CR 3.

05 Endokrin
By: Mega

ANAMNESIS PF PP DD TERAPI EDUKASI

DM Tipe 1 (4A)
 Polifagi, poliuri, Awal kasus - normal. American Diabetes Association (ADA) DM tipe 2 Insulin injected subcutaneously is Diet
polidipsi DKA: - A fasting plasma glucose (FPG) level Hiperglikemi the first-line treatment of type 1 BB sesuai IMT
Kussmaul respiration, signs of dehydration, ≥126 mg/dL (7.0 mmol/L), or sekunder diabetes mellitus (DM). The
 Penurunan BB hypotension, and, in some cases, altered mental -A 2-hour plasma glucose level ≥200 DKA different types of insulin vary Olahraga
status. mg/dL (11.1 mmol/L) during a 75-g oral with respect to onset and 3-5x seminggu , 30-45x,
3 bulan 1x: glucose tolerance test (OGTT), or duration of action. Short-, 150 min / week.
 Lelah, mual, kram otot macrovascular and microvascular complications. -A random plasma glucose ≥200 mg/dL intermediate-, and long-acting GDS < 100 makan dulu
They should undergo funduscopic examination for (11.1 mmol/L) in a patient with classic insulins are available. Short- GDS > 250 tunda latian
 Pandangan kabur retinopathy and monofilament testing for peripheral symptoms of hyperglycemia or acting and rapid-acting insulins
neuropathy. hyperglycemic crisis are the only types that can be
 Onset pada infant / administered intravenously (IV).
dadakan vital signs, funduscopic examination, limited American Diabetes Association (ADA)  Rapid (sblm makan)
vascular and neurologic examinations, and foot guidelines recommend measuring aspart, glulisine, lisspro
examination. HbA1c at least every 6 months in  Intermediet
KOMPLIKASI
patients with diabetes who are meeting  Long acting detemir
treatment goals and who have stable  Ultra long acting
 Makrovaskuler: glycemic control. For patients whose
Hipertensi, stroke therapy has changed or who are not
 Neuropati: gejala meeting glycemic goals, the guidelines
nyeri, kesemutan, recommend HbA1c testing every 3
disfungsi ereksi, kaki months.
kering

 Mikrovaskuler: ggg.
Penglihatan

 DKA: dehidrasi,
takikardi, nafas bau
keton
DM Tipe 2 (4A)
Classic symptoms: Obesitas centralis GDP ≥126 mg/dL  Biguanides Prediabetes
Polyuria, polydipsia, Hipertensi GDS ≥200 mg/dL  Sulfonylureas Self-management
polyphagia, and weight Eye hemoragi, eksudasi, neovaskularisasi TTGD ≥200 mg/dL  Meglitinide derivatives education
loss Skin achantosis nigricans HbA1C ≥6,5 Nutrition
 Alpha-glucosidase
Blurred vision Infeksi candida Physical activity
inhibitors
Lower-extremity Neuropati insulin and C-peptide levels and Smoking cessation
paresthesias Claw foof, diabetic ulcer immune markers (eg, glutamic acid  Thiazolidinediones Psychosocial care
(TZDs)
Yeast infections (eg, decarboxylase [GAD] autoantibodies), Immunizations
balanitis in men) as well as obtain a detailed family  Glucagonlike peptide–1 Glycemic treatment
history. (GLP-1) agonists Therapeutic targets
C-peptide is formed during conversion  Dipeptidyl peptidase IV Diagnosis and treatment
(DPP-4) inhibitors
 of proinsulin to insulin. An insulin or C-  Selective sodium- of vascular
peptide level below 5 µU/mL (0.6 glucose transporter-2 complications
ng/mL) suggests type 1 DM; a fasting C- (SGLT-2) inhibitors Intensification of insulin
peptide level greater than 1 ng/dL in a  Insulins therapy in type 2
patient who has had diabetes for more  Amylinomimetics diabetes
than 1-2 years is suggestive of type 2 ppropriate
 Bile acid sequestrants
(ie, residual beta-cell function). An goal setting
exception is the individual with type 2  Dopamine agonists
Dietary and
DM who presents with a very high exercise modifications
glucose level (eg, >300 mg/dL) and a Medications
temporarily low insulin or C-peptide
Appropriate
level but who will recover insulin
self-monitoring of blood
production once normal glucose is
glucose (SMBG)
restored.
Regular
monitoring for
Islet-cell (IA2), anti-GAD65, and anti-
complications
insulin autoantibodies can be present
in early type 1 but not type 2 DM. Laboratory
Measurements of IA2 autoantibodies assessment
within 6 months of diagnosis can help
differentiate between type 1 and type 2 Ideally, blood glucose
DM. These titers decrease after 6 should be maintained at
months. Anti-GAD65 antibodies can be near-normal levels
present at diagnosis of type 1 DM and (preprandial levels of 90-
are persistently positive over time. 130 mg/dL and
hemoglobin A1C
[HbA1c] levels < 7%).
However, focus on
glucose alone does not
provide adequate
treatment for patients
with diabetes mellitus.
Treatment involves
multiple goals (ie,
glycemia, lipids, blood
pressure).

General signs of diabetic ketoacidosis (DKA) may Laboratory studies for diabetic Acute Managing diabetic ketoacidosis  Only short-
 The most common early include the following: ketoacidosis (DKA) should be scheduled Pancreatitis (DKA) in an intensive care unit acting insulin is
symptoms of DKA are the  Ill appearance as follows: Alcoholic during the first 24-48 hours used for
insidious increase in  Dry skin  Blood tests for glucose every Ketoacidosis always is advisable. When correction of
polydipsia and polyuria.  Labored respiration 1-2 h until patient is stable, Appendicitis treating patients with DKA, the hyperglycemia in
The following are other then every 4-6 h Urinary Tract following points must be DKA.
 Dry mucous membranes
signs and symptoms of  Serum electrolyte Infection (UTI) considered and closely  The optimal
 Decreased skin turgor and Cystitis monitored:
DKA: determinations every 1-2 h rate of glucose
 Decreased reflexes (Bladder  Correction of fluid loss
 Malaise, generalized until patient is stable, then decline is 100

weakness, and fatigability
 Nausea and vomiting; may
be associated with diffuse
abdominal pain,
decreased appetite, and
anorexia
 Lactic Acidosis
Rapid weight loss in
patients newly diagnosed
with type 1 diabetes
 History of failure to
comply with insulin
therapy or missed insulin
injections due to vomiting
or psychological reasons
or history of mechanical
failure of insulin infusion
pump
 Decreased perspiration
 Altered consciousness (eg,
mild disorientation,
confusion); frank coma is
uncommon but may occur
when the condition is
neglected or with severe
dehydration/acidosis
 Signs and symptoms of
DKA associated with
possible intercurrent
infection are as follows:
 Fever
 Coughing
 Chills
 Chest pain
 Dyspnea
 Arthralgia
HIPOGLIKEMIA RINGAN
(4A)
The patient’s medical
and/or social history may
reveal the following:
 Diabetes
mellitus, renal
insufficiency/failu
 Characteristic acetone (ketotic) breath every 4-6 h Infection) in with intravenous fluids mg/dL/h.
odor  Initial blood urea nitrogen Females  Administer 1-3 L during  The blood
Effects on vital signs that are related to DKA may (BUN) Hyperosmolar the first hour. glucose level
include the following:  Initial arterial blood gas (ABG) Coma  Administer 1 L during should not be
 Tachycardia measurements, followed with Hypophosphate the second hour. allowed to fall
 Hypotension bicarbonate as necessary mia  Administer 1 L during lower than 200
Hypothermia mg/dL during the
 Tachypnea the following 2 hours
first 4-5 hours of
 Hypothermia  Administer 1 L every 4
Metabolic treatment.
 Fever, if infection is present hours, depending on
Acidosis  Avoid
Specific signs of DKA may include the following: the degree of
Salicylate induction of
 Confusion dehydration and central
Toxicity hypoglycemia
venous pressure
 Coma Septic Shock because it may
readings
 Abdominal tenderness develop rapidly
 Correction of during correction
hyperglycemia with of ketoacidosis
insulin and may not
provide sufficient
 Correction of
warning time.
electrolyte
disturbances,
particularly potassium
loss
 Correction of acid-base
balance
 Treatment of
concurrent infection, if
present
Assess vital signs for hypothermia, tachypnea, aboratory studies that should be Addison Pharmacotherapy he Hypoglycemia Patient
tachycardia, hypertension, and bradycardia obtained include the following: Disease The mainstay of therapy for Questionnaire includes
(neonates).  Glucose and electrolyte levels Adrenal Crisis hypoglycemia is glucose. Other the following questions:
The head, eyes, ears, nose, and throat (HEENT) (including calcium, Alcoholism medications may be administered  How well can
examination may indicate blurred vision, pupils magnesium) Anxiety based on the underlying cause or you recognize
normal to fixed and dilated, icterus (usually  Oral glucose tolerance test Disorders the accompanying symptoms. the symptoms
cholestatic due to hepatic disease), and parotid pain and/or 72-hour fasting Cardiogenic Medications used in the of low blood
 (due to endocrine causes). plasma glucose Shock treatment of hypoglycemia glucose?
re, alcoholism, Cardiovascular disturbances may include tachycardia  Complete blood count Hypopituitaris include the following:  How often do
hepatic (bradycardia in neonates), hypertension or Other tests that may be helpful m  Glucose supplements you have
cirrhosis/failure, hypotension, and dysrhythmias. Neurologic including the following: (Panhypopituita (eg, dextrose) hypoglycemic
other endocrine conditions include coma, confusion, fatigue, loss of  Blood cultures rism)  Glucose-elevating episodes?
diseases, or coordination, combative or agitated disposition,  Urinalysis Insulinoma agents (eg, glucagon)  Have you
recent surgery stroke syndrome, tremors, convulsions, and diplopia. Pseudohypogly  Inhibitors of insulin needed
 Serum insulin, cortisol levels,
 Central nervous Respiratory disturbances may include dyspnea, cemia secretion (eg, assistance in
and thyroid hormone levels
system: tachypnea, and acute pulmonary edema. diazoxide, octreotide) the past during
Gastrointestinal disturbances may include nausea  C-peptide levels
Headache,  Antineoplastic agents a
and vomiting, dyspepsia, and abdominal cramping.  Proinsulin
confusion, (eg, streptozocin) hypoglycemic
The patient's skin may be diaphoretic and warm or Imaging studies
personality Other therapies episode?
show signs of dehydration with decrease in turgor. Imaging modalities to evaluate
changes insulinomas may include the following:  Fasting hypoglycemia:  Do you check
Symptoms of hypoglycemia are fewer in elderly your glucose
 CT scanning Dietary therapy
persons and they frequently appear at a lower level before
 Ethanol intake  MRI (frequent meals/snacks
threshold of plasma glucose than in younger driving?
and nutritional preferred, especially at
persons.  Octreotide scanning  Do those close
deficiency night, with complex
carbohydrates); IV to you know
glucose infusion; IV how to
 Weight
octreotide administer
reduction, glucagon?
 Reactive hypoglycemia:
nausea and
Dietary therapy
vomiting
(restriction of refined
carbohydrates,
 Fatigue, avoidance of simple
somnolence sugars, increased meal
frequency, increased
Neurogenic or protein and fiber);
neuroglycopenic symptoms alpha-glucosidase
of hypoglycemia may be inhibitors
categorized as follows:

 Neurogenic
(adrenergic)
(sympathoadrena
l activation)
symptoms:
Sweating,
shakiness,
tachycardia,
anxiety, and a
sensation of
hunger
 Neuroglycopenic
symptoms:
Weakness,
 tiredness, or
dizziness;
inappropriate
behavior
(sometimes
mistaken for
inebriation),
difficulty with
concentration;
confusion;
blurred vision;
and, in extreme
cases, coma and
death

HIPOTIROIDISME &
TIROTOKSIKOSIS
Common symptoms of Thyroid examination Thyroid function tests for Diffuse Toxic Treatment of hyperthyroidism
thyrotoxicosis include the Thyrotoxicosis from Graves disease is associated with hyperthyroidism are as follows: Goiter (Graves includes symptom relief, as well
following: a diffusely enlarged and slightly firm thyroid gland.  Thyroid-stimulating hormone Disease) as therapy with antithyroid
 Nervousness Sometimes, a thyroid bruit can be heard by using the (TSH) Euthyroid medications, radioactive iodine-
 Anxiety bell of the stethoscope.  Free thyroxine (FT4) or free Hyperthyroxine 131 (131I), or thyroidectomy.
 Increased perspiration Toxic multinodular goiters generally occur when the thyroxine index (FTI—total mia
thyroid gland is enlarged to at least 2 to 3 times the T4 multiplied by the correction for Goiter
 Heat intolerance
normal size. The gland often is soft, but individual thyroid hormone binding) Graves Disease
 Hyperactivity nodules occasionally can be palpated. Because most Struma Ovarii
 Palpitations  Total triiodothyronine (T3)
thyroid nodules cannot be palpated, thyroid nodules Thyroid function study results in Thyrotoxicosis
Common signs of should be documented by thyroid ultrasonography, Imaging
thyrotoxicosis include the hyperthyroidism are as follows:
but overactive thyroid nodules can be demonstrated
following:  Thyrotoxicosis is marked by
only by nuclear thyroid imaging with radioiodine (I-
 Tachycardia or atrial suppressed TSH levels and elevated
123) or technetium (Tc99m) thyroid scan.
arrhythmia T3 and T4levels
If the thyroid is enlarged and painful, subacute
 Systolic hypertension painful or granulomatous thyroiditis is the likely  Patients with milder
with wide pulse pressure thyrotoxicosis may have elevation of
diagnosis. However, degeneration or hemorrhage
T3 levels only
 Warm, moist, smooth into a nodule and suppurative thyroiditis should also
skin be considered.  Subclinical hyperthyroidism
Ophthalmologic and dermatologic examination features decreased TSH and normal
 Lid lag
Approximately 50% of patients with Graves T3 and T4levels
 Stare Autoantibody tests for hyperthyroidism
thyrotoxicosis have mild thyroid ophthalmopathy.
 Hand tremor are as follows:
Often, this is manifested only by periorbital edema,
 Muscle weakness  Anti–thyroid peroxidase (anti-
but it also can include conjunctival edema
 Weight loss despite (chemosis), injection, poor lid closure, extraocular TPO) antibody - Nonspecific elevation
increased appetite muscle dysfunction (diplopia), and Proptosis (see the with autoimmune thyroid disease
(although a few patients image below). Evidence of thyroid eye disease and found in 8% of Graves patients
may gain weight, if high thyroid hormone levels confirms the diagnosis  Thyroid-stimulating antibody
excessive intake outstrips
weight loss)
 Reduction in menstrual
flow or oligomenorrhea
Presentation of
thyrotoxicosis varies, as
follows [2] :
 Younger patients tend
to exhibit symptoms of
sympathetic activation (eg,
anxiety, hyperactivity,
tremor)
 Older patients have
more cardiovascular
symptoms (eg, dyspnea,
atrial fibrillation) and
unexplained weight loss
 Patients with Graves
disease often have more
marked symptoms than
patients with thyrotoxicosis
from other causes
 Ophthalmopathy (eg,
periorbital edema,
diplopia, or proptosis)
suggests Graves disease
GOITER
 Incidentally, as a swelling
in the neck discovered by
the patient or on routine
physical examination
 A finding on imaging
studies performed for a
related or unrelated
of autoimmune Grave disease.
Palpation of the goiter is performed either facing the
patient or from behind the patient, with the neck
relaxed and not hyperextended. Palpation of the
goiter rules out a pseudogoiter, which is a prominent
thyroid seen in individuals who are thin. Each lobe is
palpated for size, consistency, nodules, and
tenderness. Cervical lymph nodes are then palpated.
(TSab) - Also known as thyroid-
stimulating immunoglobulin (TSI),
long-acting thyroid stimulator (LATS),
or TSH-receptor antibody (TRab);
found in 63-81% of Graves disease; a
positive test is diagnostic and specific
for Graves disease
Autoantibody titers in hyperthyroidism
are as follows:
 Graves disease - Significantly
elevated anti-TPO, elevated TSab
 Toxic multinodular goiter -
Low or absent anti-TPO and TSab
 Toxic adenoma - Low or
absent anti-TPO and TSab
 Patients without active
thyroid disease may have mildly
positive anti-TPO and TSab
If the etiology of thyrotoxicosis is not
clear after physical examination and
other laboratory tests, it can be
confirmed by scintigraphy: the degree
and pattern of isotope uptake
indicates the type of thyroid disorder.
Findings are as follows:
 Graves disease – Diffuse
enlargement of both thyroid lobes,
with uniform uptake of isotope and
elevated radioactive iodine uptake
 Toxic multinodular goiter --
Irregular areas of relatively
diminished and occasionally
increased uptake; overall radioactive
iodine uptake is mildly to moderately
increased
 Subacute thyroiditis –Very
low radioactive iodine uptake
Initial screening should include TSH. Anaplastic Small benign euthyroid goiters do
Given the sensitive third-generation Thyroid not require treatment. The
assays in the absence of symptoms of Carcinoma effectiveness of medical
hyper or hypothyroidism further testing Branchial treatment using thyroid hormone
is not required. An assessment of free Cleft Cyst for benign goiters is controversial.
thyroxine index or direct measurement Carotid Large and complicated goiters
of free thyroxine would be the next Artery may require medical and surgical
 medical evaluation The oropharynx is visualized for the presence of step in the evaluation. Aneurysm treatment. Malignant goiters
 Local compression lingular thyroid tissue. Further laboratory testing is based on Lymphatic require medical and surgical
causing dysphagia, The size of each lobe is measured in 2 dimensions presentation and results of screening Malformation treatment.
dyspnea, stridor, plethora using a tape measure. Some examiners make tracings studies and may include thyroid (Cystic  The size of a benign
or hoarseness on a sheet of paper, which is placed in the patient's antibodies (antithyroid peroxidase Hygroma) euthyroid goiter may be
 Pain due to hemorrhage, chart. Suitable landmarks are used and documented formerly the antimicrosomal antibodies Fibroma reduced with
inflammation, necrosis, to ensure consistent measurement of the thyroid and antithyroglobulin), thyroglobulin, Granulomato levothyroxine
or malignant gland. sedimentation rate and calcitonin in an us Disease of suppressive therapy.
transformation The pyramidal lobe often is enlarged in Graves individual at high risk for medullary the Thyroid The patient is
 Signs and symptoms of disease. carcinoma of the thyroid. Infectious monitored to keep
hyperthyroidism or A firm rubbery thyroid gland suggests Hashimoto Thyroiditis serum TSH in a low but
hypothyroidism thyroiditis, and a hard thyroid gland suggests Lipomas detectable range to
malignancy or Riedel struma. Lymphadeno avoid hyperthyroidism,
 Thyroid cancer with or
Multiple nodules may suggest a multinodular goiter pathy cardiac arrhythmias,
without metastases
or Hashimoto thyroiditis. A solitary hard nodule Medullary and osteoporosis. The
suggests malignancy, whereas a solitary firm nodule Thyroid patient has to be
may be a thyroid cyst. Carcinoma compliant with
Diffuse thyroid tenderness suggests subacute Papillary monitoring. Some
thyroiditis, and local thyroid tenderness suggests Thyroid authorities suggest
intranodal hemorrhage or necrosis. Carcinoma suppressive treatment
Cervical lymph glands are palpated for signs of Parathyroid for a definite time
metastatic thyroid cancer. Adenoma period instead of
Auscultation of a soft bruit over the inferior thyroidal Parathyroid indefinite therapy.
artery may be appreciated in a toxic goiter. Palpation Cyst Patients with
of a toxic goiter may reveal a thrill in the profoundly Pseudogoiter Hashimoto thyroiditis
hyperthyroid patient. Sarcoma respond better.
Goiters are described in a variety of ways, including Subacute  Treatment of
the following: Thyroiditis hypothyroidism or
 Toxic goiter: A goiter that is associated with Thyroglossal hyperthyroidism often
hyperthyroidism is described as a toxic goiter. Duct Cyst reduces the size of a
Examples of toxic goiters include diffuse toxic Thyroid goiter.
goiter (Graves disease), toxic multinodular goiter, Abscess  Thyroid hormone
and toxic adenoma (Plummer disease). Thyroid replacement is often
 Nontoxic goiter: A goiter without Lymphoma required following
hyperthyroidism or hypothyroidism is described Thyroid surgical and radiation
as a nontoxic goiter. It may be diffuse or Nodule treatment of a goiter.
multinodular, but a diffuse goiter often evolves Use of radioactive
into a nodular goiter. Examination of the thyroid iodine for the therapy
may not reveal small or posterior nodules. of nontoxic goiter has
Examples of nontoxic goiters include chronic been disappointing and
lymphocytic thyroiditis (Hashimoto disease), is controversial.
goiter identified in early Graves disease, endemic  Medical therapy of
goiter, sporadic goiter, congenital goiter, and autonomous nodules
physiologic goiter that occurs during puberty. with thyroid hormone is
Autonomously functioning nodules may present with not indicated.
inability to palpate the contralateral lobe. Unilobar  Ethanol infusion into
agenesis may also present like a single thyroid

CUSHING SYNDROME
Patients with Cushing
syndrome may complain of
weight gain, especially in
the face, supraclavicular
region, upper back, and
torso. Frequently, patients
notice changes in their
skin, including purple
stretch marks, easy
bruising, and other signs of
skin thinning. Because of
progressive proximal
muscle weakness, patients
may have difficulty
climbing stairs, getting out
of a low chair, and raising
their arms.
Menstrual irregularities,
amenorrhea, infertility, and
decreased libido may occur
in women related to
inhibition of pulsatile
secretion of luteinizing
hormone (LH) and follicle-
stimulating hormone (FSH),
which likely is due to
interruption of luteinizing
hormone-releasing
hormone (LHRH) pulse
nodule with hyperplasia of the remaining lobe. benign thyroid nodules
The Pemberton maneuver raises a goiter into the has not been approved
thoracic inlet when the patient elevates the arms. in the United States,
This may cause shortness of breath, stridor, or but it is used
distention of neck veins. elsewhere.
Benign goiters can be treated
with thyroid hormone. The most
widely used thyroid hormone is
levothyroxine sodium,
administered once a day.
Liothyronine sodium requires
more frequent administration.
Desiccated thyroid powder,
thyroglobulin, and liotrix are less
predictable following ingestion.
Obesity Currently, 4 methods are accepted for Alcoholism Somatostatin analogs bind and
Patients may have increased adipose tissue in the the diagnosis of Cushing Anorexia activate human somatostatin
face (moon facies), upper back at the base of neck syndrome: urinary free cortisol level, Nervosa receptors resulting in inhibition of
(buffalo hump), and above the clavicles low-dose dexamethasone suppression Bulimia ACTH secretion, which leads to
(supraclavicular fat pads). test, evening serum and salivary Nervosa decreased cortisol secretion
Central obesity may also appear as increased adipose cortisol level, and dexamethasone– Concurrent
tissue in the mediastinum and peritoneum, increased corticotropin-releasing hormone test. ritonavir and
waist-to-hip ratio greater than 1 in men and 0.8 in inhaled
women; and, upon CT scan of the abdomen, fluticasone in
increased visceral fat is evident. patients with
Skin HIV - Interferes
Facial plethora may be present, especially over the with
cheeks. Violaceous striae, often wider than 0.5 cm, dexamethasone
are observed most commonly over the abdomen, suppression
buttocks, lower back, upper thighs, upper arms, and testing (false
breasts. Ecchymosis may be present. Patients may positive)
have telangiectasia and purpura, cutaneous atrophy Depression
with exposure of subcutaneous vasculature tissue Obesity
and tenting of skin may be evident. Glucocorticoid Pseudo-Cushing
excess may cause increased lanugo facial hair. If Syndrome
glucocorticoid excess is accompanied by androgen Psychiatric
excess, as occurs in adrenocortical carcinomas, Illness
hirsutism and male pattern balding may be present
in women. Steroid acne, consisting of papular or
pustular lesions over the face, chest, and back, may
be present.
Acanthosis nigricans, which is associated with insulin
resistance and hyperinsulinemia, may be present.
The most common sites are axilla and areas of
generation. In men, frequent rubbing, such as over elbows, around the
inhibition of LHRH and neck, and under the breasts.
FSH/LH function may lead Cardiovascular and renal
to decreased libido and Hypertension and possibly edema may be present
impotence. due to cortisol activation of the mineralocorticoid
Psychological problems receptor leading to sodium and water
such as depression, retention. Cushing syndrome is also associated with
cognitive dysfunction, and cardiac structural and functional changes. Left
emotional lability may ventricular (LV) hypertrophy and impaired LV
develop. New-onset or diastolic function have been described in patients
worsening of hypertension with Cushing syndrome; however, these changes are
and diabetes mellitus, reversed upon normalization of corticosteroid
difficulty with wound excess. [10]
healing, increased Gastroenterologic
infections, osteopenia, and Peptic ulceration may occur with or without
osteoporotic fractures may symptoms. Particularly at risk are patients given high
occur. doses of glucocorticoids (rare in endogenous
Signs and symptoms hypercortisolism).
specifically associated with Endocrine
endogenous Cushing Galactorrhea may occur when anterior pituitary
syndrome include the tumors compress the pituitary stalk, leading to
following: elevated prolactin levels.
 Patients with an Signs of hypothyroidism, such as slow deep tendon
ACTH-producing reflex relaxation, may occur from an anterior
pituitary tumor: pituitary tumor whose size interferes with thyroid-
Headaches, stimulating hormone (TSH) synthesis and release.
polyuria, Similarly, other pituitary function may be impacted
nocturia, visual as well.
problems, or Low testosterone levels in men may lead to
galactorrhea decreased testicular volume from inhibition of LHRH
 Patients with and LH/FSH function. In women, low level of LHRH
tumor mass and LH/FSH lead to menstrual irregularities or
effect on the amenorrhea.
anterior pituitary: Skeletal/muscular
Hyposomatotropi Proximal muscle weakness may be evident.
sm, Osteoporosis may lead to incident fractures and
hypothyroidism, kyphosis, height loss, and axial skeletal bone pain.
hyperprolactine Avascular necrosis of the hip is also possible from
mia or glucocorticoid excess.
hypoprolactinemi Neuropsychological
a, hypogonadism Patients may experience emotional liability, fatigue,
 Patients with an and depression.
adrenal Visual-field defects, often bitemporal, and blurred
carcinoma as vision may occur in individuals with large ACTH-
underlying cause producing pituitary tumors that impinge on the optic
of Cushing chiasma.
syndrome: Rapid Adrenal crisis
 onset of Patients with cushingoid features may present to the
symptoms of emergency department in adrenal crisis. Adrenal
glucocorticoid crisis may occur in patients on steroids who stop
excess in taking their glucocorticoids or neglect to increase
conjunction with their steroids during an acute illness. It may also
hyperandrogenis occur in patients who have recently undergone
m presenting as resection of an ACTH-producing or cortisol-producing
virilization in tumor or who are taking adrenal steroid inhibitors.
women or Physical findings that occur in a patient in adrenal
feminization in crisis include hypotension, abdominal pain, vomiting,
men and mental confusion (secondary to low serum
sodium or hypotension). Other findings include
hypoglycemia, hyperkalemia, hyponatremia, and
metabolic acidosis

Malnutrisi Energy Protein ← -

(4A)
← Kwashiorkor:
1.Wajah bulat dan sembab
2.Rambut tipis, kusam,
warna seperti jagung
(kemerahan) dan tidak
sakit ketika dicabut,
rontok
3.Kedua punggung kaki
edema.
4.Bercak kehitaman di
tungkai atau bokong
(crazy pavement
dermatosis).
5.Anak rewel, apatis.
← -
- Marasmus:
1.Anak sangat kurus
2.Wajah seperti orang tua
3.Cengeng dan rewel
4.Kulit keriput
5.Iga gambang
6.Perut cekung
7.Bokong kendur dan
keriput.
- Faktor risiko: BBLR, HIV,
Infeksi TB, pola asuh yang
salah.
Viitamin Deficiency]
←
Px Fisik: Dyslipidemia-
BB/TB < 70% atau < -3SD Malnutrisi vit & Farmakoterapi:
← - Marasmus: tampak mineral ← - Vitamin A
sangat kurus, tidak ada jaringan lemak bawah dosis tinggi diberikan pada
kulit, anak tampak tua, baggy pants appearance. anak gizi buruk dengan dosis
← - Kwashiorkor: edema, sesuai umur pada saat pertam
rambut kuning kali ditemukan
mudah rontok, crazy pavement ← - Makanan
dermatosa. pemulihan gizi: ada 3 pilihan:
- - Tanda dehidrasi 1). makanan therapeutic atau
- - Demam gizi siap saji, F100 atau
- - Frekuensi dan tipe pernapasan: makanan lokal dengan densitas
pneumonia atau gagal jantung. energi yg sama terutama dari
- - Sangat pucat lemak
- Pembesaran hati, ikterus (minyak/santan/margarin).
- - Tanda defisiensi vit A pada ← - Pemberian
mata  konjungtiva kering, ulkus korneas, jenis makanan untuk
keratomalasia. pemulihan gizi disesuaikan
- - Ulkus pada mulut masa pemulihan (rehabilitasi):
- LILA < 11.5 untuk anak 6-59 bulan. Px Penunjang: ← - 1 minggu
← - Laboratorium: gula pertama pemberian F100.
darah, Hb, Ht, preparat apusan darah, urin ← - Minggu
rutin, feses. berikutnya jumlah dan
← - Antropometri frekuensi F100 dikurangi
← - Foto thorax seiring
← - Uji tuberculin.
←
 Vitamin A (Retinol)Buta
senja, kulit kering,
Xeropthalmia, Bitot’s spots
(bintik merah kehitaman
pada konjungtiva),
disfungsi imun, folikular
hyperkeratosis,
Vitamin B1 (Thiamin)Beri-
beri: neuropati, kelemahan
otot, cardiomegaly,
ophthalmoplegia, edema,
confabulasi (latah),
Wernicke-Korsakoff
syndrome, Polineuritis
- Vitamin B2
(Riboflavin)  inflamasi
bibir, scaling dan fisura
(cheilosis), lidah merah,
stomatitis angular di
bibir, seborrhea.
Defisiensi Mineral
Kalsium  osteoporosis,
Rheumatoid Arthritis,
deformasi gigi, nyeri pada
tulang.
- Besi  anemia, napas
pendek, ingatan rendah,
lidah dan mulut pucat.
← -
Yodium  goiter, rambut
rontok.
← - Zinc 
hyposmia kemampuan
acrodermatitis
entheropathica.
← -
Magnesium  kelemahan
otot, insomnia, penurunan
ingatan.
← -
Vitamin B3 (Niasin)  Glositis, pellagra (kemerahan Sesuai defisiensi
pada daerah yang terpapar matahari seperti wajah,
Diare, disorientasi, apatis, dermatitis, demensia)
- Vitamin B6 (Piridoksin)  neuropati perifer,
anemia mikrositik, glositis, seborrhea, bingung.
- Vitamin B9 (Folat)  anemia
makrositik (megaloblastik), glositis atrofi,
homosistein (faktor
pembentuk Hb) meningkat.
atrofi, homosistein (faktor
pembentuk Hb) meningkat.
← - Vitamin B12
(Kobalamin)  anemia makrositik, kelainan
neurologi (paresthesia, degenerasi)
← - Vitamin C (Asama
Askorbat)  skorbut (gusi bengkak, mudah
berdarah, gangguan penyembuhan luka),
menurunkan imun tubuh.
← - Vitamin D
(Ergokasiferol/ Kolekalsiferol)  rikets (anak),
osteomalasia (dewasa), tetanus, hipokalsemia
← - Vitamin E 
Gangguan eritrosit (anemia hemolitik)
← - Vitamin K 
Perdarahan (pemanjangan PT).
- Konsumsi makanan
yang mengandung
mineral yang sesuai.
← Besi  hati,
daging merah,
ikan.
← Kalsium  susu,
telur, ikan,
cereals.
← Flour  air
minum, ikan
laut, keju, the.
← Yodium 
seafood, susu,
sayur, sereal.
← Zinc  daging,
ikan, sayuran
hijau
(kangkung,
 Potassium  hypokalemia, bayam).
kelemahan otot, paralisis, ← Potassium 
mental confusion. daging, susu,
← - buah segar,
Flourcaries dental. sayur segar,
← - gandum.
Sodium  hiponatremia, ← Sodium  roti,
digestive disorders, sayuran, garam
penurunan ingatan, dapur.
fatigue, kelemahan.
← -
Chromiumhipertensi,
kolesterol tinggi, DM Tipe
2.

Dyslipidemia
Peningkatan/ penuruanan
fraksi lipid dalam
plasmaKenaikan
kadar kolesterol total,
kolesterol LDL, dan atau
trigliserida, serta
penurunan kolesterol HDL.
- Sakit kepala,
peningkatan BB secara
signifikan
- Faktor resiko
aterosklerosis sehingga
dapat menyebabkan
stroke, penyakit Jantung
Koroner, Peripheral Arterial
Disease (PAD), Sindroma
Koroner Akut (SKA)
Px fisik: - TTV - Farmakoterapi: dilakukan setelah
Antropometri (Lingkar perut dan IMT) Hipertrigliseride 6 minggu terapi non
Px penunjang: mi - farmakologis.- R/ simvastatin tab
← - Kolesterol total >200 Hiperkolesterol 10 mg no x S1dd tab 1 pc 
mg/dl emi golongan statin
← - Kolesterol LDL >160 (HMG CoA reduktasi inhibitor)
mg/dl ← -
← - Kolesterol HDL <40 Niasin (Vit B3) menghambat
mg/dl pada laki- laki, dan <50 mg/dl pada lipolysis, VLDL sirkulasi <<
wanita. ← -
← - Trigliserida plasma Resin asam empedu
>150 mg/dl (Kolestiramin)  menghambat
reabsorpsi asam empedu.
← -
Inhibitor reseptor kolesterol
(Ezetimibe)  menghambat
absorpsi kolesterol di usus
halus.
← -
Fibrat (Fenofibrat) 
meningkatkan lipoprotein
lipase TG <<
Non farmakoterapi:-
Terapi nutrisi medis’
Pasien dengan kadar
kolesterol LDL tinggi
dianjurkan untuk
mengurangi asupan
lemak total dan lemak
jenuh, dan
meningkatkan asupan
lemak tak jenuh rantai
tunggal dan ganda. Pada
pasien dengan resiko
tinggi perlu penurunan
LDL <100 mg/dl, riwayat
infark miokard <70
mg/dl)
2. Pada pasien dengan
trigliserida tinggi perlu
dikurangi asupan
karbohidrat, alkohol, dan
lemak.
- Aktivitasfisik1. Olah
raga sesuai kondisi dan
kemampuan.

Hiperurisemia
← Gout
artritis
← - Kadar
asam urat berlebih
← -
Px fisik:
← - Cek pembengkakan
atau radangnya
← - Arthritis
monoartikuler dapat ditemukan, biasanya
x penunjang:
← - Darah
lengkap: asam urat >7mg/dl
← - X ray:
Tampak pembengkakan
Rheumatoid Farmakoterapi: Atasi serangan
atritis - Sepsis akut:
arthritis 1. Kolkisin (efektif pada 24 jam
pertama setelah serangan nyeri
sendi timbul. Dosis oral 0,5-0.6
 Bengkak dan nyeri
sendi yang mendadak,
biasa pada malam hari
dengan rasa panas dan
kemerahan
← -
Demam, menggigil,
dan nyeri badan.
← -
Apabila serangan
pertama, 90% kejadian
hanya pada 1 sendi dan
keluhan dapat
menghilang dalam 3-
10 hari walau tanpa
pengobatan.
← -
Faktor Risiko
← Usia dan jenis kelamin
← Obesitas
← Alkohol
← Hipertensi
← Gangguan fungsi ginjal
← Penyakit-penyakit
metabolic
← Pola diet
← Obat: aspirin dosis
rendah, diuretik, obat-
obat TBC
← konsumsi alkohol
melibatkan sendi metatarsophalang 1 atau
sendi tarsal lainnya. Sendi yang mengalami
inflamasi tampak kemerahan dan bengkak.
← pendek (bila NSAID dan kolkisin
asimetris pada sendi dan
kista subkortikal tanpa erosi.
mg per hari dengan dosis
maksimal 6 mg.
2. Kortikosteroid sistemik jangka
tidak berespon baik) seperti
prednisone 2-3x5 mg/hari selama
3 hari.
3. NSAID seperti natrium
diklofenak 25-50 mg selama 3- 5
hari.
Program pengobatan untuk
mencegah serangan berulang
1. Obat: analgetik, kolkisin dosis
rendah
Kelola hiperurisemia:1. Obat-obat
penurun asam urat
Agen penurun asam urat (tidak
digunakan selama serangan akut).
Pemberian Allupurinol dimulai
dari dosis terendah 100 mg,
kemudian bertahap dinaikkan bila
diperlukan, dengan dosis
maksimal 800
mg/hari. Target terapi adalah
kadar asam urat < 6 mg/dl. 2.
Modifikasi gaya hidup
Minum cukup (8-10 gelas/hari).
Mengelola obesitas dan menjaga
berat badan ideal. Hindari
Pola diet sehat (rendah purin).

Obesitas
IMT ≥ 23 kg/m2- Lingkar
perut: laki-laki >90 cm,
wanita >80 cm.
Sindrom metabolik (3B)
x Fisik ← Px Penunjang - Asites atau orsilat Perbaikan pola makan,
← - Antropometri, IMT - - GDS edema- Massa olah ragi
← - Pengukuran lingkar - - Lipid Serum otot yang
pinggang (pada pertengahan antara iga - - Asam Urat tinggi  atlet.
terbawah dengan krista iliaka, pengukuran
dari lateral dengan pita tanpa menekan
jaringan lunak) laki-laki >90cm, wanita
>80cm.
← - TTV  hipertensi.
←

Kumpulan gejala dari: Px fisik:- IMT, lingkar pinggangObesitas - Px penunjang:- GDS >110 mg/dl Farmakoterapi:
obesitas visceral, TTVHipertensi - HDL <40 mg/dl pada pria, <50 mg/dl ← - R/
hiperglikemi, - Trigliserida ≥ 150 mg/dl. pada wanita. simvastatin tab 10 mg
dislipidemia, tekanan
darah tinggi, trigliserida
tinggi.
- Lingkar pinggang >40
inchi (90cm) pada pria,
>35 (80 cm) inchi pada
wanita.
← no x S1dd tab 1 pc
← - R/
metformin tab 500mg
no xv. S3dd tab 1 pc
← - R/
captopril tab 25mg no
xv. S3dd tab 1 pc