reduce
glucose transport in muscle cells, elevated hepatic glucose production, and increased breakdown of fat.
(Sommers & Fannin, 2015)

Since diabetic patients are hyperglycemic, they are at a higher risk for infection because an elevated
glucose encourages bacterial growth. The combination of peripheral neuropathies with numbness of the
extremities, peripheral vascular disease leading to poor tissue perfusion, and the risk for infection makes
the diabetic patient prone to feet and leg ulcers. (Sommers & Fannin, 2015)

Patient T.A 89 y/o Female, Filipino, Catholic, was admitted to the Surgery Ward of UERM Hospital
on July 24, 2018 at 6:15pm due to Chief Complaint of non-healing and progressively enlarging Left Foot
wound with duration of one (1) week. Patient was then diagnosed to have Diabetic Foot Infection, Left.
 PATHOPHYSIOLOGY
MF: NMF:
-infection -Gender (F) (OBS Hx)
-Lifestyle (Sedentary) -Age (89)
-(+) FmHx/ genetic predisposition
- 4Ps
- (+) PHx

Insulin Resistance

dysfunction of insulin-producing
pancreatic beta cells, insulin
hormone resistance in cells of the
body, or a combination of both

The resistance, and the

compensating production of
insulin by pancreatic beta cells,
may eventually lead to beta cell
failure

endogenous insulin can no longer

be secreted

struggles to store the sugar found in

the blood. Leads to the pancreas has
to produce more insulin to
compensate for this reduction in LANSOPRAZOLE:
insulin function.
Class of PPI

Block the production of acid

the inability of cells to use the by the stomach by specific
inhibition of the (H+, K+)-
insulin hormone, which inhibits
ATPase enzyme system at
the cell’s capability to absorb and the secretory surface of the
then use glucose in metabolic gastric parietal cell.,

Hyperosmolar state processes

Insulin Deficiency
Too much glucose cause to
excrete water through urine

hyperglycemia
A
Dehydation

LOOSE GREEN WATERY

STOOL
 A

Vascular changes

Atherosclerosis, in which plaques

builds up inside the arteries

Alteration in vascular hemeostasis

due toe endothelial and SMC
dysfunction

Increased glucose take most in the

endothelial cells

Too much glucose inside cells

increased release of ATP

Forms PKC Forms AGP

Increased
endothelium
Increased NFkB

B Increased platelet Increased VEGF: growth

aggregation factors angiogenesis

-growth factor
Platelet: 253
angiogenesis

ENOXAPARIN: an
anticoagulants or
antithrombotic, binds to
antithrombin III and
accelerates activity, inhibiting
thrombin and factor Xa
(LMWH)

It treat blood clots.

An inflammatory transcription factor

 C

MACROVASCULAR Complication MICROVASCULAR Complication

Peripheral Vascular
Nephrophaty
Exudation of plasma proteins

Edema/ swelling Patient has (+) Pallor, pale lips and poor skin
turgor. Patient has Stage 2 ulcerations on her
Loss of sensation lower back and sacral area, 2x3.5 cm and
3x2cm, respectively

Positive gangrene

FOOT DIABETES (+) oral candidiasis specifically in the tongue with

creamy white bumps on the tongue, gums and
tonsils
No capillary refill on both fingers of the left
and right hands and both toes of the left and
right feet. Patient is (+) for +4 Pitting Edema
on both Left and Right feet. Unable to
palpate both Dorsalis pedis pulses due
to edema.

Cerebrovascular

Glasgow Coma Scale score of 8/15, Eye

Opening responsive to speech (3), CHOLINERV: improves the pt.’s
Incomprehensible verbal sounds (2), and condition of the structural
Flexion to painful stimulus (3). The patient phospholipids of cell
was observed to be stuporous, responsive membrane.
only to tactile-stimulation, and semi-
conscious.

Coronary artery

CBC Results show decreased HgB (85 g/L),

Hematocrit (28%), RBC (3.1 x 1012/L),
MCHC (31%),

and increased RDW (20.6%), WBC (110.8

x109/L), Neutrophil (75%)