Presentasi Endokrin Lengkap Ub.pptx

Drh. M. Ar Raniri Putra (drh. ArRan)

VETERINARY ENDOCRINOLOGY [email protected]

Hormones ??

• Substansi kimia yang dihasilkan oleh kelenjar endokrin yang disekresikan ke dalam aliran darah dan akan mempengaruhi kerja jaringan/organ lain secara kimiawi.

Lipofilik hormone  protein binding

T4  T3

Testosteron  dihydrotestosteron

IGF  Liver  liver & growth place

Pancreas Sel A  glucagon  sel B  insulin  sirkulasi

Cathecolamine: hormone ketika dihasilkan oleh adrenal, neurotransmitter ketika direalese oleh nerve terminal

Progesteron dalam semen, GH dalam susu

Produksi dan Regulasi Hormon • Konsentrasi hormon ditentukan oleh perubahan laju produksinya. • Laju produksi meningkat  konsentrasi meningkat dan sebaliknya • Laju produksi dikontrol oleh sejumlah “negative feedback loops” • Konsentrasi hormon dalam tubuh: – Konsentrasi fluktuatif  insulin, hormone reproduksi – Konsentrasi konstan  thyroxine

Hormone Deficiency (Hypofunction) Penurunan/kegagalan produksi hormon

Kegagalan dalam beraksi

Gangguan dapatan

Gangguan Kongenital pd kelenjar

Endocrine function

idiopathic

Hyperfunction Neoplasia

Hormon-like substance

Endocrine Hyperfunction

Pemberian hormon

Abnormalitas Feedback

Polyuria and Polydipsia

PDHB’s In House CE- Drh. M. Ar Raniri Putra

Patogenesa polyuria • Peningkatan volume urin primer  primary polydipsia • Osmotic diuresis  glucosuria • Kurangnya jumlah tubulus yang berfungsi • Problem pada hipertositas dari renal medulla • Kekurangan sekresi ADH (vasopressin) • Penurunan sensitifitas tubulus ginjal terhadap ADH (VP)

Anti Diuretic Hormone (ADH) • Neurohypophysis Inhibit: Ethanol Glucocorticoids Phenytoin

Stimulasi: Barbiturate, nicotin, narcotic, carbamazepine, vincristin, cholinergic drugs, β adrenergic drug, chlorpropamide dsb

• ADH Secretion E. Coli endotoxin Hypokalemia hypercalcemia

Menurunkan sensitivitas tubulus renal terhadap ADH

Langkah-langkah pendiagnosaan hewan dengan Gejala PU PD

History • PU n PD  biasanya terjadi bersamaan • Polyuria vs Pollakiuria • Estimasi water intake normal – Anjing: 20-90 ml/kg/day – Kucing: 0-45 ml/kg/day

• Estimasi produksi normal urine – Anjing: 20-40 ml/kg/day – Kucing: 20-45 ml/kg/day

Physical Exam • Palpasi abdomen (bladder, kidneys n Liver) • Palpasi limfonodus  lymfosarcoma • Rectal exam (urethra n Tumor) – LUTD -> Urethra menebal – Anal sack sarcoma -> hypercalcemic, polyuria, large lymphnode

• Blood pressure (elevated: renal dz, hyperthyroidism, cushing’s, diabetes in dog, liver dz, CNS dz, hyperaldosteronism, idiopathic hypertention)

• Banyak minum?? – >90 ml/kg/day (dog) >60ml/kg/day (cat) • Water intake  variable • Seberapa banyak owner yg mengukurnya?

• Banyak pipis?? – >50ml/kg/day • Sulit diukur kalau tidak dilakukan observasi di klinik

• Ketika Pasien datang dengan keluhan PU/PD test apa yang sebaiknya pertama kali dilakukan?

URINALISIS • USG (BJ)  Jika USG >1.020 pada anjing atau > 1.030 pada kucing  Tidak konsisten dengan polyuria • USG wajib diukur dengan refraktrometer • Full Urinalysis – – – –

Casts, bacteria, cells, Protein can suggest renal disorder Glucose  DM Mild proteinuria consistent with hyperadrenocorticism – Protein losing nephropathy

Other test • Chemistry profile (BUN, Cr, SGPT, ALP, Elektrolit (Ca, K, P, Na), Glukosa) • CBC (anemia, leukositosis) • Imaging – USG renal architecture, bladder, adrenal gland, liver, Ln – X-ray  abdomen: liver size, masses, urolith, kidney – Thorax  calcification, neoplasia (hypercalcemia), effect of hypertention

Most Common Causes - Dogs • Renal Disease • Diabetes Melitus • Hypercortisolism • Pyometra • Subacute leptospirosis • Hypercalcemia • Hypoadrenocorticism • Psychogenic • Advanced Liver Disease

Most Common Causes - Cats

• Renal Disease • Diabetes Melitus • Hyperthyroidism • Pyometra • hypokalemia

Canine Hypothyroidism Drh. M. Ar Raniri Putra

Principal cells (sel folicular): Thyroglobulin Parafollicular cells : calsitonin

REGULATION

Canine Hypothyroidism • Common endocrine disorders in dogs ?? • Over diagnosed – Gejala klinis non spesifik – Diganostic test yg tidak tepat

Metabolisme hormon thyroid • Produk utama dari kelenjar Thyroid adalah Thyroxine (T4) • Triiodothyronine (T3) – Hanya 20% yang diproduksi dr kelenjar thyroid – Sisanya hasil dari proses deiodinisasi T4 di jaringan perifer • Reverse T3 (alternatif produk dr proses deiodinisasi)

Thyroid Hormone Metabolism • >99% dari T3 dan T4  protein bound • Free hormones (Free T4) – Bebas keluar masuk sel – Memiliki efek metabolik – Regulasi mekanisme umpan balik • Total T4 = Free T4 + Bound T4

Canine Hypothyroidism Etiology • Primary Hypothyroidism – Destruksi thyroid gland • Lymphocytic thyroiditis • Idiopathic thyroid atrophy

• Central hypothyroidism – Kegagalan sekresi TSH oleh pituitary • Malformasi dari pituitary • Supresi sekresi TSH dari pituitary  temporary dan reversible – Exogenous administration of glucocorticoid – Spontaneous hyperadrenocorticism

• Congenital hypothyroidism – Uncommon – Thyroid hypoplasia, aplasia, dysgenesis atau dyshormonogenesis – “fading puppy” syndrome atau disproportionate dwarfism

Clinical Features • Metabolic features – Lethargy – Exercise intolerance – Weight gain dan obesity

Dermatological features • • • • • • •

Terjadi di lebih 85% kasus Alopecia Dryness Abnormal keratinitation (Scaling)  seborrhoea Hyperpigmentation Gangguan persembuhan luka Pada kasus yang ekstrim, terjadi akumulasi mucopolysaccharides dibawah kulit yang menyebabkan penebalan kulit, khususnya di wajah myxoedema

• Neuromuscular – Myopathy – LMN dz – Laryngeal paralysis dan megaoesophagus – Mixoedema coma • Cardiovascular – DCM • Reproductive – Anestrus – Infertilitas – Penurunan libido jantan

Diagnosis • Clinical pathology – QBC: non regenerative anemia often presen – Biochemistry • • • •

Hypercholesterolaemia (>75% cases) Hyperlipidemia ↑ALP, ALT ↑ fructosamine (up to 80%)

Total T4 • Berguna sebagai screening test • Kebanyakan anjing dengan hypoTh memiliki nilai TT4 yang rendah. • Akan tetapi beberapa anjing dengan penyakit tertentu (ESS) memiliki nilai TT4 yang rendah juga • Test lanjutan dibutuhkan apabila nilai TT4 rendah, rendah dalam batas normal atau sangat tinggi

Beberapa yang akan menurunkan nilai TT4 • • • • • • •

Glucocorticoid Sulphonamides Anticonvulsan Furosemide Euthyroid sick syndrome (ESS) Thyroid hormone autoantibodies Breed (sight hounds have lower T4 values)

Euthyroid Sick Syndrome • Gastrointestinal diseases • Pulmonary diseases • Cardiovascular diseases • Renal diseases • Infiltrative and metabolic disorders • Inflammatory conditions • Myocardial infarction

• • • • • • •

Starvation Sepsis Burns Trauma Surgery Malignancy Bone marrow transplantation

Free T4 • Ada 2 metoda pengukuran – Analogue techniques • Tidak lebih baik dari nilai TT4

– Equilibrium dialysis • Gold standard in dogs • Lebih sensitif dan spesific dibandingkan TT4

Advantages – free T4 • Free T4 is biologically active portion – Diffuse into cells – Exerts negative feedback on pituitary • Changes in total T4 with illness and drugs may not affect fT4 • Equilibrium dialysis assay is less affected by thyroid hormone autoantibodies

Disadvantages-fT4 • Must be run with Equilibrium dialysis (ED) (kebanyakan lab manusia menggunakan analogue technique) • Expensive (ED)

T3 & rT3 • Poor indicator of thyroid function – 80% is produced in extra-thyroidal tissues • Tidak ada perbedaan T3 in normal dogs, hypothyroid dogs dan ESS dogs. • Anti-T3 autoantibodies are more common than antiT4 • rT3 partly increased in ESS dogs and after drug application

TSH • Lack of negative feedback on pituitary should lead to elevation of TSH • Combination with fT4 or T4 (High TSH & Low fT4 or T4) – Sensitivity 87% – Specificity almost 100%

100 & 50

Feline Hyperthyroidism Drh. M. Ar Raniri Putra

Etiology • Hypethyroidism (thyrotoxicosis)  gangguan multisistemik, yang diakibatkan karena berlebihnya konsentrasi hormone thyroid • 98 % Adenomatous hyperplasia • 2 % carcinoma • 70% terjadi bilateral • Cause unknown • Hypotheses : – BPA (Bysphenol A)  coat dalam kaleng – PBDEs (PolyBrominated Dyphenil Ether)  Limbah  Tinggi dalam tubuh ikan. – Genetics

Canned food and Hyperthyroidism • Risk factors: Flea sprays, indoors, herbicides, canned food (scarlett et al, 1988) • Increased risk in cats that prefer fish or liver or giblets flavored canned food (Martin et al, 2000) • Cats fed pop-top canned food at any time had 2.5x to 5x risk of hyperthyroidism VS cats fed dry food (Edinboro et al. 2004)

Breed • Siamese • Himalayan • Purebred

Decreased risk

• DSH  increase risk

Sex • Male and female equal

Age • Middle-aged Older cat (>4yo, average : 12-13th)  increased risk

Historical Findings • • • • • • • • •

Weight loss Hyperactivity Polyphagia PU/PD Vomiting Diarrhea Decreased Appetite Large fecal volume Anorexia

88% 61% 49% 36% 44% 15% 16% 8% 7%

Physical Findings • • • • • • • •

Goiter (enlargement of Thyroid Glnd) 83% Thin 65% Heart murmur 54% Tachycardia 42% Gallop 15% Aggression 15% Unkempt 9% Thick claws 6%

Diagnosis • Thyroid palpation: ↑size may indicate HyperTh • Laboratory : CBC,Blood Chemistry, Urinalysis • Imaging (USG, Xray, Scintigraphy) • Diagnostic test

Thyroid Palpation

Classic Palpation Technique Norsworthy Technique

Thyroid palpation (Score) • • • • • • •

0 : not palpable, 1 : 1-<3mm 2: 3-<5mm 3: 5-<8mm 4: 8-<12 mm (kacang kedelai) 5: 12 -<25 mm 6 : >25mm (uang logam 100rp)

• Conclution: – Euthyroid 0-3

- Hyperthyroid ≥ 4

Diagnosis • Urinalysis (Variable USG (40-60% >1.040) but concurrent (masked) renal disease USG<1.040, mild proteinuria) • CBC – Leukositosis, eosinopenia, increased PCV

• Chemistry profile – Increased ALT (90%) – Creatinine umumnya lowered  loss of muscle mass & increase GFR – Azotemia (20%)  increase protein intake and protein catabolism or HYperThy with concurrent renal dz

• Blood pressure (high)

• Serum total T4

TT4

10% of hyperthyroid cat 40% of early or mild hyperthyroid cat Have TT4 within 1/3 uuper in reference range

Euthyroid Sick Syndrome • • • • •

Gastrointestinal diseases Pulmonary diseases Cardiovascular diseases Renal diseases Infiltrative and metabolic disorders • Inflammatory conditions • Myocardial infarction

• • • • • • •

Starvation Sepsis Burns Trauma Surgery Malignancy Bone marrow transplantation

Diagnostic test Therapy

Drug

Dose

Route

Sampling times

Assay

euthyroidism

HyperT

T3 Suppression

Liothyronine

20 mg q8h for 7 doses

Oral

0 and 2-4 hours after last dose

Total T4

<20 nmol/l with >50% suppression

>20nmol/l ± <35% suppression

TSH Stimulation

Bovine TSH

0.5 IU/kg

IV

0 and 6 hours

Total T4

>100% increase

Minimal to no increase

rhTSH

25ug/cat

IV

1 and 6-8 hours

Total T4

>100% increase

Minimal to no increase

TRH

0.1 mg/kg

IV

0 and 4 hours

Total T4

>60% increase

<50% increase

TRH Stimulation

Hyperthyroid dengan Cardiac disease • Hyperthyroid  metabolisme rate meningkat  HR meningkat  Cardiac Output meningkat  penebalan dinding otot jantung • ECG abnormalities : Arrythmia, tachycardia, increase R-wave amplitude (lead II), Prolong QRS, Shortened Q-T interval

Hyperthyroid dengan CKD • Hyperthyroid  GFR meningkat • GFR meningkat  akan membuat ginjal terlihat dalam kondisi yg sangat baik  ketika berlangsung lama  kidney damage • CKD akan tidak terlihat atau terlihat tidak terlalu parah (unmask) apabila terjadi pada kucing dengan hyperthyroidism

• Serum TT4 dan renal parameter harus dicek ulang setelah 30 hari post treatment

Anti-thyroid drug Reversible Diet Treatment Thyroidectomy irreversible Radioactive iodine

Treatment • Antithyroid drugs – Methimazole/Thiamazole (Felimazole ®) : 2.5mg/cat q12h

• Transdermal 2.5 mg/ 0.1ml  apply 0.1ml to inner pnna (wear gloves) – Carbimazole (Vidalta ®) : 5mg/cat q12h – Recheck every 2-4 weeks in first 3mo – Thereafter every 3-6 mo’s

• Diet  hills Y/d

• Radioactive Iodine  the best treatment • Surgical  risk of damaging of the parathyroid gland

CANINE CUSHING’S SYNDROME: AN OVERVIEW

Dr. Harvey Cushing (1869-1939)

Hypothalamus

CRH (+)

Pituitary pars distalis

cortisol (-)

ACTH (+)

Adrenal cortex

Cortisol

cortisol (-)

KAUSA DARI HYPERCORTISOLISM 

Pituitary-dependent hypercortisolism (PDH)    





Most common Persisten sekresi ACTH Micro atau macroadenoma dari pars distalis Bilateral adrenal hyperplasia ACTH merangsang sekresi cortisol tapi negative feed back cortisol thd ACTH tidak terjadi  [cortisol] dan [ACTH] ↑ ↑

Adrenal Tumor Cortex secara autonom mensekresikan cortisol  Negative feed back cortisol terhadap ACTH tetap terjadi  [cortisol] ↑ sementara [ACTH]↓ 



Iatrogenic = pengobatan corticosteroid dlm waktu yg lama

PREDISPOSITIONS 

Usia 



2-16 tahun, adrenal tumor  rata2 11 tahun

Breed Pred Dog : Poodle, boston terrier, boxer, dachshund PDH;  german shepherd and toy poodle  adrenal tumor  Cat : none 



Sex pred Dog: none, but female make up 70% of adrenal tumor  Cat: female 

CLINICAL SIGN 

Pu.PD (90%) Due to ADH antagonism  Decreased renal tubular water permeability  Decreased vasopressin secretion 



Polyphagia 

Direct effect of glucocorticoid, or can be due to an anti insulin effects (77-87% dogs)

CLINICAL SIGNS: SKIN Bilaterally symmetrical alopecia (55-90%)  Thin skin 

Skin tears easily in cats  Decubital ulcers in severe cases  Pembuluh darah subcutis terlihat jelas 

Hyperpigmentation  Comedones 

CLINICAL SIGNS : MUSCLE 

Muscle atrophy and lethargy 



Direct effect of glucocortioids

Abdominal enlargement (93-95%) Wasting Abd. Muscle  Redistribution of fat to ventral abdomen  Hepatomegaly induksi vakuolisasi sel hati dan akumulasi glikogen 

Muscle Atrophi

Pot belly

CLINICAL SIGNS 

Respiratory system Panting is common abd. Fat n disposisi lemak yg berlebih pada thorax, kelemahan otot respirasi  Dyspnea due to pulmonary embolism 





Obesity Endocrine system Insulin resistance  Diabetes is common in dogs and cats with hypercortisolism 



Infertility Malebilateral testis atrophy, penurunan libido  Female (bitches) prolonged unestrus 



Nervous system 

Seizures, blindness, circling due to macroadenoma

DIAGNOSIS

History and PE are the most important “tests” in diagnosis of hyperadrenocotism.

DIAGNOSIS 

Urinalysis 



CBC 



Isosthenuria, proteinuria Lymphopenia, eosinopenia, neutrophilia, monocytosis (stress leukogram)

Serum chemistry Elevated ALP (90% dog), 5-40 times  elevated ALT, hyperglycemia, hypernatremia, hypercholesterolemia (90%), hypokalemia (50%) 



Blood pressure 

Mild elevation in 80% of dogs

DIAGNOSTIC IMAGING 

Radiography Hepatomegaly  Mineralized adrenal tumors (35%)  Pulmonary metastasis 



Ultrasound Adrenal hyperplasia vs atrophy vs tumor  Liver and kidney imaging 

PITUITARY ADRENAL FUNCTION TESTS 

Screening tests To establish a diagnosis of hyperadrenocortisism  LDDS, ACTH stimulation tests 



Differentiation Tests To differentiate pituitary from adrenal tumor  HDDS, endogenous ACTH 

PITUITARY-ADRENAL FUNCTION TEST 

Basal cortisol 



Not useful

ACTH stimulation Test      

Cortisol measured before and 60-90 min after 5ug/kg synthetic ACTH IM Use normal value specific for your lab Cats may have cortisol peak 30 or 60 minutes Highly sensitive Tidak akurat pd kasus adrenal tumor Akurat dalam kasus iatrogenic hypercortisolism

TECHNIQUE Ambil darah 2ml untuk mengukur basal cortisol  Inject 5 ug/kg synthetic ACTH IM  Collect blood sample (2ml) in 30 min, 60 min and 90 min  Ensure the tube are labelled correctly 

PITUITARY-ADRENAL FUNCTION TEST 

Dexamethasone Supression Tests Low dose (0.01-0.015 mg/kg)  High dose (0.1 – 1 mg/kg) 

TECHNIQUE  Ambil

darah 2ml untuk dilakukan pengecekan basal cortisol (0 Jam)  Injeksikan 0.01 mg/kg dexamethasone (LDDS) atau 0.1 mg/kg (HDDS) Vena cephalica (sebaiknya menggunakan IV cath)  Ambil darah kembali untuk di cek Cortisol pada 4 jam dan 8 jam post injeksi Dexamethasone

THE GRAPHICS BELOW SHOWS POSSIBLE LDDST RESULTS 16

14

12

?PDH/ADH

10

PDH

8

Normal

6

HypoAd or Iatrogenic hyperAd

4

2

0 0

4

8

RATIO OF URINE CORTISOL AND CREATININE (UCCR) Sebaiknya gunakan urin pertama yang keluar dipagi hari  Ukur urine cortisol dan creatinine dalam mmol/L  Ratio >35  Cushing’s  High negative predictive value  Very non specific 



Large breed

•have ratio >35 too 

dissect

TREATMENT (OBAT) 

Adrenocorticolytic Drugs 



Mitotane

Steroidogenesis Inhibitors 

Ketoconazole, methyrapone dan trilostan

MITOTANE (LYSODERM, OP-DDD) 

Dosis induksi 



 

50 mg/kg/day dibagi menjadi bid for 7-10 days

Maintenance phase 



Dimulai ketika pre dan post ACTH stim test berada di kisaran low-normal 50mg/kg/week (divided)

Relapses sering terjadi



Adrenalectomy diperlukan ketika relapse sering terjadi Adrenocorticolytic drug  Also useful for adrenal tumors Higher doses  Useful when surgery is not indicated 

SIDE EFFECTS Inappetance  Anorexia  Vomiting  Collapse  Diare  Ataxia 

Owner harus mempersiapkan prednisone kalau side effect muncul

STEROIDOGENESIS INHIBITORS Ketoconazole  Metyrapone  Trilostane 

Ketoconazole

Hepatotoxic

Methyrapone

Digunakan di manusia, tidak dihewan

Trylostane

TRILOSTANE (VETORYL) Low water solubility  better with food  Dikonversi di hati 

SURGERY Adrenalectomy  tumor adrenal  Hypophysectomy  PDH 

Introduction to Diabetes Mellitus in Dogs n Cats

Hyperglycemia • Blood glucose > ref. Range • Clinical signs occur when the renal threshold is exceeded – 180-220 mg/dl in dog – ?-300 mg/dl in cat – Results in glucosuria  osmotic diuresis  PU/PD

Ruleouts for Hyperglycemia • DM – Type 1 or type 2

• Stressed cats  epinephrine release • hyperAd or drug (corticosteroid atau dextrose) • Hyperglycemia from glucocorticoids not always accompanied by glycosuria

Pathophysiology • Type 1 – Destruction/loss of beta cells – May be partial  associated with pancreatitis

• Type 2 – Insulin resistance/dysfunctional beta cells – Can be obesity-related

• Dogs are more like Type 1, cats more like type 2, but all fall somewhere on continuum between the two

DM Type 2 • Insulin resistance – Fat  cytokine  prevent of insulin action  pankreas produksi lebih banyak insulin  cell B hypofunction due to over work

• Dysfunctional B-cell – ↑↑ Glucose + ↑↑ Fatty acid  toxic to B-cell  apoptosis  dysfunctional  ↓ insulin

• Insulin  lebih cepat.. Lebih baik..  ↑remission

Causes of DM in dogs • Genetic predispositions – Australian terrier, Schnauzer, Samoyed, mini schnauzer, fox terrier, keeshond, bichon frise, Poodle, Husky

• Age – 8-15 yo (most over 10 yo)

• Obesity increases risk 3 – to 5 fold • Female 2x more likely than male • Dogs weighing less than 23 kg greater risk (small – medium dog) • Doggy snack • Drugs: Glucocorticoid

Clinical Signs • Polyuria • Polydipsia • Polyphagia  satety center has an insulin mediated uptake of glucose • Weight loss

Diabetic cataracts • Most occur in dogs • Glukosa akan dimetabolisme melalui sorbitol pathway  sorbitol dan fruktosa  osmotic disruption • Bisa terjadi sangat cepat • Biasanya terjadi 5-6 bulan setelah terdiagnosa • Sering terjadi pada pasien DM yg tdk terkontrol

Diabetic cataracts

Treatment • Dietary – High fiber – Avoid excessive amounts of protein – Avoid excessive amounts of fat

Insulin currently used In dogs

• Porcine lente/ Caninsulin (most common) • Humulin N • Lantus

Cause of DM in Cats • • • • •

Chronic pancreatitis Obesity Sex: neutered males more common Most are over 10 yo Infection and other illness (bacterial ginggivitis and UTI) • Drugs  glucocorticoid

Diabetic neuropathy • Seen in cats • Plantigrade posture the hocks touching the ground • Cause is unknown

Initial diagnostics • • • • •

Urinalysis • Urinalysis – Glycosuria CBC – Proteinuria Chemistry profile – Ketonuria Urine culture – Bacteriuria +/- Fructosamine • Chemistry – hyperglycemia – Liver enzyme abnormality • Due to lipidosis n pancreatitis

– Pre renal azotemia – ↑ Cholesterol

Stress Hyperglycemia

• Stress hypergycemia  Big enemy • 1 high BG not enough – repeat fasted measurment

Dietary • In cats – Obligate carnivores – Amino acid signals insulin release – Maintain necessary glucose levels from amino acids and not dietary carbohydrates

Feeding schedule

Exercise

• If typically fed free choice, continue • Minimum of 2 meals daily

• Promote weight loss • Glucose lowering effect

Insulin currently used In cats

• • • •

Porcine lente PZI Humulin N Glargin/ Lantus (most common)

Treatment Goal • Eliminate clinical symptoms • Avoid ketoacidosis • Diabetic remission (?) – Kalau >6bl treatment belum ada tanda2 remission  kecil kemungkinan akan remission

Insulin starting doses Dogs • 0.5-1 IU/kg bid

cats • 0.5-1 IU/kg atau 1-3 IU/cat

Before or After meal??? Post prandial BG

Post prandial BG

Insulin

• Sometimes insulin + food in the same time: not good enough • 30 minutes prior to food can give superior result

Insulin

Monitoring Insulin Therapy • Clinical Signs – Signs of hypoglycemia – PU/PD – Body condition – Appetite

• Fruktosamine • Spot BG

Oral Hypoglycemic Drugs • Increasing Insulin secretion  glipizide • Inhibit glucose release  metformin  can be toxic in dog n cat • Decrease glucose absorption  acarbose • Increase sensitivity to insulin  thiazolodine  very toxic in cats

• Kontraindikasi – Hypoglycemia – Development of ketonuria – Lack of response – hepatotoxic

Thank you..

Signalment and History Milk, Anjing mix malthese-westie, usia 10 tahun, jantan sudah dikebiri Datang dengan keluhan muntah dan lethargic.

Clinical Signs Clinical symptoms include • vomiting  1o GI atau 2oGI ?? • Lethargy • DM • HyperA • polyuria, • Kidney dz • polydipsia, • limfosarcoma • decrease of body weight for a couple of month. • DM • CKD

DDx awal • Diabetes Melitus • Kidney disease • HyperA

Diagnostic plan • Hematology • Kimia darah : BUN, Cr, SGPT, ALP, Total bilirubin, Glukosa • Urinalysis

Haematology : within normal limit Blood chemistry: Urinalysis USG : 1020 pH : 5 Leukocyte: Protein : +1 Glucose : +4 Keton : +3 SGPT Urobilinogen : Total Protein Erythrocyte : +4

77 5.6 Albumin 3.3 ALP 834 Total Bilirubin 7.39

< 50 5.4-7.1 2.3-3.2 <105 0.1-0.3

u/l gr/dl gr/dl u/l mg/dl

Blood Glucose 514 Ureum 38.6 Creatinin 0.9

60-100 10-20 1-2

mg/dl mg/dl mg/dl

Diagnosa • Diabetes Ketoacidosis – DDX : HyperA

Treatment Rehidrasi Insulin Antibiotik Prescription diet w/d

Result.... • Insulin resistance