GANGGUAN METABOLISME

KARBOHIDRAT, PROTEIN DAN LEMAK

Oleh
SUS DERTHI WIDHYARI

DIVISI PENYAKIT DALAM

DEPT KLINIK REPRODUKSI DAN PATOLOGI
FAKULTAS KEDOKTERAN HEWAN – IPB
 METABOLISM
• Metabolism is the process your body uses to get
or make energy from the feed.
• Feed is made up of proteins, carbohydrates, and
fats.
• Metabolism consists of anabolism (the buildup of
substances) and catabolism (the breakdown of
substances).
• The term metabolism is commonly used to the
breakdown of food into energy.
Cow Metabolism
Muscle
Feed Digest Bone
Fat
Circulation Reproduction
 METABOLISM
• Enzymes break proteins down into amino acids, fats into
fatty acids, and carbohydrates into simple sugars (for
example, glucose).
• In addition to sugar, both amino acids and fatty acids can
be used as energy sources by the body when needed.
• These compounds are absorbed into the blood, which
transports them to the cells.
• The body can use this fuel right away, or it can store the
energy in their body tissues, such as liver, muscles, and
body fat.
Digestive Process - Monogastrics
Proteins Fats Starch

MOUTH amylase

Maltose

STOMACH proteases

Peptides

SMALL peptidases bile salts amylase

lipases maltase
INTESTINE
Amino Fatty Glucose
acids acids

= main site of absorption

Dok. Sus derthi

 LIVER ANABOLISME
Glikogen ADIPOSE
Glucose
Glucose- 6- P glucose (from gut)
Glu Glu-6-P
HMP
pyruvat Amino Acids Pyruvate
AA (from gut) Acetyl CoA
TCA
Acetyl-CoA Protein Chylomicra
Fatty Acid
TCA
Fatty Acid (from gut
Triglyceride
VLDL Triglicerid Chylomicra
remnants
VLDL VLDL

Amino Acids

AA MUSCLE BRAIN
Acetyl-Co A
Protein TCA Acetyl-CoA TCA
Pyruvat
Pyruvat
Glu Glucose Glucose Glu-6-P

Glycogen
Dok. Sus derthi
Metabolisme post-absorptive state
JALUR BIOKIMIA PRODUKSI ENERGI
 METABOLISME KARBOHIDRAT

GLIKOGEN

glikogenolisis  glikogenesis

GLUKOSA

glikolisis  glukoneogenesis

LAKTAT
Digestive Process - Ruminants
Nonprotein N Feed
(NPN) proteins Carbohydrates Fats

RUMEN/ Cellulose Starches

RETICULUM Hemicellulose Sugars

RUP
Microbial protein Volatile fatty
(essential AA) acids (VFA’s) Glucose

LIVER
Glucose

OMASUM
VFA’s

ABOMASUM
RUP
Microbial protein

Peptides

SMALL Fats
Peptides
INTESTINE
Fatty acids &
Amino acids Glucose glycerol

= microbial action; RDP = rumen degraded protein; RUP = rumen undegraded protein; = main site of absorption = some absorption

Dok. Sus derthi

Energy Pathways and Metabolites
GANGGUAN METABOLISME
• Penyakit non infeksius dan bersifat sistemik
• Gangguan metabolisme :
1. Gangguan metabolisme karbohidrat
2. Gangguan metabolisme protein
3. Gangguan metabolisme lemak
• Kejadian diinduksi oleh ketidak seimbangan antara
input dan output atau berhub dgn hasil metabolit
 Glukosa
• Jika kadar glukosa darah dalam batas normal  sebagian
besar jaringan menggunakan glukosa sebagai sumber
energi.
• Kelebihan glukosa akan disimpan sebagai glikogen.
Sintesis glikogen dari glukosa disebut glikogenesis.
• Simpanan glikogen terbatas sehingga kelebihan glukosa
yang lain diubah menjadi lemak (lipogenesis).
• Jika kadar glukosa darah turun, tubuh mengubah glikogen
kembali menjadi glukosa (glikogenolisis)
Hormon Insulin :

 Menurunkan kadar glukosa darah

 Menekan pembentukan glukosa
 Meningkatkan konversi glukosa menjadi lemak
 ↑ permeabilitas membran sel jar (otot maupun adiposa)
 Menghambat glukoneogenesis di dalam hati
 Meningkatkan pembentukan glikogen di hati dan hambat
glikogenolisis oleh hormonal
Hormon pertumbuhan, glukokortikoid,
epinefrin, glukagon

 mengurangi pengambilan glukosa oleh

jaringan
 mobilisasi asam lemak bebas dari jar
meningkat
 Meningkatkan glukoneogenesis melalui
katabolisme protein, menurunkn penggunaan
glukosa oleh jar
  pembentukan glikogen di hati dan otot
 ↑ glikogenolisis
 Meningkatkan proses glukoneogenesis
 Metabolic Disorders
• Metabolic disorder is any disease that is caused by an
abnormal chemical reaction in the body's cells.
• Most disorders involve either abnormal levels of
enzymes or hormones, or problems with how those
enzymes or hormones work.
• When the metabolism of body chemicals is blocked or
defective, it can cause a buildup of toxic substances in the
body or a lack of substances needed for normal body
function, either of which can lead to serious symptoms
GANGG. METABOLISM KARBOHIDRAT

• Gangguan metabolisme karbohidrat → munculnya

keadaan hipoglisemia, hiperglisemia, ketonuria,
glukosuria
• Jika homeostasis gagal dan glukosa darah
melebihi kadar normal (pada diabetes mellitus),
kelebihan glukosa akan diekskresi dalam urin.
• Ekskresi glukosa dalam urin hanya terjadi jika
ambang ginjal untuk reabsorbsi glukosa
terlampaui.
• Kadar glukosa pd monogastrik (anjing) sekitar 60-110 mg/dl,
sedang pd ruminansia (sapi) sekitar 45-75 mg/dl. Pada burung
(unggas) sekitar 209-399 mg/dl). Manusia sekitar 70 -110
mg/dl

• Ambang renal glukosa

• Pd sapi dan kambing sekitar 100 mg/dl
• Pd anjing sekitar 180-220 mg/dl
• Pd kucing sekitar 290 mg/dl
• Pd kuda sekitar 150 mg/dl
 Analisa Glukosa
 Plasma atau serum
 Antikoagulan menggunakan Kalium oksalat dan NaF
(Natrium Flourida)
→ Berfungsi sbg antibeku dan menghalangi glikolisis.
→ dengan cara menghambat kerja enzim Phosphoenol
pyruvate dan urease shg kadar glukosa stabil.
Sebanyak 1 ml untuk 10 ml darah)

Alat spektrofotometer atau glukometer

Glukometer akan mengukur konsentrasi glukosa dalam darah (mg/dl).
Prolonged exposure of serum or plasma to
leukocytes,platelets and erythrocytes →
consume glucose and lower glucose
concentration
Decline 5%-10% per hour
Removing serum or plasma 30-60 minutes after
blood collection
Blood in cool environment decreased glucose
consumption
Increase consumption →
leukocytosis,thrombocytosis,erythrocytosis
GANGGUAN METABOLISME
KARBOHIDRAT

Diabetes Mellitus
Ketosis
Pregnancy Toxemia
• HIPERGLISEMIA
• HIPOGLISEMIA
 HIPERGLIKEMIA
 Peningkatan kadar glukosa darah

 Hiperglikemia terjadi akibat dari :

 Intake glukosa ↑
 Produksi glukosa ↑
(glikogenolisis hepatik atau glukoneogenesis ↑)
 Pemanfaatan glukosa oleh jaringan ↓

 Keadaan diabetes timbul akibat ketidak seimbangan dalam

interaksi pankreas, hipofisis dan adrenal
 Physiologic
Hyperglycemia

• Fear, Excitement, Stress (Cat)

• Following a meal
• Glucocorticoid associated
• Hyperglisemia akibat Fear, Excitement
→Katekolamin (epinephrin dan nor epinephrin)dihasilkan
medulla adrenal
• stimulai glikogenolisis pd hati
• Uptake glukosa oleh myocyt, dan adiposit menurun

• Hyperglisemia akibat stress

• → hormon glukokortikoid (cortisol)
stimulai glukoneogenesis di hati
 Pharmacologic Hyperglycemia
- Injeksi glukosa (IV,oral)
- Terapi glukokortikoid,
- Pemberian xylazin, ketamin
Xylazin atau detomidin: inhibit insulin release, reduces of
glucose utilization by hepatocytes, myocytes, and adipocytes
Ketamine : stimulates the release of epinephrine → increased
glycogenolysis
 Pathologic Hyperglycemia

•Diabetes Mellitus
(tipe I → Idiophatic (dogs)
tipe II → Pancreatic insular amyloidosis (cats)

•Endocrine : hyperadrenocorticism, (Insulin

resistance), hyperpituitarism
•Pancreatic ( pancreatitis, pancreatic carcinoma)
•Hipertiroidis → Increased tissue breakdown and
carbohydrate metabolism
Infectious : sepsis, bovine viral diarrhea
(BVD)
Infeksi BVD (bovine viral diarrhea)
merusak sel ß menyebkan insulin 
 penggunaan glukosa oleh sel
adiposit, hepatosit,myosit 
Diabetes Melitus
Insulin ↓
 glukosa sulit masuk sel
 hiperglikemia & energi intrasel ↓
 METABOLISM KARBOHIDRAT

Kadar glukosa diatur oleh hati, jar ekstrahepatik dan hormon

agar tetap mantap di dlm darah.
Tubuh menyeimbangkan kadar glukosa → sintesis glikogen,
pemecahan glikogen, dan sintesis lemak
Msknya glukosa kedalam sel (organ hati, otot dan jaringan
adiposa) tgt pada insulin, sedang sel mata, ginjal, sel darah
dan sel syaraf tdk tgt insulin
• Kelebihan glukosa dirubah menjadi sorbitol oleh aldosa
reduktase
 Sorbitol dehidrogenase merubah sorbitol menjadi fruktosa (mis.
Sel ginjal, syaraf, lensa, tdk punya SD)
 Peningkatan sorbitol → peningkatan tekanan osmotik disertai
pergerakan air ke dlm sel; produksi glikoprotein meningkat shg
terjadi penebalan pembuluh kapiler
 Komplikasi berupa mikroangiophaty, retinophaty, nephropathy,
neurophaty
 Hepatic Lipidosis

Infiltrasi lipid yang terjadi pada kucing gemuk

yang mengalami penurunan BB dengan cepat.
Causes : kelaparan, DM, excess cortisol
Tanda klinis : depresi, ataxia, paresis, seizure,
hipersalivasi, vomiting, icterus
X-ray  pembesaran hati
Patogenese : VLDL menurun  akumulasi
lemak dalam hati  sumbatan aliran bile
ke portal icterus
Hepatic Lipidosis

Akumulasi lemak dalam hati

 Hipoglikemia

 Increased insulin secretion : pancreatic beta cell neoplasia

(insulinoma)
 Decreased insulin antagonist (hipoadrenocorticism, growth
hormone, hipopituitarism)
 Decreased gluconeogenesis
- (hepatic insuficiency, starvation, severe malnutrition)
 Decreased glycogenolysis (rare)
 Increased uptake of glucose by target cells
 HIPOGLISEMIA

• Hyperinsulinism
• Hypoadrenocorticism
• Primary (Addison’s disease)
• Secondary (ACTH deficiency)
• Liver dysfunction
• Ketosis (Ruminant)
• Pregnancy Toxemia (Ewe)
• Chronic starvation
• Chronic malabsorption
• Anoreksia menyebabkan hipoglisemia

• Hepatosit mempertahankan kadar glukosa melalui

glukoneogenesis (asam lemak dan asam amino)
• Glukoneogenesis tdk mampu menyediakan glukosa yang cukup
 Ketosis
• Ketosis salah satu kasus disertai keadaan hipoglisemia dan
ketonemia
• Kondisi fisiologis (nafsu makan menurun, kelaparan, produksi
susu tinggi) dan patologis (penyakit displecement abomasum,
metritis)
• Glukosa darah menurun dari 50 mg/dl menjadi 20-25 mg/dl
• Kejadian sering pd sapi perah yang memiliki produksi susu
tinggi (1-2 bulan post partum)
● Diproduksi oleh rumen dan omasum
• Mobilisasi as lemak meningkat dari jar adiposa
• Badan-badan keton : Aseton, asetoasetat dan β hidroksi butiric
acid
• Akumulasi badan keton dlm darah → ekskresi dalam susu dan
urin (diagnostik test ketosis)
• Gejala klinis lemah,penurunan prod susu, dan berat badan
(jarang fatal)
  Ketosis
 (Acetonemia pada Sapi,
 Pregnancy Toxaemia Of Sheep)

 Ketonaemia, ketonuria, hypoglycemia,

 Penurunan nafsu makan, tremor atau inkoordinasi
.
 Kasus ini sering dihubungkan dgn produksi susu yg tinggi
dan sering dijumpai pada umur 5 – 8 tahun.
Ketosis
• Keton uria mendahului kejadian ketonemia (pd ambang renal
keton rendah) → deteksi dini ketosis sub klinis

• Diekskresi melalui ginjal  H+ diserap diganti ion bikarbonat,

Na dan K turut diekskresikan melalui urin
Any
questions?
GANGGUAN LEMAK
 Lipid
• Lipids play very important roles in maintaining
the structure of cell membrane (cholesterol, phospholipids),
cell growth (cholesterol),
steroid hormone synthesis (cholesterol), and energy metabolism
(triglycerides).

• Since lipids are highly hydrophobic, they have to be packed into

lipoproteins as water-soluble particles in blood circulation

• A lipoprotein is a particle consisting of a core of hydrophobic lipids, i.e.,

triglycerides (TG), cholesteryl esters (CE), surrounded by a polar layer of
phospholipids (PL), unesterified cholesterol (FC), and apolipoprotein(s)
 NORMAL LIPID METABOLISM
Lumen Enterocyte

lymph
Triglyseride Mono
glyceride triglyceride chylomicron chylomicron
Bile Fatty acid
acid lipase

Fatty Acid Fatty acid

Capillary
Fatty acid

1. Hydrolysis. 2. Emulsification 3. micelle formation 4. absorption

• Cholesterol
• Triglicerida (Triasilgliceral)
• Phospholipid
• Nonesterified faftty acids

Plasma Lipid
 KOLESTEROL

• Sintesis kolesterol di hati, 2 mol asetil ko A mengalami

kondensasi membentuk asetoasetil ko A → HMG Ko A (3
hidroksi 3 metil glutaril ) →menjadi asam mevalonat →
menjadi kolesterol
• Di hati kolesterol berbentuk kilomikron dirubah menjadi
lipoprotein
 LIPOPROTEIN
☺Lipoprotein disintesis di hati dan usus halus, dan disekresikan
ke dalam plasma
☺Transport Lemak di dalam darah (Lipoprotein)
• Kilomikron → penyerapan melalui limfe
• VLDL → Membawa lipid dari hati ke jar perifer. Fatty liver :
ketidak seimbangan antara sintesis TG hepatic dan sekresi
VLDL.
• HDL → kolesterol perifer dibawa ke hati
• LDL → membawa kolesterol ke jaringan perifer, mengendap
pd membran sel. LDL partikel cukup kecil meninggalkan
pembuluh darah dan masuk cairan ekstraseluler, dpt jg
berpindah diantara sel.
• Pada manusia sebagian besar sbg LDL kolesterol
• Pada Sapi konsentrasi HDL dan LDL seimbang
• Kucing dan Anjing konsentrasi HDL tertinggi
• HDL kucing 5-6 kali lebih besar dibanding LDL

• Anjing dan kucing resisten thd atherosklerosis

• Proses pemecahan lipid oleh lipase a.l. :
- Lipase lambung (degradasi trigliserida)
- Lipase pankreas (emulsi lipid di usus)
- Lipase lipoprotein (sel endotel )
- Lipase hepatic (hidrolisa TG pd LDL)
- Hormon sensitive lipase (epineprin dan
glukagon, hidrolisis TG menjadi Asam
lemak)
• Lipoprotein lipase (LPL) is necessary for removing VLDL
and chylomicron fatty acid from the blood
• LPL activity is increased by insulin and thyroid hormone
• The free fatty acids diffuse into cells and are either
resynthesized to triglycerides and stored in adipocytes or used
for energy in myocytes and other cells.
• Lipoprotein lipase is the major enzyme involved in triglyceride
clearance, deficiency of this enzyme has been considered as a
possible cause of hypertriglyceridemia

Lipoprotein lipase
(LPL)
 Metabolic Disorders

• Metabolic disorder is any disease that is caused by an

abnormal chemical reaction in the body's cells.
• Most disorders involve either abnormal levels of
enzymes or hormones, or problems with how those
enzymes or hormones work.
• When the metabolism of body chemicals is blocked or
defective, it can cause a buildup of toxic substances in the
body or a lack of substances needed for normal body
function, either of which can lead to serious symptoms
•Hiperlipidemia

•Hipolipidemia
 Sinonim Hyperlipidemia

• Lipaemia, hyperlipaemia and

hyperlipoproteinaemia, hyperlipidemia all refer
to increased serum lipids
• Hyperlipidemia is the increased concentration
of triglyceride (hypertriglyceridemia),
cholesterol (hypercholesterolemia), or both in
the blood.
Hiperkolesterolemia dapat terjadi akibat :

Produksi kolesterol meningkat di hati

Lipolisis intravaskuler menurun
Defisiensi lipoprotein lipase
 Hiperlipidemia

• Produksi meningkat oleh sel hati (hepatosit) dan sel usus

(enterosit)
- Equin hiperlipemia atau hiperlipedemia
- Postprandial hiperlipidemia
• Procesing lipoprotein intravaskuler terganggu
- Hipotiroid, Neprotic syndrom, defisiensi lipoprotein lipase
Causes of Hyperlipidemia

• Hyperlipidemia to occur in all pets for a few hours after eating.

• The cholesterol and triglyceride levels then return to normal due to the
action of fat metabolism enzymes.
• If your dog has a deficiency of or a defect in these enzymes, they will be
unable to clear the fat from their blood stream, which results in
persistently high fat levels.

• Schnauzer dogs have a genetic predisposition to hyperlipidemia due to

defective enzymes.
 Causes Hyperlipidemia

Physiological
postprandial lipemia (after fat meal consumption)

Postprandial hyperlipidemia is physiological and transient, and

typically resolves within 7–12 h after a meal, depending on the fat
content of the meal
 Causes of Hyperlipidemia
Primary hyperlipidemia: Hereditary / congenital defects
due to genetic or idiopathic causes (such as a mutation in
a receptor protein)
• The cholesterol and triglyceride levels then return to
normal due to the action of fat metabolism enzymes.
• Schnauzer dogs have a genetic predisposition to
hyperlipidemia due to defective enzymes
• Deficiency or a defect in enzymes, they will be unable to
clear the fat from their blood stream, which results in
persistently high fat levels.
• Reported to occur in: Brittany spaniel , Doberman
Pinschers, Rottweilers and domestic cats
Secondary hyperlipidemia:

• Hyperlipidemia can also develop

canine diabetes,
hypothyroidism,
Cushing's disease (hyperadrenocorticism),
liver disease,
canine pancreatitis and
certain kidney diseases.

It is important to have your veterinarian check for these dog

illnesses if hyperlipidemia is identified.
Phatogenesis of Secondary Hyperlipidemia

. Hyperlipidemia due to Hormonal disturbance

• Increased lipolysis by :
- catecholamines (epineprin dan noreepineprin)
- Glucagon
- Adrenocorticotropin
- Growth hormone (GH) or Somatotropic
(STH)

• Decreased lipolysis by:

- Insulin
- Tiroid
 Hormone
(Adrenalin, Glucagon, ACTH)
Lipolysis
Receptor (7TM)

Activates

Adenylyl
Cyclase
ATP c-AMP

Insulin
blocks this Activates lipase
step
Triacylglycerols Glycerol +
Fatty acids Blood

Adipose Cell 69
• Hormon Insulin
→ promote the storage of lipids
→ Meningkatkan aktivitas lipoprotein lipase (LPL)

Diabetes melitus → defisiensi Insulin

 aktivitas LPL menurun
 Lipolisis meningkat (lemak sbg sumber energi)
→hipertrigliserida, hiperkolesterol dan VLDL ↑
 Adenylyl cyclase Phosphodiesterase

ATP c-AMP AMP

Enhanced by glucagon Enhanced by insulin

Inactive Kinase Activated Kinase

Inactive Lipase Activated Lipase

(Hormone-sensitive
Phosphatase Lipase)

Insulin favors formation

of the inactive lipase Triacyl- Glycerol +
glycerol Fatty Acids
71
• Thyroid Hormone (Thyroxine and Triiodotyronine)
→promote cellular uptake and utilization of lipid

• Hypercholesterolemia
- Increased cholesterol formation
- Decreased use of cholesterol
- The activity of lipoprotein lipase decreases

Hypothyroidism → Hypercholesterolemia
-Receptor and LPL lipase activity are reduce
-Cholesterol use decreases and cholesterol
synthesis increases.
Hyperlipidemia due to Hyperadrenocorticism

• Hyperadrenocorticism is the condition with

increase Cortisol → increased lipolysis and
decreased lipoprotein lipase activity may result
hypertriglyceridemia or hyperlipidemia

• Effects of cortisol on fat metabolism:

mobilization of fatty acids due to reduced
transport of glucose into cells causing fatty acids
to be released
• Efek kortisol terhadap metabolisme lemak :
• mobilisasi asam lemak akibat berkurangnya pengangkutan
glukosa ke dalam sel-sel lemak sehingga menyebabkan asam-
asam lemak dilepaskan
• pembentukan lemak yang berlebihan dan terjadi penumpukan
lemak di beberapa jaringan tubuh yang berlangsung lebih cepat
daripada mobilisasi dan oksidasinya.
Hyperlipidemia due to Pancreatitis

• This condition is observed in dogs

• In Pancreatitis is thought to release inhibitors of
lipoprotein lipase so triglyceride and cholesterol
concentrations are increased
Hyperlipidemia due to Cholestasis

• Severe hypercholesterolemia may occur in association with

cholestasis because excretion in the bile is the major route for
removal of excess cholesterol from the body
Hyperlipidemia due to Nephrotic syndrome

Hypercholesterolemia is secondary to enhanced

synthesis of cholesterol-containing lipoproteins.

Lipoprotein synthesis presumably is stimulated by

hypoalbuminemia and decreased plasma osmotic
pressure (unknown)

Proteinuria (albuminuria)associated with Protein

losing nephropathy (PLN), is often associated
with hyperlipidemia in dogs.
• Symptoms of Hyperlipidemia

• The symptoms of hyperlipidemia are variable

and range from asymptomatic (no symptoms)
to severe episodes of canine pancreatitis, vision
disturbances and seizures.
• Most dogs with hyperlipidemia will exhibit
intermittent signs of vomiting, diarrhea and/or
abdominal discomfort.
• The presence of hyperlipidaemia may be of little clinical
significance.

• However, it may be associated with a range of clinical signs:

• Abdominal signs--anorexia, vomiting, diarrhoea
• Acute necrotising pancreatitis--anorexia, vomiting, diarrhoea,
localised abdominal pain
• Ocular abnormalities--lipid keratopathy, arcus lipoids corneae,
stromal dystrophy, lipid in the aqueous humour, lipemia retinalis
• Dermatological manifestations-- cutaneous xanthomata, pruritus,
Alopecia
• Central nervous system disturbances-- seizures, neuropathies,
cerebral arthrosclerosis.

CLINICAL SIGNS OF HYPERLIPIDEMIA

Ocular disease
• Several ocular manifestations of hyperlipidemia, such as
lipemia retinalis, lipemic aqueous, and lipid keratopathy
have been reported in dogs
• Recently, solid intraocular xanthogranuloma formation
was reported as a unique disorder of hyperlipidemic
Miniature Schnauzer
• xanthogranuloma is a deposition of yellowish cholesterol-
rich material that can appear anywhere in the body in
various disease states.
• Lipid keratopathy occurs as a result of hyperlipidemia,
which is the condition of having a high level of lipids, or
fat molecules, in the blood.
• Lipid keratopathy condition in which deposits of lipids,
or fats, infiltrate the cornea of the eye.
• Cholesterol and triglycerides are the essential lipids in the
body. These fats are insoluble
• To travel through the bloodstream to your dog's organs
and tissues, they require the help of lipoproteins
• When an insufficient amount of lipoproteins are formed,
the cholesterol cannot circulate through the blood as
efficiently and it accumulates.
• The excess lipids form deposits within the blood vessels,
as well as on the cornea of the eye.

Lipid keratopathy in dog

• Atherosclerosis
• Atherosclerosis is a condition where the arteries become
narrowed and hardened due to a buildup of plaque around
the artery wall.
• Plaque is made up of fat, cholesterol, calcium, and other
substances found in the blood.
• hardening and narrowing of the arteries due to silently
and slowly blocks arteries, putting blood flow at risk. It’s
the usual cause of heart attacks, strokes, and peripheral
vascular disease
• HDL is believed to remove some of the bad cholesterol
from plaque in clogged arteries and transport it back to
the liver, where it is eliminated.
• The body sends a type of white blood cell (macrophages)
to clean up this cholesterol, but, sometimes, the cells get
stuck at the affected site.
• the plaque eventually, breaks open. If this happens,
platelets gather in the affected area and can stick together,
forming blood clots. This can block the artery, leading to
life-threatening complications, such as stroke and heart
attack.
• Diagnosis of Hyperlipidemia

• Hyperlipidemia is diagnosed if
triglyceride level greater than 500mg/dl
cholesterol level greater than 300mg/dl.
Milky appearance of
plasma or serum
 Alat Spektrofotometer
• Analisis kolesterol di dalam serum/p;asma
Serum stabil pada 40C selama 5-7 hari, pd suhu -200C
selama 3 bulan, dan pd suhu -700C selama beberapa tahun

• Analisis trigliserida di dalam serum/plasma

• Di dalam serum TG stabil pada 40C selama 5-7 hari, pd
suhu -200C selama 3 bulan, dan pd suhu -700C selama
beberapa tahun
  Hipokolesterolemia

 Prod kolesterol menurun

 Protein losing enteropathy
 Hypoadrenocorticism
Any
questions?
PLASMA PROTEIN
DAN KELAINAN
 PROTEIN PLASMA

• Jika jaringan kekurangan prot, protein plasma dapat

digunakan sbg sumber prot dlm jaringan
• Prot plasma sbg tempat simpanan yang labil dan dpt
digunakan sbg sumber AA bagi jar yang memerlukan
 PLASMA PROTEIN
Albumin, Globulin dan fibrinogen
Albumin dan fibrinogen dibentuk di
hati oleh sel hepatosit
Globulin dibentuk di kel limfoid dan
sumsum tulang (oleh Limfosit β dan
sel plasma)
Protein Pathways and Metabolites
 AMONIA
• Dibentuk di mukosa usus,
degradasi protein dan urea
oleh bakteri rumen, glutamin
di ginjal
• Hasil degradasi protein
amonia (NH3), bersifat
toksik bagi susunan
syaraf,shg diubah di hati
menjadi urea.
Hiperammonemia
• Amonia diekskresikan oleh Dapatan : Cirrhosis hati (alkohol,
ginjal sbg NH4+ hepatitis, obstruksi sal. Empedu)
(pengatur keseimbangan
asam basa) Herediter : def. enzim pd siklus
urea
METABOLISME PROTEIN
 Plasma Vs Serum
 Plasma  komponen cairan dari darah
yang mengandung fibrinogen terlarut.
(darah diisi antikoagulan)

 Serum darah adalah cairan bening yang

memisah setelah darah dibekukan (tanpa
antikoagulan).
Serum tidak mengandung fibrinogen.
Analisa Plasma Protein
• Analisa plasma protein menggunakan plasma atau
serum
• Alat spektrofotometer, refraktofotometer
• Kadar protein sekitar 5.5-7.5 g/dl
• Globulin (TP – Albumin)
• Rasio Albumin/Globulin (A/G) berkisar
0.5-1.50
 Beberapa Istilah
• Protein dyscrasia : protein memiliki struktur abnormal

• Dysproteinemia : konsentrasinya yang abnormal

• Panhiperproteinemia : konsentrasi protein scr keseluruhan

meningkat

• Panhipoproteinemia : konsentrasi protein menurun scr

keseluruhan
 Protein Plasma

Albumin mol prot yang paling kecil. Berperan di

dlm tek osmotik. Albumin pertama lepas dari
pemb darah jika permeabilitas pemb darah
terganggu

Gamma globulin penting di dlm sistem

kekebalan)
Fraksi globulin dilihat menggunakan
elektroforesis
 HIPERPROTEINEMIA
• Dehydration
• Inflammation (infection, non infectious)
• Neoplasia →Increased globulin level
(plasma cell myeloma)
• Hiperfibrinogenemia
 HIPOPROTEINEMIA

Produksi protein plasma menurun

(malnutrition,malabsorption, pancreatic
insufficiency, liver disorders )

Kehilangan protein plasma meningkat

(hemorrhage,exudation,nephrophathy)
Absorbsi protein menurun
Katabolisme protein meningkat (kanker)
 ALBUMIN

Hiperalbuminemia
Jarang terjadi, kadang pd dehidrasi

Hipoalbuminemia
a. Hemoragi
b. Gangguan pd glomerulus (protein losing nephropathies)
c. Gangguan gastrointestinal
d. Peny. Hepatis → prod albumin menurun
e. Malnutrisi,
f. Nekrosa hati, fibrosis hati, hepatitis,
hepatoinsufficiency
 GLOBULIN

Hiperglobulinemia
Inflamasi kronis sistemik, myeloma sel plasma,
limfosarkoma

Hipoglobulinemia
Imunodefisiensi, kegagalan transfer pasif imunoglobulin
pada neonatus
PUSTAKA

• Stockham SL, Scott MA. Fundamentals of Veterinary Clinical

Pathology. Iowa State Press

• Kaneko JJ. Clinical Biochemistry of Domestic Animals. Ed

ke-3. New York: Academic Press.

• Ruckebusch, Phaneuf LP, Dunlop R. Physiology of Small and

Large Animals. Philadelphia: B.C. Decker Inc.
TERIMA KASIH