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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.