Diabetes Mellitus 2 and Chronic Kidney Disease

8/13/2019 Diabetes Mellitus 2 and Chronic Kidney Disease

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PATHOPHYSIOLOGY

Etiologic Factor

I- Predisposing Factors

Factors Present Justification

Gender According to Huether and McCance (2012),

incidence of Type 1 DM in gender is similar

in males and females.

Race Huether and McCance (2012) stated that

races like non-Hispanic blacks,

Hispanic/Latino, American Indians, Alaska

Natives, Asian Americans, and Pacific

Islanders have between 1.5 and 2.2 times

the risk of whites.

Family history According to Huether and McCance (2012),

there are between 10% and 13% of

individuals with newly diagnosed type 1 DM

have a first-degree relative with type 1 DM.

Age It affects people primarily after 40 years of

age, as mentioned by Huether and McCance.

Socioeconomic

status

It is more common among those lower

income countries.

II- Precipitating Factors

Factors Present Justification

obesity Obesity is a risk factor because and it is the


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major contributor to insulin resistance

through adipokines released in adipose

tissue (McCance & Huether, 2010).

Physical inactivity Inactivity increases serum triglycerides ad

cholesterol and decreases the HDL

Symptomatology

Type 2 Diabetes Mellitus

Symptoms Present Justification

hyperglycemia In type 2 DM, elevated serum glucose level

happens when there is insufficient insulin

produced by the beta cell. The less sensitive

the insulin receptor, the higher concentration

of glucose is retained in the bloodstream

(Porth, 2010).

Polydipsia Because of elevated serum glucose levels,

water is osmotically attracted from body cells,

resulting in intracellular dehydration and

stimulation of thirst in hypothalamus (Huether

& McCance, 2008).

Polyuria Hyperglycemia acts as an osmotic diuretic;

the amount of glucose filtered by the

glomeruli of the kidneys exceed that which

can be reabsorbed by the renal tubules;

glucosuria results, accompanied by large

amounts water lost in the urine (Huether &

McCance, 2008).

polyphagia Depletion of cellular stores of carbohydrates,

fat, and protein results in cellular starvation


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and a corresponding increase in hunger

(Huether & McCance, 2008).

Recurrent infection Growth of microorganisms is stimulated by

increased glucose levels; impaired blood

supply hinders healing (McCance & Huether,

2010).

Our patient had undergone gram staining

culture and sensitivity in her sputum and

urine. The result was both had the presence

of Staphylococcus aureus and Candida

infections. Moreover, the patient had a

cellulitis in the left leg and the wound was

gram stained, cultured, and being treated by

different antibiotics. It also had S. aureus and

candidal infections.

Genital pruritus Hyperglycemia and glycosuria favor fungal

growth; candidal infections, resulting in

pruritus (McCance & Huether, 2010).

Visual changes Blurred vision occurs as water balance in theeye fluctuates because of elevated blood

glucose levels; diabetic retinopathy is

another cause of visual loss (McCance &

Huether, 2010).

Our patient had already undergone

extracapsular cataract extraction in the left

eye last 2010. She said that months or years

after she was diagnosed with type 2 DM, her

vision fluctuates until there was luring on her

left eye.

Paresthesia Paresthesias are common manifestation o

diabetic neuropathies (Jameson, 2010).


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Fatigue and

lethargy

Metabolic changes result in poor use of food

products, contributing to lethargy and fatigue

(McCance & Huether, 2010).

Dyslipidemia Dyslipidemic because of the mild lypolysis.

Myelodysplastic Syndromes

Symptoms Present Justification

Pallor, dyspnea,

fatigue

Pallor, dyspnea, and fatigue are initial

symptoms of anemia because one problem

of MDS is insufficient production of RBCs

Skin infection Leukopenia is also one the problem f MDS

due to immature blast cells.

Prolonged wound

healing

Platelets are the responsible for clotting. If

there is low amount of platelet, prolonged

wound healing ise xpected


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SCHEMATIC DIAGRAM

Predisposing Factors:

Age

Gender

Race

Family history

Genetic predisposition

Precipitating Factors:

Obesity

Physical inactivity

Insulin receptors are

less sensitive to insulin

Presence of adipokines, increase serum FFA,

intracellular deposits of triglycerides and cholesterol,

and inflammatory cytokines

Decrease beta cell

mass & beta cell

dysfunction

Insulin

resistance

Relative insulin

deficiency

Glucose cannot pass

through the cell

B

A

Increase in insulin

counterregulatory hormones


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High blood glucose

level

Pancreatic beta cells compensate by

increasing the insulin output

Increase insulin level in

the plasma

Stimulates beta cells to

produce more insulin

Less sensitivity to

insulin receptors

High serum

glucose level

B

B

hyperglycemia

hyperinsulinemia

Increase

HGT result


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B

B2B1

Beta cell

exhaustion

Over workload of the

pancreatic beta cells

Impaired insulin

secretion

Beta cell

dysfunction

hypoinsulinemia

Glycogenolysis in the liver

(breakdown of glycogen)

Mild lypolysis

(fat breakdown)

Gluconeogenesis

(formation of glucose)

Protein

breakdown

Amino acid

formation

Liberation of FFA and

glycerol

A


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Polyphagia

High osmotic

pressure in th

plasma

Chronic

hyperglycemia

B2

dyslipidemia

Cellular starvation

Polydipsia

Depletion of cellular

stores of carbohydrates,

fats, and protein

atherogenesis

Increased lipid synthesis in

hepatocytes (steatosis)

Nonalcoholic fatty

liver disease

B1

Glucosuria

Osmotic

diuretic

High f iltration

of glucose

Intracellular

dehydration

Abnormal liver

function tests

creased triglycerides

and LDL and

decreased HDL

C

Polyuria

GOOD

PROGNOSIS

If not treated:

Coronary artery

disease

Stroke

Peripheral vascular

disease

Treatment:

Lipid lowering agent

Antihypertensives

atherectomy

Genital pruritus,

recurrent

infections

Antibiotics

FAIR

PROGNOSIS

F


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C

Aldose reductase

catalyzes glucose to

sorbitol

Increased advanced

glycosylation end product

Microvascular

diseases

Hyperperfusion in

retinal plasma flow

and activation of PKC

Vascular cell

proliferation, enhanced

contractility, and

increased permeability

Capillary occlusion

Capillary endothelial

cell is damaged

Sorbitol interferes

with ion pumps

Sorbitol is converted into

fructose by sorbitol

dehydrogenase

Increasedintracellular osmotic

pressure

D

Cell injury in

e ithelial cells

Inactivation of

nitric oxide

Vasoconstriction

Demyelination of

Schwann cells

Decreased nerve blood

flow in vaso nervorum

Aldose reductase

catalyzes glucose to

sorbitol

C3C1 C2 Paresthesia, tingling

sensation, absence of ankle

reflexes, numbness


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C2C1

Retinal

ischemia

Treatment:

Aldose reductase

inhibitor

GOOD PROGNOSIS

If not treated:

Diabetic retinopathy

Treatment:

Regular eye examination

Laser photocoagulation

Limit valsalva maneuver

Aspirin therapy

Glycemic and blood

pressure control

If not treated:

cataract

GOOD PROGNOSIS

Extracaps

catarac

extractio

C3

Treatment:

Vitamin B12and folatesupplement

Antidepressants/anticonvulsants

Adequate salt intake

Avoidance of dehydration and

diuretics

If not treated:

Diabetic neuropathy

GOOD PROGNOSIS

ual changes,

mplete blindness


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First 5 years

D

Hyperfiltration and

hypoperfusion in the kidneys

Increased afferent

arteriole dilatation

Renal vasodilation

occurs

Greater mesangial

matrix production

Increase intraglomerular

pressure

Increased GFR and

protein excretion

Glomerular hypertrophy and

mesangial volume expansion

proteinuria

D1

Increased sodium

excretion

Sodium deficit and

volume depletion

D2

Hardening of the

nephrons

Diabetic

nephrosclerosis

D3


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5-10 years

: Stage 2 CKD

D1

Begins to excrete small

amounts of albumin

Increases glomerular

capillary permeability

Progression increased in

intraglomerular pressure

Excretion of big amount

of albumin

Nephron injury

Juxtaglomerular

apparatus secretes renin

hypoproteinemia

Microalbuminuria/

proteinuria

D2

Renin converts

Angiotensinogen to Ang I

ACE converts Ang I to

Ang II in the lungs

Decreased plasmacolloid osmotic pressure

Aldosterone increases waterretention and increase BP

Ang II stimulates adrenal

gland to secrete aldosterone

Water retention in

tissues D2

D2

dema,

asarca

D1

Mild decrease in GFR

60-89mL/min

Treatment:

ACE inhib

Treatment

ARBS

Treatment

Decreas

OFI

D3


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D1

Renal scarring

Increased serum

creatinine and urea

concentration

Increased glomerular

permeability and filtration

Glomerular capillary

hypertension

proteinuria

Increased tubular

protein reabsorption

Tubulointerstitial

fibrosis

Increase

creatinine and

urea

E


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Stage 3 CKD

Increase cardiac

output

Systemic hypertensionIncrease loss of

nephrons

E

Moderate decrease in

GFR 30-59mL/min

More kidney damage Impaired renal

synthesis of calcitriol

Anemia

Decreased production

of RBCs

Impaired erythropoietin

production

Pallor, fatigue,

weakness,

dyspnea

Hypertrophy of the

myocardium

Increase afterload and

increase heart workload

Decreased calcium

intestinal absorption

Serum phosphate

binds to calcium

hypocalcemia

E1

E2

Blood transfusion,

oxygen administration

E3


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E1

Stimulates parathyroid

gland to produce PTH

Vitamin D deficiency

If not treated:

Vascular

calcification

(mitral, tricuspid,

and aortic

sclerosis)

hypercalcemia

Hyperparathyroidism

Treatment:

Vitamin D

replacement

Phosphorus

supplements

Sunlightexposure

If not treated:

osteomalacia

FAIR PROGNOSIS

Congestive heart failure

BAD PROGNOSIS

Treatment:

Hyperphosphatemia

control

Al OH

GOOD

PROGNOSIS


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F

Serum viscosity

Decreased tissue

perfusion

RAAS activation

vasoconstriction

Decrease blood flow

to the kidneys

Increase cardiac

output

High blood pressure

F

Familial

monosomy 7

abnormality

Myelodysplastic

syndrome

Refractory

anemia (RA)

RA with ringed

sideroblasts

Refractory

cytopenia

with

multilineage

d s lasia

MDS-

Unclassified

RA with

excess blasts

thrombocytopenialeukopeniaerythrocytopenia

Anemia, fatigue

dyspnea, pallor

Infection Decreased clotting

factor, increased

bleeding

Treatment:

Blood

transfusion

O2 therapy

Treatment:

antibioticsTreatment:

antihemorrhagic


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Hypertrophy of the

myocardium

Increase afterload and

increase heart workload

Decreased myocardial

contractility

F

Ventricular

remodelling

Increase preload

Myocardial

infarction

Stretched the myocardium

and constrict the arteriesTroponin I (+)

F

E2


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STAGE 4 CKD

STAGE 5 ESRD

F

Hypoxia of the

myocardium

Decreased

contractility

Increased residual of

blood in the left ventricle

Left ventricular

hypertrophy

Regurgitation of

blood into the lungs

Venous pulmonary

congestion

F

E3

Moderate

hypertension

Severe decrease ofGFR 15-29ml/min

metabolic acidosis

Kidney failure; GFR

of


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Pulmonary edema

Treatment:

O2 administration

Diuretics

Decrease OFI and

sodium intake

GOOD

PROGNOSIS

Pulmonary

hypertension

F

If not treated:

Shock and suffocation

DEATH

BAD PROGNOSIS


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Narrative Form of Schematic Diagram

Diabetes mellitus (DM) is caused by various factors. Some books may indicate

that DM is idiopathic but specifically, DM results from a severe, absolute lack of insulin

caused by loss of beta cells in the pancreas; wherein fact, beta cells are the one

responsible for the release of insulin, only hormone know to have a direct effect in

lowering blood glucose levels.

Diabetes mellitus has two types: type 1 DM and type 2 DM. Type 1 DM is

previously known as insulin-dependent DM because and type 2 DM is non-insulin-

dependent DM, however, these terms are obsolete because many individuals of type 2

DM eventually require insulin treatment for control of glycemia (Jameson, 2010). In line

with this, patient AU was diagnosed with type 2 DM, accordingly, we will explain the

pathophysiology of this type of DM.

Type 2 DM is a heterogeneous condition that describes the presence of

hyperglycemia in association with relative insulin deficiency (Porth, 2010). There are

various factors that contribute to type 2 DM. One factor that has a great cause on a

person to have type 2 DM is obesity. Obesity is a major contributor to insulin resistance

through several mechanisms like presence of adipokines, increases serum free fatty

acids (FFA), intracellular deposits of triglycerides and cholesterol, and inflammatory

cytokines will make the insulin resistant. Insulin resistance is defined as suboptimal

response of insulin-sensitive tissues to insulin. It is an abnormality of either the insulin

molecules, down-regulation of insulin receptors, decrease or abnormal activation of

postreceptor kinases, and alteration of glucose transporter. So, when a person eats

food that is rich in carbohydrates, it breaks down and turns into glucose and moves into

the bloodstream. The body detects that there is an increase in blood glucose level;

therefore, insulin is stimulated to control the glucose level in the plasma. However, in

patients with type 2 DM the insulin doesnt bind to insulin receptors in the cell. The

insulin receptors are less sensitive, though the pancreas continues to produce some

insulin, but it is not enough to meet the bodys needs. When the body cells are less


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sensitive to insulin, glucose cannot enter into the cell causing high blood glucose level

(hyperglycemia). Beta cells secrete more insulin to compensate the hyperglycemia. As

time goes by, insulin receptors continue to be less sensitive and more glucose is

retained in the plasma. Therefore, more insulin are produced by the beta cells leading to

hyperinsulinemia, and so on and so forth. In due to over workload of the pancreas

specifically the beta cells in producing insulin, insulin response will decline due to beta

cell exhaustion and dysfunction. Impaired insulin secretion or relative insulin deficiency

is the result of beta cell dysfunction.

On the other hand, genetic predisposition is also a risk factor for type 2 DM.

according to some studies; there are incidences of genetically beta cell dysfunction and

decrease beta cell mass. And because of this, insulin counterregulatory hormones

(catecholamines, cortisol, growth hormone, and glucocorticoid) will increase.

Consequently, when the insulin secretion is impaired it cannot function well on its

job in maintaining the homeostasis of glycogen and glucose. Deficiency of insulin

causes a mild lypolysis, glycogenolysis, and protein breakdown. The products are

essential in gluconeogenesis that will result in high blood glucose level formationthe

more the patient will be hyperglycemic.

Originally, insulin is the one responsible for glycogen synthesis and decreases

gluconeogenesis, increase triglyceride synthesis and inhibits adipose cell lipase, and

decreases protein breakdown. But when there is impaired insulin secretion the insulin

cannot perform its function well, therefore, fats, protein, and glycogen will catabolize. In

the adipose tissue, there is only a mild lypolysis because the body has still relative

amount of insulin left. Moreover, free fatty acids and glycerol will now circulate freely in

the bloodstream and contributes to the formation of more glucose. Increase in FFA will

lead also to increase lipid synthesis in hepatocytes. This lipid storage in the liver maylead to nonalcoholic fatty liver diseases and abnormal liver function test. This is also

responsible for dyslipidemia and can cause macrovascular diseases (Jameson, 2010).

Lipid lowering agents like statins and antihypertensives. By the same token, there will

be glycogenolysis in the liver and more glucose is producedchronic hyperglycemia is


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expected. And also, same will happen in proteins; proteins catabolize and amino acid is

formed and this may contribute in the production of glucose.

As what have mentioned above, chronic hyperglycemia will happen if the body

will continue to produce more glucose when the body cannot compensate its high sugar

level. In line with this, the initial manifestation of type 2 DM will occur. The classical

symptoms are polyphagia, polydipsia, and polyuria. Polyphagia happens when the cell

depletes energy or food source and results in cellular starvation and increase hunger.

On the other hand, polydipsia is an intracellular dehydration due to the attraction of

water into the plasma, consequently, due to high blood glucose level. Thus, intracellular

dehydration stimulates the thirst mechanism of hypothalamus. Polyuria occurs when

there is too much water is being secreted in the urine because the amount of glucose

filtered by the glomeruli of the kidney exceeds that which can be reabsorbed by the

renal tubules. Glucosuria is present and may also contribute to fungal growth called

genital pruritus or any infections due to attraction of microorganisms on a high sugar

level environment.

Furthermore, Huether and McCance (2012) stated that chronic complications of

DM are associated with metabolic alterations, primarily hyperglycemia. Strict blood

control of blood glucose significantly reduces complications. If there is a macrovascular

complication of DM, there is also microvascular diseases primarily due to

hyperglycemiadiabetic retinopathy, neuropathy, and nephropathy.

Firstly, DM retinopathy is caused due to retinal ischemia resulting from blood

vessel changes and RBC aggregation. Hyperglycemia causes hyperperfusion in retinal

plasma flow and vascular pericyte loss because of the activation of protein kinase C

(PKC) that contributes to vascular cell proliferation, enhanced contractility, and

increased permeability. Because of this, the capillary endothelial cell is damage withloss of tight junctions, capillary occlusion that will lead to retinal ischemia and may lead

to visual changes and complete blindness. By the same token, polyol pathway also has

also a central role in initiating diabetic cataract formation. The enzyme aldose reductase

catalyzes the reduction of glucose to sorbitol through a polyol pathway. That is why

aldose reductase inhibitor are given to patients to inhibit the enzyme during the


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catalyzation. Sorbitol is slowly converted into fructose by the enzyme sorbitol

dehydrogenase. Osmotic stress in the lens caused by sorbitol accumulation induces

apoptosis in lens of epithelial cells leading to the development of cataract. Usual

management for persons with cataract is cataract surgery or extracapsular cataract

extraction.

Secondly, hyperglycemia increases ICF sorbitol (due to polyol pathway) that can

contribute to nerve edema. Increases advanced glycosylation end-products (AGEs)

formation can cause inactivation of nitric oxide, a potent vasodilator that will result to

vasoconstriction, decrease nerve blood flow in the vaso nervorum, and ischemic injury

and demyelination of Schwann cells. Nerve edema and demyelination of Schwann cells

may alter sensorimotor function. This alteration in the nerve function is called diabetic

neuropathy. Paresthesia, tingling sensation, numbness, and absence of ankle reflexes

are the manifestations of DM neuropathy.

Lastly, DM nephropathy is a chronic complication that causes DM patients to

have chronic kidney disease (CKD) or eventually will lead to end-stage renal disease

(ESRD). With DM nephropathy, early glomerular hemodynamic changes include

hyperfiltration and hyperperfusion which result in microalbuminuria. Increase afferent

arteriole dilation due to a dysfunction of basic and constrictive autoregulatory

inflammatory response contributes to increase intraglomerular pressure exacerbated by

systemic hypertension which is associated to greater mesangial matrix production.

Renal vasodilation may first occur and there will be an increase in GFR and increase

protein excretion. During the first 5 years of DM, thickening of the glomerular basement

membrane, glomerular hypertrophy, and mesangial volume expansion occur as the

GFR returns to normal. There are some instances that the nephrons will harden due to

excessive use and will develop diabetic nephrosclerosis. After 510 years, 40% of

individuals begin to excrete small amounts of albumin in the urine. Microalbuminuria is

defined as 30300 mg/dL in a 24-hr collection or 30300 g/mg creatinine in a spot

collection. Macroalbuminuria progresses over the next 10 years in some individuals.

Once macroalbuminuria is present, there is a steady decline in GFR, and 50% of

individuals reach ESRD in 710 years. Hypoproteinemia will result to increase albumin


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excretion. Normally, protein increases plasma colloid osmotic pressure; however, due to

protein excretion water will congest into tissues and will lead to edema and maybe

anasarca. Once macroalbuminuria develops, blood pressure slightly rises and the

pathologic changes are likely irreversible.

During hyperfiltration, large amount of sodium will also be filtered and excreted

through urine; sodium deficit and volume depletion will stimulate the juxtaglomerular

apparatus to secrete renin. Renin will now convert the angiotensinogen from the liver to

angiotensinogen I. As angiotensin I flow into the lungs, an enzyme cleaves of the

structure of angiotensin I and will convert it into angiotensin II. This enzyme is called

angiotensin-converting enzyme. Angiotensin II is a potent vasoconstrictor and promotes

high blood pressure. Other function of angiotensin II is to stimulate the adrenal gland to

produce aldosteronepromotes water retention, increases blood volume and increases

blood pressure. This activation from stimulation of renin to the production of aldosterone

is called renin angiotensin aldosterone system. In patients with DM, hypertension will

increase the vascular resistance result to the progression of intraglomerular pressure

and exacerbate the glomerular capillary permeability adding more injury into nephrons.

Prevention of the RAAS activation is the important intervention to prevent further

damage to kidneys. ACE inhibitor, ARBS, Ca channel blocker, aldosterone inhibitor, and

decrease OFI are some of the treatment regimens to prevent hypertension and water

retention.

Stage 2 CKD has a mild decrease in GFR of 60-89 mL/min; plasma creatinine

concentration increases by a reciprocal amount; because there is no regulatory

adjustment for creatinine, plasma levels continue to rise and serve as an index of

changing glomerular function. As GFR declines also, urea clearance increases. As the

glomerular pressure continues to increase, proteins are still permeable due to

hyperfiltration. There will be an increase in tubular protein reabsorption and will further

bought fibrosis to tubulointerstitium. Increase losses of nephrons are prominent. There

is a hypothesis that surviving nephrons are able to compensate the loss of other

nephrons by hyperfunction in their rates of filtration, reabsorption, secretion and


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excretion. However, the continued loss of functioning nephrons and the adaptive

hyperfiltration can add insult to injury.

As the kidney damage progresses, nephrons continue to injure and there will be

a moderate decrease of GFR of 30-59 mL/min (Stage 3 CKD). The kidneys now will not

be able to produce erythropoietin and the productions of RBCs are reduced. Patients

with CKD are prone to anemia. Pallor, fatigue and weakness are the initial

manifestations and may have dyspnea due to impaired gas exchange. Supposedly, the

hemoglobin carries the oxygen molecule for tissue perfusion and carries carbon dioxide

for gas exchange in the lungs.

Moreover, damage to the kidneys can also impair the synthesis of calcitriol.

Calcitriol is a hormone responsible for calcium absorption in the intestines. If there is

decrease intestinal absorption of calcium, the serum calcium level also decreases. To

compensate for the low amount of calcium in the blood, it will stimulate the parathyroid

gland to produce parathormone (PTH). PTH is the one responsible in increasing serum

calcium level and stimulation of calcitriol. But, due to impairment of calcitriol, the PTH

will retain in the bloodstream leading to more complication like hyperparathyroidism.

Hypercalcemia is caused by excessive production of PTH. Intake of phosphorus-riched

foods is needed because, physiologically, calcium is inversely proportional to

phosphorus. An increase of either of those two electrolytes will be a reduction of the

other, and vice versa. If these are not treated, complications like vascular calcifications

will be prone to your patient. In line with this, our patients echocardiography impression

shows aortic, mitral, and tricuspid sclerosis. Sclerosis is the hardening of a soft tissue

and maybe due to calcification of serum calcium.

As mentioned above, damage of the kidneys result to impairment of calcitriol or

Vitamin D. Vitamin D and phosphorus supplements and sunlight exposure are thetreatment for vitamin D deficiency. Osteomalacia is one of the complications if not

treated immediately.

In addition, more kidney damage will result to moderate hypertension and severe

decrease of GFR will rapidly to occur. GFR of 15-29mL/min indicates the 4thstage of


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CKD. One complication of severe decrease in GFR is metabolic acidosis. Progression

of kidney failure will lead to the last stage of CKD, the end-stage renal disease where

uremia, pericarditis, azotemia, other cardiovascular disorders are present and slowly the

patient will meet its death. Dialysis and kidney transplant are the management for

ESRD.

In addition, chronic hyperglycemia also makes the blood more viscous. Serum

viscosity may lead to poor tissue perfusion to all organs especially the kidneys. The

RAAS will be activated and increase vascular resistance is the product of its activation.

Vasoconstriction may increase cardiac output, increase the afterload, and increase

heart workload. Hypertrophy of the myocardium will result due to its workload until it

decreases its myocardial contractility. Normally, the heart remodels as a compensatory

mechanism to increase workloadmyocardial contraction will increase as well as its

preload. Pathologically, our patient had a positive Troponin I and indicates myocardial

infarction. Therefore, increase contraction will stretched the myocardium and constrict

the coronary arteries. Hypoxia in the myocardium will happen and thus, decreasing its

normal contractility. The chamber especially the left ventricles was hypertrophied and it

cannot pump the whole blood towards the systemic body. Left ventricular hypertrophy

will occur and there will be a minimal or increased residual of blood in the left ventricles.

Because of this, the ventricle cannot pump the whole blood and some amount of blood

will regurgitate back to the lungs. The regurgitation of blood is easy on her case

because the patient had already calcified leaflets or valves called sclerosis. Therefore,

there will be a venous pulmonary congestion with the presence of crackles in the lungs.

The congestion in the lungs will lead to pulmonary edema and because of increased

pressure; there will be also a pulmonary hypertension. Medications and other treatment

regimen should be intervened immediately. Oxygen therapy and diuretics should be

rendered and decrease OFI and sodium intake should be strictly followed. Shock andsuffocation will be the major complication when not treated and may impend to death.

Diabetes Mellitus 2 and Chronic Kidney Disease

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Transcript of Diabetes Mellitus 2 and Chronic Kidney Disease