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Acute Complication of Diabetes – dr. Fitria Na berhubungan dengan osmolalitas.

Benda keton
bersifat asam, tubuh kita punya range normal pH yaitu
Komplikasi akut pada diabetes adalah komplikasi yang
7.35-7.45, kalau keton dalam darah terlalu asam
terjadi dalam waktu singkat, meliputi diabetes
jadinya asidosis. Kalau ada keton di darah, akan
ketoasidosis (DKA), hiperglikemia dan kondisi
akibatkan ketonuria (untuk mendeteksi); standar DAK
hiperosmolar/nonketotik (HHNK), dan hipoglikemia.
ya keton di dalam darah. Kalau ini berlanjut maka bisa
Hipoglikemia terjadi karena penggunaan insulin yang berujung passed out.
berlebih, efek samping insulin, overdosis insulin
(berhubungan dengan terapi nanti). Hipoglikemi Our bodies live and die at the cellular level. The
berbahaya, karena jika 5 menit saja otak tidak dapat billions of cells in our bodies must maintain alkalinity,
asupan gula, maka akan terjadi penurunan kesadaran, in order to function and stay alive. The first line of
bahkan berujung kematian. defense against disease is a proper pH balance.
Disease can only grow in an acidic body, which makes
A. Diabetic Ketoacidosis a condition favorable for the growth of bacteria,
yeast, fungus, mold, viruses, and any other unwanted
Terjadi ketika sel otot menjadi sangat kelaparan organisms. Cancer always strikes those with an over-
(sangat butuh energi) dan menyebabkan tubuh acidic body. 
menggunakan “energi emergensi” dengan memecah
lemak yang terdapat benda keton. Glukoneogenesis An acidic state causes a lack of oxygenation at the
membongkar lemak dan membongkar protein sebagai cellular level. When the pH level falls below 7.4, there
cadangan akhir benda keton. is less than the maximum oxygen in the blood. Blood
carries the maximum oxygen at pH 7.4 (alkaline).
Biasanya terjadi pada pasien DM tipe 1, terdapat Without proper oxygenation, unfriendly bacteria,
gangguan produksi sel. Keadaan di mana tidak mold, and viruses will prosper.
cukupnya insulin untuk menyeimbangkan kenaikan
gula darah When the human body is in an acidic state, it will try
to shield itself from the damaging acid by storing the
(1) bisa karena extreme stress or illness that leads to acid in fat cells. The body tries to prevent the acid
infection and body will produce adrenaline. from eating holes in tissues. When the acid level is
high in the body, calcium is also depleted. Your body
When stressed, the body prepares itself by ensuring
may make fat cells in order to store unwanted acid for
that enough sugar or energy is readily available.
its own protection. This process may save your vital
Insulin levels fall, glucagon and epinephrine
organs from severe damage. By returning to a
(adrenaline) levels rise and more glucose is released balanced pH level, you may lose unwanted fat cells.
from the liver. At the same time, growth hormone and
cortisol levels rise, which causes body tissues (muscle Osteoporosis is an acidic problem. As the body
and fat) to be less sensitive to insulin. As a result, becomes more acidic, calcium is depleted. The body
more glucose is available in the blood stream. will then leach calcium from bones, teeth, and tissue
to make up for this loss. One of the first warning signs
(2) atau karena lupa mengonsumsi insulin is calcium deposits in the body, which come from the
1. Patofisiologi
calcium in our teeth and bones and not from Infeksi 40%, infeksi saluran kemih, missed insulin
nutritional calcium.  treatment 25%, previously unknown diabetes 15%,
lainnya 20%.

Associated causes: myocardial infarction, trauma


Untuk diagnosis DKA ada 3, yaitu acidemia (dalam (kepala), stress, surgery, complicated pregnancy,
darah), ketonimia (ph <7), hiperglikemia. cerebrovascular accident. Produksi urin normal

2. Sign and Symptom

Terjadi polyuria dan polydipsia (enuresis/ngompol),


dehidrasi (dicirikan dengan takikardi dan
orthostasis/posisi yag kalo duduk trs langsung bangun
jadi berkunang kunang), abdominal pain (adanya
nausea and vommiting), fruity breath (bau acetone),
kussmaul breathing (napas cepat dan dalam), change
in mental status (coma, combative/agressive).

3. Precipitationg Factor

25% terjadi pada penderita DM tipe 1 (ga tau


awalnya), 40% karena infeksi, bisa juga karena obat
(steroids/hormon antiperadangan antiinflamasi,
thiazides/obat hipertensi, bobutamine/obat perkuat
kontraksi jantung, dan turbutaline/obat asma), insulin
tidak teratur karena takut hipoglikemi dan takut berat
badan naik, stress karena chronic disease.

4. Diagnosis

- Dehydration
- Acidotic/Kussmaul breathing with fruity smell, tergantung berat badan, gender (0.5-1cc/kgBB/jam).
- abdominal pain/ditention, vomiting,
K+? Kalo K+ kurang dari 3.3 maka jangan diberikan
- altered mental status ranging from disorientation
insulin dulu. Na K, untuk transport ion, dan banyak
to coma
terdapat di tubuh, yg paling penting di otot jantung,
+ Hyperglycemia >300mg/dL and glucosuria berujung pada aritmia kalau terganggu (terlalu rendah
+ Ketonemia and ketonuria K). Hubungan K dengan insulin: tiap kali glukosa
+ Metabolic acidosis pH <7.25, serum bicarbonate insulin mengalami binding, ketika masuk ke dalam sel
<15mmol/L, anion gap >10 akan terdapat pengiring, yaitu K. Kalau K nya kurang
dan ttp ditambah insulin, maka akan semakin rendah
Anion gap: [Na]+[K]-[Cl]+[HCO3]  berbedaan
K nya. Makanya kalau hiperkalemi, dikasihnya gula
natrium dengan kalium
dan insulin juga.
5. Komorbiditas
B. Hyperglycmia Hyperosmolar State/Nonketotic
A high lever of blood glucose may interfere blood
circulation (level >600mg/dL) tinggiiiiiiii bgt gulanya,
darah mengental; glucose uptake by the cells
decreases, the glucose passed from blood to urine
causing dehydration by drawing tremendous amounts
of fluid from the body (hiperosmolar). It’s common in
DM type 2 patient. Trigger factor: high-dose steroid,
diuretics, infection, illness, stress or drinking excessive
alcohol.

1. Patophysiology

Pasien biasanya datang dengan keadaan tidak


sadar.

C. Hypoglycemia

Adalah situasi klinis dengan ditandai penurunan


konsentrasi gula darah yang dapat menyebabkan
munculnya gejala dan tanda (a level that may induce
symptms or signs); ditandai juga dengan penurunan
kesadaran dan mengubah stimuasi saraf simpatis,
mengubah sistem hormon adrenalin (cemas,
berdebar, berkeringat, tremor) yang biasanya
meningkat ketika dalam keadaan
stress/hipermetabolisme/jadi resmponsif dan aware.
Plasma glucose level less than 50mg/dL is generally
considered the threshold. Hypoglycemia typically
arises from abnormalities in the mechanism involved
in glucose homeostasis.

1. Whiple Triad

The documentation of low blood sugar; presence of


symptoms; reversal of these syptoms when the blood
sugar level is stored to normal. Dikasih permen, bukan
roti gandum or other source of carbs; krn beda
polisakaridanya, permen lebih sederhana, dan
harusnya membaik gejalanya.
2. Physiology d. Autoimmune hypoglycemia: insulin antibodies
and insulin receptor antibodies
e. Hormonal deficiency: hypoadrenalism
(corlisol), hypopituitarism (growth hormone in
children), glucagon deficiency, epinephrine.
f. Critical illnesses: cardiac, hepatic, renal
disease, sepsis with multiorgan failure
g. Pregnancy, exercise, starvation
h. Renal glycosuria
i. Ketotic hypoglycemia of childhood
j. Adrenal insufficiency
k. Hypopituitarism

4. Treatment

Dexitrose: 25g IV bolus slowly

Glucagon: for unconcious patients at home or if IV


access is difficult, 0.5 to 1mg IM/subcutaneously,
Mekanisme glukoneogenesis may repeat in 20min

Penurunan pada subkutan/periferal, induce sinyal ke Oral Glucose: for concious, cooperative patients,
otak, resulting in rasa makan/lapar. Kalau lapar + chewable glucose tablets 25 to 100g
hipoglikemi, otomatis akan mendatangkan
Target gula >70mg/dL biar nyampe ke otak cui
mekanisme blocking insulin; maka kontrainsulin akan
keluar yaitu glukagon, ia yang akan merangsang 5. Complication
pelepasan glukosa dari liver/hati.
Acute sequelae could lead to coma, cardiac
3. Ethiology dysrithmia, and death; the risk of permanent
neurologic deficits increases with prolonged
a. Fasting Hypoglycemia hypoglycemia (memory impairment, diminished
language skills, ataxia); cardiovascular event.
- Nesidioblastosis is a rare cause of fasting
hypoglycemia in infants and are rare in adults
- Inherited liver enzyme deficiencies that restrict
hepatic glucose release (deficiency of glucose-6-
phosphatase, fructose-1,6-diphosphatase, pyruvate
carboxylase, phosphorylase, glycogen synthase)

b. Drugs

Ethanol (alkohol, efek ke liver), haloperidol, quinine,


sallcylates, sulfonamides; oral hypoglycemic,
phenylbutazone, p-aminobenzoic acid, methanol,
isoniazide, triciyclic antidepressant, fluoxatine,
sertraline, , thiazide diuretics, lithium.

c. Endogenous insulin or insulin-receptor-


mediated hypoglycemia

- Insulin-producing tumours of pancreas (islet cell


adenoma or carcinoma/insulinoma)
- Non-beta-cell tumor

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