Carbohydrate Metabolism

Prof. Agus Bagiada MD

Department of Biochemistry Faculty of
Medicine Udayana University
Block the endocrine and metabolic
disorder team
 Introduction
What is CH
classification.; Poly, Oligo, Disaccharida, monosac
The important CH for our body:
Amylum/starch/pati : polysacharida

Hydrolized: di-saccarida mono saccharide

Hexosa and pentosa

Glucosa and ribosa.

Metabolism : Anabolism and catabolism
 What is metabolism
Metabolism is the sum of all of the
enzymes-catalyzed reactions that take
place in cells and can be viewed as having
two contrasting processes :
* catabolism : energy yielding reactions in which
complex mol are broken down to small molecule
* anabolism : energy requiring reactions in which
simple precursor molecule are converted into
complex mol.
 Energy yielding in catabolism
Catabolism of C-H, lipids, aa to a simpler
end-product such as CO2, H2O and
amonia is accompanied by the synthesis
of ATP.
ATP is utilized for various cellular functions
such as :
synthesis of protein,RNA,DNA for growth, adaptation and repair,
synthesis of fat and glycogen,
performance of mechanical work,
active ion transport,
absorptions of nutrients against the gradient.
GLUCOSE ABSORPTION
 Glucose transport pathways

Glucose, hydrophilic nature, can not penetrate lipid bilayer; specific

transporterproteins are required for facilitated diffusion into cells

Facilitative glucose carriers (GLUTs)

Class I : high-affinity binding proteins GLUT1,
GLUT3, GLUT4, and lower-affinity transporter
GLUT2
Class II : GLUT5, GLUT7, GLUT9, and GLUT11 or
myoinositol transporter (HMIT1) have a very low
affinity for glucose and preferentially transport
fructose
Class III : GLUT6, GLUT8, GLUT10, GLUT12
Sodium-glucose cotransporters (SGLTs)
 Structure of typical GLUT
Oligosaccharide

Outside

Membrane

Inside

COOH
NH2
 Pathway involved in the
pathogenesis of T2DM
Glucose

Glucose transporter
Glucose

Hexokinases Glucose-6-phosphatase
P
Glucose-6-phosphate

HEXOSAMINE BIOSYNTHESIS PENTOSE PHOSPHATE

PATHWAY PATHWAY

GLYCOLYSIS GLYCOGEN SYNTHESIS

Fig. Cellular fate of glucose showing the major metabolic pathways:

glucose transports and phosphorylation, glycolysis, glycogen synthesis,
pentose phosphate pathway, and hexosamine biosynthesis pathway
Bouche et al. Endocrine Reviews 25: 807-830, 2004
 GLUT-2
Glucokinase
Glucose G-6-P ATP
NIMGU
Beta cell pancreas

Glu-
NIMGU ins
cose (+)
NEFA
Glucose uptake GLUT-4
Glucose Glycerol Triglyceride
(+) (+)
ins (+) ins ins
Insulin-sensitive tissue
Insulin-independent tissue Adipose tissue

NIMGU Glycogen
ins cats
(+) (+)
Glucose G-6-P ins
GLUT-4 (+) CO2

Glycolysis

ins (+)
Skeletal muscle
 CH Metabolism.
1. Glycolysis. Oxid of Glucose/glycogen pyruvat &
lactate.
2. The oxidation of pyruvat to acetyl-CoA: prior to
TCA cycle.
3. TCA Cycle: the final common pathway for
oxidation of CH,fat and protein.
4. The HMP-shunt : alternative pathway for
glucose oxidation
5. Oxidative phosphorylation in respiration chain of
Mitochondria.
GLYCOLYSIS
 GLYCOLYSIS
3 stages of glycolysis
1. Investment stage (2 ATP invested)
2. Splitting stage (compound of 6 Carbon
splitt into 2 substance of 3 Carbon atom)
3. Yielding stage (4 ATP produce)
Total ATP production on glycolysis are 2 ATP
Slide 3 of 22
 Sequence of reaction in glycolysis
D-glucose Glucose 6-P (enzyme hexokinase and glucokinase, ATP and
Mg)
Glucose 6-P Fructose 6-P (enzyme isomerase)
Fructose 6-P Fructosa 1,6- 2P (phosphofructose isomerase, ATP,Mg)
Fructose 1,6-2P dihidroxy aceton-P + glyceral dehide 3-P (aldolase)
Glyceraldehid 3-P 1,3 bisphosphoglycerate (gliceraldehid 3-P
dehydrogenase NAD dependent)
1,3 bisphosphoglycerat 3- phosphoglycerat (phosphoglycerat kinase, Mg
ATP)
3-phosphoglycerate 2 posphoglycerate (phosphoglycerat mutase)
2-phosphoglycerat phosphoenol pyruvate (enolase, Mg)
Phosphoenol pyruvat (enol) pyruvat (pyruvat kinase, Mg, ADP)
Enol pyruvat keto pyruvat (spontaneous)
Keto pyruvat L(+)- Lactate (lactate dehydrogenase NAD dependent)
Oxidation of pyruvat to acetyl-CoA.
Before entering TCA-cycle, pyruvat must
be oxidatively decarboxylated to acetyl
CoA.
Catalyze by pyruvat dehydrogenase
complex
Need thiamin pyrophosphate as enzyme
 Overview of Metabolism
protein polysaccharides lipids
ADP + Pi ADP + Pi ADP + Pi
ATP ATP ATP
amino acids hexoses
fatty acids
ADP + Pi pentoses
ADP + Pi ADP + Pi
ATP ADP + Pi
ATP
ATP
pyruvate ATP
urea
acetyl-CoA ADP + Pi
urea O2
ATP
cycle
electron transport
e- chain
citric acid oxidative
cycle phosphorylation
CO2

ATP
TCA CYCLE
 The Citric Acid Cycle
Final stage for the metabolism of
carbohydrates, fats and amino acids.
Oxidative cycle

- requires oxygen
- aerobic
Also called the Krebs cycle

for Hans Krebs who first described it.

 The Citric Acid Cycle
acetyl CoA

citrate
oxaloacetate A
cis-aconitate A99 step
step
process
process that that
malate
takes
takes the
the
isocitrate
acetate
acetate from from
acetyl-CoA
acetyl-CoA
fumarate and
and converts
converts
-ketoglutarate itit to
to CO
CO22
succinate succincyl
CoA
 Citric Acid Cycle Enzymes
acetyl CoA
Aconitase
Aconitase
Citrate
Citratesynthase
synthase citrate
oxaloacetate
cis-aconitate
Malate
Malate
dehydrogenase
dehydrogenase Aconitase
Aconitase
malate isocitrate

Fumarase Isocitrate
Isocitrate
Fumarase
dehydrogenase
dehydrogenase
fumarate
-ketoglutarate
Succinyl
Succinyl
dehydrogenase
dehydrogenase succinate succincyl -Ketoglutarate
-Ketoglutarate
CoA dehydrogenase
dehydrogenase
Succinyl complex
SuccinylCoA
CoAsynthase
synthase complex
 Energy & the Citric Acid
acetyl CoA Cycle H O
citrate 2

oxaloacetate
cis-aconitate H2O
NADH

malate isocitrate
CO2
H2O +
NADH
fumarate
-ketoglutarate

FADH2 Coenzyme A
succinate succincyl
CoA
GTP CO2 + NADH
+ Coenzyme A GDP
OXIDATION PHOSPHORYLATION
Itis occur in inner mitochondrial
membrane of mitochondria (respiration
chain)
Couple of oxidation and phosphorylation
1 mol of NADH oxidized 3 ATP
1 mol of FADH2 2 mol ATP
1 GTP produce 1 mol ATP
 Pentosa Phosphate Pathway
The primary pathway for formation of
nucleotide, DNA and RNA.
This pathway branched from glycolysis at
a level of G-6P.
This is also describe of shunt rather than
pathway.
Important Enzymes are G6PDH, PGK,
PGM, Enolase, Pyruvate Kinase(PK), LDH
Pentosa Phosphate Pathway (3)
The major product is NADPH
In nucleated cell, with active lipid biosynthesis,
NADPH used in redox reactions biosynthesis
of fatty acid, cholesterol and steroid hormon and
bile salts.
Liver used for hydroxilation reactions for
detoxification and excretion of drugs.
RBC shunt about 10% of glucose use primary
for the reduction of gluthation an important
intermediate in antioxidant defence.
 ROS
Fig.11.10
 The Beneficial effect of ROS
Phagocytosis killed bacteria
 The harmfull effects of ROS
RBC not involved in phagosytosis, however RBC have high O2
tension in arterial blood and heme iron content, ROS are formed
continously in RBC.
Oxidase such as xantine oxidase can produce radical superoksid
and H2O2 directly.
Hb oxidized to Met-Hb that does not bind or transport O2. Its can
presipitate in RBC as Heinz bodies and may also release heme,
which react to H2O2 and superoksid radical to produce hidroxil
radical oxidize lipid membrane lipid peroxidation reactive
carbonyl species such as MDA, 9-hydroxi noneal which react with
protein, damaging the integrity of cell membrane and the actions of
trasport protein, collapsing ion gradient and leading to cell death.
Similar process occur in nucleated cells. Damaging of DNA
contribute to cellular aging
 Gluconeogenesis

The synthesis of glucose from

noncarbohydrate precursors
Occurs primary in the cytosol
Liver & kidney cortex (glucose)
Substrates for gluconeogenesis:
1. Lactate
2. Amino acids
3. Glycerol
4. Propionate
 Gluconeogenesis
During fasting and starvation, when glycogen
liver is depleted, gluconeogenesis is essential
for blood glucose homeostasis
The energy provide from the metab of fat
release from adipose tissue, and carbon
skeleton provided from 3 sources such as
lactate, amino acids, and glycerol release from
triglyceride during lipolysis in adipose tissue.
Substrates for Gluconeogenesis 1. Lactate
2. Amino acids
3. Glycerol
4. Propionyl-CoA

Figure 16.4: Outline of pathways for glucose synthesis

from the major gluconeogenic precursors
1. Lactate:

Figure 16.5: The Cori cycle

The glucose-alanine cycle (chapter 20; NH3)

2. Amino acids:
Many amino acids can be converted to glucose; they are referred
to as glucogenic.
3. Glycerol:
In general, lipids are poor gluconeogenic precursors.
In animals, fatty acids cannot undergo net conversion to
carbohydrates.
4. Propionate: propionyl-CoA
Generated either from the breakdown of some amino acids or
from the oxidation of fatty acids with odd numbers of carbon
atoms.
 ethanol
Ethanol Consumption and Gluconeogenesis:

Not only is ethanol a poor gluconeogenic precursor; it also inhibits

gluconeogenesis and can cause hypoglycemia.
Ethanol is metabolized primarily in the liver, by alcohol
dehydrogenase:
Ethanol + NAD+ acetaldehyde + NADH + H+
This reaction shifts the equilibrium of the lactate dehydrogenase
reaction toward lactate synthesis instead of pyruvate formation;
the same mechanism shifts the equilibrium of cytosolic malate
dehydrogenase.
 Glucose homeostasis
Plasma glucose concentration reflects
the balance between :
1. Glucose intake (abs from the gut)
2. Tissue utilization (glycolisis,PPP, TCA
cycle, glycogen synthesis)
3. Endogenous production of glucose
(glycogenolysis, gluconeogenesis)
Control of glucose homeostasis
Control by:
1. Anabolic hormone, insulin and insulin like
growth factor.
2. Several catabolic hormone (glucagon,
cathecolamine, cortisol, and GH = anti insulin
= counter-regulatory hormone
Glucose level acts as a signal that initiate the islet
hormonal response. Glucose stimulates the
secretion of insulin and suppresses glucagon
secretion.
 Insulin
Prepro insuline Proinsulin insulin.
Preproinsuline (single chain) lost 24 aa
Proinsuline (insuline sequence
intersperced by conecting aa = C-peptide)
Proinsuline split into insuline + C-peptide
Insuline ( 2 chain alpha and beta chain
link by 2 disulfida bonds)
 Insuline signaling pathway
Tyrosine kinase pathway : binding of insulin
to receptors, activate the tyrosin kinase which
auto phosphorylates the receptors than initiates
further intracellular phosphorylation.Tyrosine
kinase can phosphorylate other protein such as
the insulin receptor substrat-1 (IRS-1) than in
turn generate signal which affect glucose
transport and glycogen synthesis.
G-protein pathway.
 Fig. Insulin signaling pathway that regulate
glucose metabolism in muscle cells and adipocytes
(Shepherd and Kahn, 1999)
 Metabolic effect of insulin
Insulin promotes an anabolic state: storage of
CH and lipid, and synthesis of protein.
Insulin acts on 3 main target tissues,

the liver, muscle and adipose tissue.

In the liver insulin stimulate both glycolysis and
glycogen synthesis. Its also suppresses lypolisis
and promote the lipogenesis (synthesis of long
chain fatty acids). The lipids are than packages
into VLDL blood.
 In the peripheral tissue, insulin induces
lipoprotein lipase an enzyme that hydrolize
VLDL liver and dietary chilomicron into glycerol
and fatty acids
In adipose tissue insuline also stimulates
triglyceride synthesis from glycerol and fatty
acids
In muscle insulin increase glucose transport,
glucose metabolism and glycogen synthesis.
Insulin also increase cellular uptake of amino
acids and stimulate protein synthesis.
 Insulin resistance
Patient with type 2 DM, sometimes present with
hyperglycemia together with high plasma insulin
concentration.
This inconsistency due to tissue insensitivity to
insulin, known as insulin resistance
In insulin resistance, glucose is not efficiently
utilized by tissue
Within a target cells, insulin resistance may be
caused by defect of several levels (pre receptor,
receptor, post receptor, glucose transport.)
 Insulin resistance (cont..)
Rarely, a mutation in the insulin receptor
gene may cause extreme resistance.
Resistance is also caused by antireceptor
antibody.
Defect in receptor signaling (tyrosine
kinase activity or protein phosphorylation
may also cause insulin resistance.
By defective enzyme such as glycogen
syntase or pyruvate dehydrogenase.
 Insulin and C-peptide
Insulin consist of 2 peptide chains link by 2 disulfide
bonds.
The -chain contain 21 aa and the -chain 30 aa. MW is
5500 Da.
The precursor of insulin in beta cell of the islet of
Langerhans is a single chain of preproinsulin. During
insulin synthesis 24 aa cleaved from preproinsulin by
peptidase yielding proinsulin
Proinsulin consist of the insulin sequence intersperced by
Connecting peptide (C-peptide).
At the final stage of insulin synthesis proinsulin split into
insulin and C-peptide both are released from the
cell.This is exploited in the clinical lab. to assess beta cell
function, in patien Th/ by exog. Insulin.
 Metabolic effect 0f Glucagon
A small, single chain 29 aa peptide, MW 3485
Da.
Its main effect is the mobilization of the fuel
reserves, for maintenance of blood glucose level
between meals.
Glucagon inhibits glucose-utilizing pathway and
the storage of metabolic fuels.
Acts rapidly in liver to stimulate glycogenolysis
and inhibits glycogenesis, glycolisis and
lipogenesis. Than activated gluconeogenesis
and ketogenesis.
 Glucagon action
The first stage of glucagon actions is
binding to specific membrane receptors,
glucagon-receptor complex causes the
binding of 5GTP to G protein complex
dissociation of G protein subunit
stimulate adenylate cyclase which convert
ATP to c.AMP activate c-AMP
dependent protein kinase through
phosphorylation of regulatory enzyme of
CH and lipid metabolism.
 Hyperglycaemia
Folin-Wu : 80-120 mg%
O-toluidin : 60-100 mg%
Glucose oxidase: 50-100 mg%

Morethan normol value (depend to

method used hyperglycaemia
Hyperglycaemia is a toxic substrate
Auto oxidation ROS as free radical
AGEs formation non enzymatic glycation
basa schiff amadori products AGEs
HbA1c glycated Hb
Polyol pathway sorbitol fructose
Enz. Aldose reductase and sorbitol
dehydrogenase
Increasing NADH/NAD+ ratio
Accumulation of sorbitol on the
lens cataract and retinopathy
diabetic
In clinical study found that in
diabetic patient with HbA1c
7,38% detected 44% of
retinopathy.
 Fig 20.22
 HbA1c
Diatas7% kontrol DM buruk
6-7 % baik
Dibawah 6% terkendali
 Intervention to effect better control
means fewer complications
EVERY 1% Reduced Risk*
reduction in HBA1C

Deaths from diabetes - 21%

Heart attacks - 14%

Microvascular complications - 37%

1%
Peripheral vascular disorders - 43%
*p<0.0001
DCCT&UKPDS:
Reducinghyperglycaemiareducesincidentrisk&progressionof UKPDS 35 BMJ 2000;321:405-412
 Hypoglycaemia
Blood glucose level < 45 mg% (2,5 mmol/l)
hypoglycaemia
Hypoglycaemia caused by:
Over exercise, external insuline>>, insulinoma,
fasting, inhibition of endogenous glucose
production.
Sign and symptom : palpitation, sweating,
trembling, and feeling hunger
If it is continue neuroglycopenia confuse
and unconciousness fatal.
Hypoglycaemia is medical emergency.
Parathyroid

Keshav Magge MD
March 7, 2007
 Parathyroid
The parathyroid glands develop at 6 weeks and
migrate caudally at 8 weeks
The paired superior parathyroid glands develop
with the thyroid gland from the fourth branchial
pouch and are generally consistent in position,
residing lateral and posterior to the upper pole of
the thyroid at the level of the cricothyroid cartilage.
The paired inferior glands descend with the
thymus from the third branchial pouch and
occasionally migrate to the level of the aortic arch
or, rarely, fail to migrate, remaining in the high
neck.
Parathyroid
 Anatomy
Superior glands usually dorsal to the RLN at
level of cricoid cartilage
Inferior glands located ventral to nerve
Usually derive most of blood supply from
branches of inferior thyroid artery, although
branches from superior thyroid supply at least
20% of upper glands.
Glands drain ipsillaterally by superior, middle,
and inferior thyroid veins.
 Calcium Homeostasis
The parathyroid cells rely on a G-protein-coupled membrane
receptor designated the calcium-sensing receptor (CASR), to
regulate PTH secretion by sensing extracellular calcium levels
PTH secretion also is stimulated by low levels of 1,25-
dihydroxy vitamin D, catecholamines, and hypomagnesemia.
 Calcium Homeostasis
PTH is synthesized in the
parathyroid gland as a
precursor
hormone,preproparathyroid
hormone, which is cleaved
first to proparathyroid
hormone and then to the
final 84-amino-acid PTH.
Secreted PTH has a half-life
of 2 to 4 minutes. In the
liver, PTH is metabolized
into the active N-terminal
component and the relatively
inactive C-terminal fraction
 Calcium homeostasis
The calcium-sensing receptor (CASR) is expressed
on the surface of the parathyroid cell and senses
fluctuations in the concentration of extracellular
calcium.
Increased PTH secretion leads to an increase in serum
calcium levels by increasing bone resorption and
enhancing renal calcium reabsorption.
PTH also stimulates renal 1- Hydroxylase activity,
leading to an increase in 1,25-dihydroxy vitamin D,
which also exerts a negative feedback on PTH
secretion
 Calcium homeostasis
PTH functions to regulate
calcium levels via its actions
on three target organs, the
bone, kidney, and gut.
PTH increases the
resorption of bone by
stimulating osteoclasts and
promotes the release of
calcium and phosphate into
the circulation.
 Calcium homeostasis
At the kidney, PTH acts to limit calcium excretion at the distal
convoluted tubule via an active transport mechanism.
PTH also inhibits phosphate reabsorption (at the Proximal
convoluted tubule) and bicarbonate reabsorption.
PTH and hypophosphatemia also enhance 1-hydroxylation of
25-Hydroxyvitamin D, which is responsible for its indirect
effect of increasing intestinal calcium absorption.
 Hyperparathyroidism
Affects approximately 100,000 patients a year
Primary hyperparathyroidism occurs in 0.1 to
0.3% of the general population and is more
common in women (1:500) than in men
(1:2000).
Primary hyperparathyroidism is characterized by
increased parathyroid cell proliferation and PTH
secretion which is independent of calcium levels.
 Hyperparathyroidism
Etiology unknown, but radiation exposure, and
lithium implicated, associated with MEN1, and
MEN 2A

Enlargement of a single gland or parathyroid

adenoma in approximately 80% of cases,
multiple adenomas or hyperplasia in 15 to 20%
of patients and parathyroid carcinoma in 1% of
patients
Hyperparathyroidism Clinical Sx
Kidney stones, painful bones, abdominal groans,
psychic moans, and fatigue overtones
Kidney stones calcium phosphate and oxalate
Osteopenia, osteoporosis, and osteitis fibrosa cystica,
is found in approximately 15% of patients with
PHPT. Increased bone turnover can usually be
determined by documenting an elevated blood
alkaline phosphatase level.
Peptic ulcer disease, pancreatitis
Psychiatric manifestations such as florid psychosis,
obtubdation, coma, depression, anxiety, fatigue
 Hyperparathyroidism
Hypercalcemia can be from other sources.
Intact PTH measurement and elevated
PTH level very sensitive for
hyperparathyroidism
 Pre-operative localization
Thepredictive value of ultrasonography,
magnetic resonance imaging, or thallium-
technetium dual isotope scintigraphy
ranges from 40 to 80 percent
 Pre-operative localization
99mTechnetium-labeled Sestamibi, aka Cardiolite, was
initially introduced for cardiac imaging and is
concentrated in mitochondria-rich tissue.
It was subsequently noted to be useful for parathyroid
localization because of the delayed washout of the
radionuclide from hypercellular parathyroid tissue when
compared to thyroid tissue.
In one prospective study of 387 patients the sensitivity
for single adenomas was 90 percent, but 27 percent of
double adenomas and 55 percent of hyperplastic glands
were missed
 Pre-operative localization
Single-photon emission computed tomography (SPECT),
when used with planar sestamibi, has particular utility in the
evaluation of ectopic parathyroid adenomas, such as those
located deep in the neck or in the mediastinum. Specifically,
SPECT can indicate whether an adenoma is located in the
anterior or posterior mediastinum.
 Pre-operative localization
Intraoperative parathyroid hormone testing
introduced 1993
Used to determine the adequacy of parathyroid
resection.
When the PTH falls by 50% or more in 10 minutes
after removal of a parathyroid tumor, as compared
to the highest preremoval value, the test is
considered positive and the operation is
terminated.
 Surgery
Bilateral neck exploration is gold standard
With pre-operative imaging techniques can have
minimally invasive focused surgery towards adenoma
Can have 99-Tc Sestamibi timed within 3 hours of
surgery to intra-operatively localize parathyroid adenoma
using hand held geiger probe
Can have sequential Sestamibi scan and repeat
technetium injection 10 minutes prior to surgery
In this setting intra-operative PTH level testing
questionable
 Surgery
Rush medical Center, 2007
220 patients, 49 had BNE, 60 had BNE w/ ioPTH level monitoring,
and 110 had MIPS with io PTH level monitoring
At 3 months postoperatively, mean serum calcium and intact PTH
levels were similar between groups, and eucalcemia rates were
same
The ultimate rates of persistent disease and recurrence were also
similar.
Operative time was shorter in group 3 compared to group 2 ( P < .
001) but not group 1.
Frozen sections and patient charges were significantly lower in
group 3 compared to groups 1 and 2 (P < .005).
When can do minimally invasive, cheaper and quicker
 Parathyroid carcinoma
1% of cases of primary hyperparathyroidism
15% of patients have lymph node metastases
and 33% have distant metastases at
presentation.
 Parathyroid carcinoma
Intraoperatively, cancer is suggested by the
presence of a large, gray-white to gray-brown
parathyroid tumor that is adherent to or invasive
into surrounding tissues
bilateral neck exploration, with en bloc excision
of the tumor and the ipsilateral thyroid lobe.
Modified radical neck dissection is
recommended in the presence of lymph node
metastases
 Surgery
If on exploration, hyperplasia found, can remove and
reimplant, or preferably subtotal parathyroidectomy
leaving approx 50 mg of tissue (as reimplantation has 5%
failure rate).
Bilateral upper cervical thymectomy also performed with
hyperplasia because of supernumerary glands occur in
20% of patients
With autotransplantation, 12 to 14 pieces inserted into
belly of brachioradialis muscle
Sternotomy performed to find a missing gland, generally
not at initial operation, and after localizing studies
performed
Intra-op PTH measuring helpful as well during sternotomy
to make sure got the gland
Secondary Hyperparathyroidism
In pts with chronic renal failure
Deficiency of 1,25-dihydroxy vitamin D as
a result of loss of renal tissue, low calcium
intake, decreased calcium absorption, and
abnormal parathyroid cell response
Normally treated medically
Secondary Hyperparathyroidism
Surgical
treatment is indicated and
recommended for patients with
bone pain,
pruritus, and a calcium-phosphate product >=70,
Ca greater than 11 mg/dL with markedly elevated
PTH
Calciphylaxis
progressive renal osteodystrophy,
soft-tissue calcification
 Tertiary Hyperparathyroidism
Long standing renal failure s/p renal transplant
autonomous parathyroid gland function and tertiary HPT.
Can cause problems similar to primary
hyperparathyroidism
Operative intervention
symptomatic disease
autonomous PTH secretion persists for more than 1
year after a successful transplant
subtotal or total parathyroidectomy with
autotransplantation
 Post Operative Complications
Hypocalcemia (Chvosteks and
Trousseaus sign)
Vocal cord paralysis after RLN injury