Endocrinology Practical

FIGURE 20-1 Copyright © McGraw-Hill Companies
Figure 20–1 Locations of the major

endocrine glands.
In addition to the large endocrine glands shown
at the left here, there are widely distributed
endocrine cells as well as various other tissues
in organs (right) throughout the body with
endocrine functions.
Not shown are adipocytes, which exert important
endocrine functions, and the many tissues in
which paracrine signalling is important.
Copyright © McGraw-Hill Companies

Figure 20–2 Pituitary gland.
The pituitary gland is composed of an anterior
part and a posterior part that is directly attached
to the hypothalamus region of the brain by an
infundibular stalk.
The gland occupies a fossa of the sphenoid

bone called the sella turcica (L. Turkish saddle).

Figure 20–4 Pituitary gland.
Histologically the two parts of the pituitary gland
reflect their origins, as seen in this low-
magnification section of an entire gland.
The infundibular stalk (IS) and pars nervosa

(PN) of the neurohypophysis resemble CNS
tissue, while the adenohypophysis’ pars distalis
(PD), pars intermediate (PI), and pars tuberalis
(PT) are typically glandular in their level of
staining. X30. H&E.

Figure 20–5 The hypothalamic-hypophyseal tract
and portal system.
(a) The hypothalamic-hypophyseal tract consists of
axons extending from the hypothalamic supraoptic and
paraventricular nuclei, through the infundibulum and
into the pars nervosa of the posterior pituitary, where
peptide hormones they carry are released for capillary
uptake.
(b) The hypothalamic-hypophyseal portal system, with
blood from the superior hypophyseal artery, consists of
two capillary networks connected by the hypophyseal
portal vein. The primary plexus surrounds the
infundibulum and median eminence, and the second is
throughout the pars distalis and drains into the
hypophyseal veins.
Figure 20–6 Pars distalis: Acidophils, basophils,
and chromophobes.
(a, b) Most general staining methods simply allow the
parenchymal cells of the pars distalis to be subdivided
into acidophil cells (A), basophils (B), and
chromophobes (C) in which the cytoplasm is poorly
stained. Also shown are capillaries and sinusoids (S) in
the second capillary plexus of the portal system. Cords
of acidophils and basophils vary in distribution and
number in different regions of the pars distalis, but they
are always closely associated microvasculature that
carries off secreted hormones into the general
circulation. X400. H&E. (c) The same area is seen after
staining with Gomori trichrome. X400.
and chromophobes.
and chromophobes.
Figure 20–9 Pars intermedia.
The pars intermedia (PI) lies between the pars distalis
(PD) and the pars nervosa (PN), with many of its
basophilic cells (B) usually invading the latter.
Remnants of the embryonic hypophyseal pouch’s
lumen are usually present in this region as colloid-filled
cysts (C) of various sizes. Function of this region in
humans is not clear. X56. H&E.

Figure 20–11 Pars nervosa: neurosecretory bodies
and pituicytes.
The pars nervosa of the posterior pituitary consists of
modified neural tissues containing unmyelinated axons
supported and ensheathed by glia cells called pituicytes
(P), the most numerous cell present. The axons run
from the supraoptic and paraventricular hypothalamic
nuclei, and have swellings called neurosecretory
(Herring) bodies (NB) from which either oxytocin or
vasopressin is released upon neural stimulation. The
released hormones are picked up by capillaries (C) for
distribution. X400. H&E.
Figure 20–12 Location and blood supply of the
adrenal glands.
The paired adrenal glands are located at the superior
pole of each kidney and each consists of an outer
cortex that produces a variety of steroid hormones and
an inner medulla that produces epinephrine and
norepinephrine. This anterior view of the left adrenal
gland and kidney shows the blood vessels supplying
these glands.

Figure 20–13 Ultrastructure of cortical
adrenalocytes.
TEM of two adjacent steroid-secreting cells from the
zona fasciculate shows features typical of steroid-
producing cells: lipid droplets (L) containing cholesterol
esters, mitochondria (M) with tubular and vesicular
cristae, abundant SER, and autophagosomes (A),
which remove mitochondria and SER between periods
of active steroid synthesis. Also seen are the
euchromatic nuclei (N), a Golgi apparatus (G), RER,
and lysosomes. X25,700.

Figure 20–14 Adrenal gland.
Inside the capsule of each adrenal gland is an adrenal
cortex, formed from embryonic mesodermal cells,
which completely surrounds an innermost adrenal
medulla derived embryologically from neural crest cells.
Both regions are very well vascularized with fenestrated
sinusoidal capillaries. Cortical cells are arranged as
three layers: the zona glomerulosa near the capsule,
the zona fasciculata (the thickest layer), and the zona
reticularis.

Figure 20–15 Adrenal cortex.
The steroid-secreting cells of the adrenal cortex are arranged differently to
form three fairly distinct concentric layers, the zonae glomerulosa (G),
fasciculata (F), and reticularis (R), surrounding the medulla (M). Shown here
are sections from two adrenal glands, stained with H&E (left) and Mallory
trichrome, in which the sparse collagen appears blue (right).
(a, b) Immediately beneath the capsule (C), the zona glomerulosa consists of
rounded clusters of columnar cells principally secreting the mineral corticoid
aldosterone.
(c, d) The thick middle layer, the zona fasciculata, consists of long cords of
large, spongy-looking cells mainly secreting glucocorticoids such as cortisol.
(e, f) Cells of the innermost zona reticularis, next to the medulla (M), are small,
better stained, arranged in a close network and secrete mainly sex steroids.
Cells of all the layers are closely associated with sinusoidal capillaries.
Left: X20 H&E.; a, c, e: X200. H&E. b, d, f: X200. Mallory trichrome.

Figure 20–16 Adrenal medulla.
The hormone-secreting cells of the adrenal medulla are
chromaffin cells, which resemble sympathetic neurons.
(a) The micrograph shows that they are large pale-
staining cells, arranged in cords interspersed with wide
capillaries. Faintly stained cytoplasmic granules can be
seen in most chromaffin cells. X200. H&E.
(b) TEM reveals that the granules of norepinephrine-
secreting cells (NE) are more electron-dense than
those of cells secreting epinephrine (E), which is due to
the chromogranins binding the catecholamines. Most of
the hormone produced is epinephrine, which is only
made in the adrenal medulla. X33,000.

Figure 20–18 Thyroid gland.
The thyroid is a highly vascular, butterfly-shaped gland
surrounding the anterior surface of the trachea just
below the larynx.

Figure 20–19 Thyroid follicular cells and parafollicular cells.
(a) A low-power micrograph of thyroid gland shows the thin capsule (C), from
which septa (S) with the larger blood vessels, lymphatics, and nerves enter
the gland. The parenchyma of the organ is distinctive, consisting of colloid-
filled epithelial follicles of many sizes. The lumen of each follicle is filled with a
lightly staining colloid of a large gelatinous protein called thyroglobulin. X12.
H&E.
(b) The lumen (L) of each follicle is surrounded by a simple epithelium of
thyrocytes in which the cell height ranges from squamous to low columnar.
Also present are large pale-staining parafollicular or C cells (C) that secrete
calcitonin, a polypeptide involved with calcium metabolism. X200. H&E.
(c-e) C cells may be part of the follicular epithelium or present singly or in
groups outside of follicles. Thyrocytes (T) can usually be distinguished from
parafollicular C cells (C) by their smaller size and darker staining properties.
Unlike thyrocytes, C cells seldom vary in their size or pale staining
characteristics. C cells are somewhat easier to locate in or between small
follicles. c and d: X400. H&E; e: X400. Mallory trichrome.

Figure 20–20 Ultrastructure of thyroid follicular and
parafollicular cells.
(a) TEM of the follicular epithelium shows pseudopodia and
microvilli extending from the follicular thyrocytes (T) into the
colloid of the lumen (L). The cells have apical junctional
complexes, much RER, well-developed Golgi complexes, and
many lysosomes. Inside the basement membrane (BM) of the
follicle, but often not contacting the colloid in the lumen, are
occasional C cells (C). To the left and right of the two C cells
seen here are capillaries intimately associated with the follicular
cells, but outside the basement membrane. X2000.
(b) A TEM of a C cell, with its large Golgi apparatus (G),
extensive RER, and cytoplasm filled with small secretory
granules containing calcitonin. X5000.

Figure 20–22 Parathyroid glands.
The parathyroid glands are four small nodules
normally embedded in the capsule on the
posterior surface of the thyroid gland.

Figure 20–23 Parathyroid principal cells.
(a) A small lobe of parathyroid gland, surrounded
by connective tissue septa (S), shows mainly
densely packed cords of small principal cells (P).
Older parathyroid glands show increasing
numbers of much larger and acidophilic
nonfunctional oxyphil cells (O) that may occur
singly or in clumps of varying sizes. X60. H&E.
(b) Higher magnification shows that principal
cells have round central nuclei and pale-staining
cytoplasm. Cords of principal cells secreting
PTH surround capillaries (C). X200. H&E.
Figure 20–23 Parathyroid principal cells.
(a) A small lobe of parathyroid gland, surrounded
by connective tissue septa (S), shows mainly
densely packed cords of small principal cells (P).
Older parathyroid glands show increasing
numbers of much larger and acidophilic
nonfunctional oxyphil cells (O) that may occur
singly or in clumps of varying sizes. X60. H&E.
(b) Higher magnification shows that principal
cells have round central nuclei and pale-staining
cytoplasm. Cords of principal cells secreting
PTH surround capillaries (C). X200. H&E.
Figure 20–24 Pineal gland.
(a) The micrograph shows a group of pinealocytes surrounded by
septa (S) containing venules (V) and capillaries (arrows). Also seen is
an extracellular mineral deposit called a corpus arenaceum (CA) of
unknown physiologic significance but an excellent marker for the
pineal. X200. H&E.
(b) At higher magnification the numerous large pinealocytes (P) with
euchromatic nuclei can be compared to much fewer astrocytes (A) that
have darker, more elongated nuclei and are located mainly within
septa and near small blood vessels (V). Capillaries (arrow) are not
nearly as numerous as in other endocrine glands. At the lower left is a
port of a very large corpus arenaceum (CA), the calcified structures
also known as brain sand. Along the septa run unmyelinated tracts of
sympathetic fibers, associated indirectly with photoreceptive neurons in
the retinas and running to the pinealocytes to stimulate melatonin
release in periods of darkness. Levels of circulating melatonin are one
factor determining the diurnal rhythms of hormone release and
physiologic activities throughout the body. X400. H&E.
Growth hormone testing
ASST. LECTURER .SABA THAER
Objective : Structure ,synthesis and secretion
Role of growth hormone
Factors affection on growth

hormone
Applied
Type of growth hormone blood test

Growth hormone :
 Is a peptide hormone that stimulates growth, cell
reproduction, and cell regeneration in humans. Also
known as somatotropin, because it synthesized and
secreted by the somatotrophs of the anterior pituitary
gland.
Structur of growth
hormone:
 Polyp peptide =single chaine
 Mo. Weight =21.000 Da
 Amino acids= 191
 Disulphide bridge =2
 human & monkey growth hormones have
same biological activity so the same
therapeutically effective.
Transport of  Growth hormone is transported in blood by GH-
bindingproteins (GHBPs).Half-life and
growth Metabolism Half-life of circulating growth
hormone is about 20 minutes. Itis degraded in
hormone: liver and kidney.
Functions :
ACTING ON LIVER
STIMULATE
TO PRODUCE
HYPERTROPHY AND
INSULIN LIKE
HYPERPLEASIA OF
GROWTH FACTOR
THE CELL
.1
METABOLIC EFFECT
Men - < 5 Women - <
ng/mL 10 ng/mL
Reference
range :
Newborns -
5-23 ng/mL
Stimulation
factors :
Hypoglycemia
Factors Protein rich
affecting of diet
growth high Amino

acid in blood
hormone: Sleep
Glucagon
hormone
 Inhibition factors :
Factors  Hyperglycemia
affecting of  Increase free fatty acid

 excess GH feeds back to inhibit its own
growth secretion
hormone:  Excess cortisol

Applied
of
growth
hormone
Hypersecretion :
Acromegaly gigantism
Hyposecretion:
 Dwarfism
Preparing for growth hormone
blood test :
 fast for a specific period of time before the test
 stop taking the vitamin biotin, or B7, at least 12 hours before the test
 stop taking certain prescription medications a few days before the
test, if they might interfere with the test results

Note :
 It’s uncommon for people to have GH levels outside the typical

range, so GH tests aren’t performed routinely.
 Growth hormone may not offer enough information to help in

diagnosis since levels of GH in body naturally rise and fall throughout
the day.
 Doctor may order IGF1 together with growth factor because the
level of IGF1 more stable .
Types of growth
hormone blood
test:
 GH suppression test
 GH stimulation test
GH suppression test
 A GH suppression test helps in

confirm if body produces too much
GH.
 For this test, a healthcare
professional will use a needle or IV
to take a blood sample. Next,
they’ll ask patient to drink a sweet
solution containing glucose, a type
of sugar.
 then give a few more samples of
blood at timed intervals during the 2
hours after drinking of the solution.
GH stimulation test:
 A GH stimulation test helps in

diagnose an excess or deficiency in
GH production.
 For this test, a healthcare
professional will generally use an IV
to take an initial blood sample.
They’ll then give a medication that
triggers the body to release GH.
 The healthcare professional will
monitor patient and take several
more blood samples at timed
intervals over 2 hours.
oral glucose tolerance test
ass .lec :suhad taha mohammed

Objectives
 Diagnosing Diabetes
Illustrate the principle of the test
Outline the indication of the test
Interpret the results of the test
Understand the precautions of the test.
Diagnosing Diabetes
Fasting Plasma Glucose (FPG)
– Glucose level after not having food or drink for at least 8 hours
Result
– Normal - <100 mg/dl
– Prediabetes - 100 – 125 mg/dl
– Diabetes - >126 mg/dl
Random Plasma Glucose(RPS)
– Glucose level at any time of the day when severe diabetes symptoms are
present.
Result
– Diabetes - > 200 mg/dl
HgbA1c
– test measures average blood glucose for the past 2 to 3 months.
Result
– Normal - less than 5.7%
– Prediabetes - 5.7% to 6.4%
– Diabetes - 6.5% or higher
• Oral Glucose Tolerance Test (OGTT)
– a two-hour test that checks the blood glucose levels before and 2 hours
after consuming a high sugar drink
• Result
– Normal - less than 140 mg/dl
– Prediabetes - 140 mg/dl to 199 mg/dl
– Diabetes - >200 mg/dl
Regulation of blood glucose
The Fed State ( Absorptive State);

The period from the start of absorption
until absorption is completed.
The Fasting State;

Begins approximately 2 to 4 hours after a
meal ( when blood glucose levels return
to basal levels) and continues until blood
glucose levels begin to rise after the start
of the next meal.
Oral glucose tolerance test (OGTT)
• Evaluate glucose tolerance in subjects with equivocal

features of diabetes mellitus and do not have fasting
blood glucose values in excess of 140 mg/dL.
Indication for test
1- family history of diabetes
2- obesity
3- Unexplained episodes of hyperglycemia
4- history of recurrent infections
5- in women, history of delivery of large infants, stillbirth, neonatal death,

premature labor, and spontaneous abortions.
6- transitory glycosuria or hyperglycemia during pregnancy, surgery, trauma,

stress, and MI.
Patients preparation
1- Normal diet & carbohydrate intake (150 g/dl) for 3 days.
2- Overnight fast ( 10-16 hours ).
3-Resting for 30 min (seated) prior to test .
4- No smoking during test .
5- No drugs known to interfere with test , e.g. steroids

Protocol
 Glucose load : adult 75g of glucose dissolved in 250 ml of water,

children 1.75 g/kg.
 Must be performed in morning and to remain seated during test .
 Glucose load given in flavored water and consumed within 5 min.
 Urine glucose estimations are not essential during test but useful
if renal glycosuria a possibility.
 Blood samples : basal ( pre-glucose) , 60min, 90min,120min.

Interpretation
Normal Blood Glucose :
Basal : < 5.6 mmol/L ( 100 mg/dl)
Intermediate sample : < 11.1 mmol/l ( 200 mg/dl)
2 hr sample : < 7.8 mmol/l ( 140 mg/dl)
HbA1c : 5-5.5 % ( B.G=100-125mg/dl)

2-h Oral Glucose Tolerance Test (OGTT)
Objectives of the test; Diagnosis of Diabetes Mellitus and Intermediate
Hyperglycemia
When OGTT is not indicated ?
 persistent fasting hyperglycemia > 140 mg/dl
Persistent fasting normal glucose
Patients with overt diabetes mellitus

Glucometer vs enzymatic estimation
Glucometer Enzymatic estimation
1- fast 1- fast ( not like glucometer)

2- cheep 2- easily done in lab
3- easily done by any person 3- precise & reliable ( there is a
4- not precise ( no control) control –standard)
The roles of vit. D3 and
calcium in the body
DR.RAYAN ZAIDAN
DEPARTMENT OF PHYSIOLOGY
AL−KINDY COLLEGE OF MEDICINE
Objectives
1-Discuss the physiological effects of parathyroid
hormone on calcium and phosphate levels?
2-List the factors that regulate calcium concentration in
the blood? State the effects of vitamin D?
3-Identify the clinical conditions resulting from the
disturbance in parathyroid hormone secretion?
Function of calcium in the body
1‫ ـ‬Calcium is very essential in muscle contraction.
2‫ـ‬Building strong bones and teeth.
3‫ـ‬Blood clotting mechanism.
4‫ـ‬Regulating heartbeats and fluid balance within the
cells.
5‫ـ‬Nerve impulse transmission.
Role of vit.D3
Vit. D3 hormone function to increase calcium level in the
body by inducing the proteins involved in active intestinal
calcium absorption and stimulation of active intestinal
absorption of phosphate.
It is essential for promotion of bone growth, helps to control
the concentration of calcium in the body and it is vital for
the development of strong bones.
Vit. D deficiency results in rickets in children, and
osteomalacia in adults.
Parathyroid Hormone:
Normally there are four parathyroid glands in humans; they are located immediately
behind the thyroid gland.
Removal of half the parathyroid glands usually causes no
major physiological abnormalities. However, removal of
three of the four normal glands causes transient
hypoparathyroidism, but its complete removal is lethal
because it is essential to life.
It controls the level of calcium and phosphate in the
blood by the movement of calcium and phosphate from
the bone to blood and excretion of phosphate by the
kidney.
Calcium level is controlled by:
1-Parathyroid hormone.
2-Calcitonin (by thyroid gland, reduce calcium and oppose
the effect of PTH).
3-Metabolites of vitamine D “1,25
dihydroxycholecalceferol”.
Calcium is absorbed from the first half of the small intestine
partly by active transport and partly by the help of vitamin
D.
The level of calcium is 10 mg/dl(9.4 mg/dl) or 5 meq/L in SI
units and is present in 3 forms:
1- Non diffusible through the capillary membrane form
41%: bound to protein.
2-About 9 % of the calcium is diffusible ,but non ionized.
3-The remaining 50 %of the calcium in the plasma is both
diffusible and ionized.
The diffusible form is performing physiological functions.
1-Maintain membrane permeability.
2-Activation of enzymatic process involved in muscular
contraction.
3-Release of neurohormones and neuropeptides.
4-Excitability of neuromuscular system.
5-Involvement in clotting mechanism.
6- It acts as hydroxypeptide in the bone, responsible for the
strength of the bone.
The phosphate level is 3-4 mg/dl as follows:
85% in bone, 14% intracellular, 1% extracellular fluid.
The amount of phosphate in the blood affects the level of
calcium, calcium and phosphate in the body react in
opposite way, so whenever we have hypercalcemia we
have hypophosphatemia.
Parathyroid hormone acts on calcium and phosphate
through:
1- Parathyroid Hormone Increases Calcium and
Phosphate Absorption from the Bone.
2-Parathyroid Hormone Increases Intestinal Absorption
of Calcium and Phosphate:
3-Parathyroid Hormone Decreases Calcium Excretion
and Increases Phosphate Excretion by the Kidneys
It increases phosphate excretion in the urine and decreases
renal tubular reabsorption of phosphate and increase
reabsorption of calcium.
Clinical conditions:
1-Hypofunction of the parathyroid hormone
(hypoparathyroidism):
This leads to decrease in calcium concentration in the
blood → abnormal function of the neuromuscular
system → hyperexcitibilty.
In children may lead to laryangeal spasm →asphyxia
and death.
⚫ Hypoparathyrodism may be mild and we have twitching of the
facial muscles elicited by mild stimuli (chvostek' s sign) .
⚫ By occlusion of blood flow to the hand like by a
sphygmomanometer, there will be flexion of the wrist and
thumb, extension of the fingers (trousseau's sign).
(trousseau's sign).
2-Hyperparathyroidism:
The cause may be:
Primary: tumor in the gland
Secondary: vitamin D deficiency or chronic renal
failure.
Excessive mobilization of calcium and phosphate from
the bone. If x ray is taken to the bone we will see a
cyst filled with fibrous tissue (osteitis fibrosa cystica).
Other complication is renal stones, CNS excitability,
constipation, weakness and hypophosphatemia.
Osteitisfibrosacystica
Aging and bone loss
● Peak bone density is achieved in the third or fourth decade,
thereafter, bone density declines throughout life.
● Bone loss occurs in both men and women, however, bone loss
accelerates in women after menopause. Osteoporosis resulting
from the bone loss increase the risk of fractures.
● The primary factor responsible for postmenopausal bone loss is
estrogen deficiency, estrogen decrease bone resorption, in part by
antagonizing the bone resorptive action of PTH, it also has been
suggested that estrogen regulates calcium handling by the
intestine and kidney and production of PTH, 1,25
dihydroxyvitamin D3 and calcitonin.
Estrogen replacement is an effective treatment for
postmenopausal loss, particularly if used in conjunction with
regular exercise, calcium supplements and perhaps
calcitonin.
THANK YOU
Year 2
Practical: Endocrine System Module
Laboratory Diagnosis of Bacterial Infection

in Diabetic Foot Ulcer
By
Assist. Prof. Dr. Humam Kasem Hussein
Diagnostic tests are indicated when the cause of a skin lesion or
disease is not obvious from history and physical examination
alone. These include:
1. Biopsy.
2. Scrapings.
3. Tzanck Testing.
4. Nail clipping.
5. Wound swabs.
Skin Biopsy
There are several types of skin biopsy:
∙ Punch biopsy
∙ Shave biopsy
∙ Wedge excision biopsy
In a punch biopsy, a tubular punch (diameter usually 4 mm) is

inserted into deep dermal or subcutaneous tissue to obtain a
specimen, which is snipped off at its base.
Shaving with a scalpel or razor blade may be done for more
superficial lesions. Bleeding is controlled by electrodessications.
Wedge excision of skin using a scalpel can be done for larger or
deeper biopsies, which are closed by sutures.
Skin Scrapings
Skin scrapings help diagnose fungal infections.

For fungal infection, scale is taken from the border of the lesion and
placed onto a microscope slide.
Then a drop of 10 to 20% potassium hydroxide (KOH) is added,

between five and fifteen minutes, in order to dissolve skin cells.
Hyphae, budding yeast, or both confirm the diagnosis of tinea or
candidiasis.
Tzanck Testing
Tzanck testing can be used to diagnose viral disease, such as herpes

simplex and herpes zoster, and is done when active, intact vesicles are
present.
An intact blister is the preferred lesion for examination. The blister

roof is removed with a sharp blade, and the base of the vesicle is
scraped with a scalpel blade. The scrapings are transferred to a slide
and stained with Wright stain or Giemsa stain. Multinucleated giant
cells are a sign of herpes infection.
Nail clipping
Keratinized portion nail, is also a possible site for residing of fungus,
should be sampled as nail clipping. Nail clipping is taken from any of
the discolored or thickened part of the nail. Following steps should be
considered during specimen collection:
Wound swabs.
1. Where possible specimens should be collected before starting any

antimicrobial therapy.
2. Use aseptic technique.
3. If the area to be swabbed is dry, moisten the swab with sterile water or
saline.
4. Sample the wound by moving the swab across the wound surface in a
zigzag motion, at the same time as rotating it between the fingers.
Immediately placed into the transport medium.
5. Label the sample.
6. If a large quantity of pus is present, aspirate into a syringe and send to
the laboratory in a sterile container.
Skin or Nail Culture
A skin or nail culture is a laboratory test to look for and identify germs
that cause problems with the skin or nails.
Mold and yeast are two types of fungus. Both can cause allergic
reactions. Fungal spores can circulate in the air and may cause allergic
rhinitis when inhaled.
How the Test is Performed
A sample of skin may need to be taken. Before the skin sample is

removed, you will likely receive a shot (injection) of numbing medicine to
prevent pain.
A small sample of a fingernail or toenail may be taken. The sample is sent

to a lab. There, it is placed in a special dish (culture). It is then watched to
see if bacteria, viruses, or fungi grow. It may take up to 3 weeks to get
results of a nail culture.
Further tests can be done to identify the specific germ that is causing
problem. This can help to provider determine the best treatment.
Why the Test is Performed
This test may be done to diagnose the cause of:
• A bacteria or fungus infection of the skin, finger, or toenail.
• A skin rash or sore that appears to be infected.
• A skin ulcer that is not healing.
*Normal Results
A normal result means no disease-causing germs are seen in the culture.
Some germs normally live on the skin. These are not a sign of infection
and are considered a normal finding.
*Abnormal Results
An abnormal result means bacteria, fungus, or virus is present. This may

be a sign of infection.
Common skin infections caused by bacteria include:
• Impetigo.
• Diabetes foot ulcers.
Common skin infections caused by fungus include:
• Athlete's foot.
• Nail infections.
• Ringworm.
Risks
Risks include slight bleeding or infection in the area where the skin
sample was removed.
Biochemical Tests of Fungi
Biochemical Tests of Bacteria
The test kit enables the following tests:
1. ONPG: test for β-galactosidase enzyme by hydrolysis of the substrate

o-nitrophenyl-b-D-galactopyranoside.
2. ADH: decarboxylation of the amino acid arginine by arginine dihydrolase.
3. LDC: decarboxylation of the amino acid lysine by lysine decarboxylase.
4. ODC: decarboxylation of the amino acid ornithine by ornithine decarboxylase.
5. CIT: utilization of citrate as only carbon source.
6. H2S: production of hydrogen sulfide.
7. URE: test for the enzyme urease.
8. TDA (Tryptophan deaminase): detection of the enzyme tryptophan deaminase:
Reagent- Ferric Chloride.
9. IND: Indole Test-production of indole from tryptophan by the enzyme
tryptophanase . Reagent- Indole is detected by addition of Kovac’s reagent.
10. VP: the Voges-Proskauer test for the detection of acetoin (acetyl methylcarbinol)
produced by fermentation of glucose by bacteria utilizing the butylene glycol
pathway.
11. GEL: test for the production of the enzyme gelatinase which liquefies gelatin.
12. GLU: fermentation of glucose (hexose sugar).
13. MAN: fermentation of mannose (hexose sugar).
14. INO: fermentation of inositol (cyclic polyalcohol).
15. SOR: fermentation of sorbitol (alcohol sugar).
16. RHA: fermentation of rhamnose (methyl pentose sugar).
17. SAC: fermentation of sucrose (disaccharide).
18. MEL: fermentation of melibiose (disaccharide).
19. AMY: fermentation of amygdalin (glycoside).
20. ARA: fermentation of arabinose (pentose sugar).
Thank You for Listening
Endocrine lab.
Part 1
Hashimoto thyroiditis
The specimen photographs shows a

diffusely enlarged thyroid with
ill-defined whitish nodular areas
secondary to fibrosis.
The patient presents with myxedema

from hypothyroidism, and the serum
TSH is elevated. There is an increased
risk for subsequent development of
B-cell non-Hodgkin lymphoma.
Hashimoto thyroiditis
Note chronic inflammation characterized

by infiltrates of CD8+ and CD4+ T
lymphocytes forming much of the
lymphoid infiltrates, including a lymphoid
follicle seen here. The remaining thyroid
follicles become atrophic, and the
epithelial cells undergo Hürthle cell
change, with abundant pink cytoplasm.
there can be painless enlargement

of the thyroid. Laboratory findings include
antithyroglobulin and antimicrosomal
(thyroid peroxidase) antibodies detected in
serum.
Graves disease
At low magnification, this thyroid

hyperplasia is characterized by many
papillary infoldings within follicles.
Patients may present with fever,

diarrhea, heat intolerance, tachycardia,
weight loss, tremor, and nervousness
(thyrotoxicosis). Exophthalmos and
infiltrative dermopathy (pretibial
myxedema) are characteristic of Graves
disease.
Graves disease
At higher magnification, the tall
columnar appearance of the
hyperplastic follicular epithelial
cells is evident. Small, clear
vacuoles appear next to each cell,
indicating scalloping
of colloid.
The feedback on the pituitary

decreases the serum TSH, whereas
the serum T4 is high.
Thyroid-stimulating
immunoglobulin
may be present.
Multinodular goiter
Multinodular goiters are often

asymmetric, although both
lobes become enlarged.
Most patients remain euthyroid,

bothered only by the mass
effect. Larger masses may be
removed because of fixed airway
obstruction, dysphagia, or
superior vena cava syndrome.
Colloid Goiter
Shown here from a goiter are

enlarged thyroid follicles lined
with inactive, flattened
epithelial cells and filled with
abundant stored colloid.
The endemic form is secondary

to dietary iodine deficiency. In
the sporadic form of the
disease, the etiology may be
unknown.
Thyroid follicular adenoma
This cross-section through a

resected lobe of thyroid gland
reveals an encapsulated round
neoplasm with a uniform brown
appearance, surrounded by a rim
of normal thyroid.
A follicular adenoma forms a

palpably firm painless nodule and
is more common in middle-aged
women.
Thyroid follicular adenoma
This follicular adenoma is composed of

recognizable follicles that are small
and packed closely, whereas the
adjacent normal thyroid has compressed
and flattened follicles at the lower right.
There is no invasion visible here.
Most follicular adenomas do not

function, but a rare hyperfunctioning
adenoma, or toxic adenoma, can be a
cause of hyperthyroidism. Some toxic
adenomas have a G protein– coupled
receptor mutation (GNAS1).
Follicular carcinoma
This follicular carcinoma is composed of

small, closely packed recognizable
follicles. There is invasion seen here into
venous spaces at the left.
These carcinomas account for 5% to 15%

of thyroid cancers, and more in persons
with iodine deficiency.
Follicular carcinoma
Vascular invasion is evidence of

malignancy in a follicular carcinoma.
Follicular carcinoma is the second

most common thyroid malignancy. It tends
to metastasizes hematogenously to
locations such as lung or liver.
Papillary carcinoma
this cross-section through an excised

thyroid gland shows a large mass
which is cystic and contains papillary
excrescences. The other small lesion
is also a papillary carcinoma.
These neoplasms may be multifocal,

as seen here, because of the
propensity to invade lymphatics
within thyroid, and metastases to
adjacent lymph nodes are common.
Papillary carcinoma constitutes up to
85% of all thyroid carcinomas.
Papillary carcinoma
This carcinoma has papillae with thin

fibrovascular cores that lined by cells with
nuclei that appear clear (empty) on H&E
staining after formalin fixation. Another
microscopic feature is the round
laminated concretion, a psammoma body.
Papillary carcinomas are indolent tumors

that have a long survival, even with
metastases.
Anaplastic carcinoma
Shown here are highly
pleomorphic spindle cells
infiltrating into adjacent skeletal
muscle on the right. Both
epithelioid and spindle cells are
seen.
Anaplastic carcinoma is the least

common thyroid malignancy and
the most aggressive. It is rapidly
growing and invasive to involve
adjacent esophagus with
dysphagia or trachea with
dyspnea.
Medullary carcinoma
The tumor here composed of sheet of

uniform small cells are with adjacent
normal thyroid visible at the lower left.
There is pink hyaline material with the
appearance of amyloid.
These neoplasms derived from thyroid C

cells which are responsible for secretion
of calcitonin.
Endocrine lab.
Part 2
Pituitary adenoma
This large pituitary adenoma (a

macroadenoma) impinges on
the ventricular system as shown
here.
There is elevation in intracranial

pressure producing symptoms of
headache, nausea, and vomiting.
Pituitary adenoma
Note the solid monotonous

pattern of uniform rounded cells
and capillary channels.
The most common pituitary

adenoma (30% of cases) in adults
secretes prolactin, whereas
20% are null-cell adenomas that
do not secrete a hormone but can
exert a mass effect.
Comparison of atrophic, normal,
and hyperplastic adrenal glands
The topmost pair of adrenal glands
are atrophic, characteristic of either
idiopathic Addison disease or
long-term use of corticosteroids.
The normal adrenals at the center

have a well-defined rim of golden
cortex and a center of reddish
medulla.
The hyperplastic pair of adrenals at

the bottom are typical of increased
ACTH secretion either from a
neoplasm, such as a small cell lung
carcinoma, which results in Cushing
syndrome, or from a pituitary
adenoma, resulting in Cushing disease.
Waterhouse-Friderichsen syndrome
These adrenals have a dark-red to black

color from extensive hemorrhage.
This condition is a consequence of

endotoxin release from Neisseria
meningitidis organisms causing septicemia
and disseminated intravascular
coagulopathy.
Adrenal adenoma
This well - circumscribed, uniformly

yellow-tan mass is adrenocortical
adenoma.
This patient has hypertension,

hypokalemia and high serum
aldosterone. These findings are
consistent with an
aldosterone-secreting adenoma (Conn
syndrome).
Adrenocortical Adenoma
Microscopically, the tumor cells are

lightly eosinophilic and are filled with
small lipid vacuoles. They are often
organized in nests or cords.
Adrenal cortical adenomas represent

the most common primary adrenal
lesion. They may be functioning
(producing aldosterone, cortisol, or sex
hormones) or nonfunctioning.
Adrenocortical Carcinoma
This tumor is large and exhibits areas of

hemorrhage and necrosis. It has destroyed
the upper pole of the kidney.
Adrenal cortical carcinomas are relatively

uncommon. They have a bimodal age
distribution, with peaks in the first and fifth
decades of life.
Adrenocortical carcinoma
This section shows adrenal tumor

with venous invasion, a feature
consistent with adrenocortical
carcinoma.
Adrenocortical carcinomas
often are hormonally functional
and can lead to Cushing syndrome
from glucocorticoid secretion, or
there can be sex steroid hormone
secretion with clinical features of
masculinization in a woman or
feminization in a man.
Pheochromocytoma
pheochromocytomas are often circumscribed, soft, and

yellowish white to reddish brown. The larger tumors
often have areas of necrosis, hemorrhage, and cyst
formation.
The complete symptomatic triad of sweating attacks,

tachycardia, and headaches clinically suggests the
presence of a pheochromocytoma, but is seen in less
than one-fourth of patients. Hypertensive episodes are
usually intermittent, but at times may be sustained.
Pheochromocytoma
this adrenal medullary neoplasm

composed of large polygonal to spindle
chromaffin cells. The cells are arranged
in nests with adjacent smaller
sustentacular cells, surrounded by
abundant intervening capillaries.
This patient had episodic hypertension

from secretion of catecholamines.
Pheochromocytomas follow the 10%
rule—10% are bilateral, malignant,
nonhypertensive, or extraadrenal in
location.
Fat necrosis in acute pancreatitis
Yellow-tan foci of fat necrosis are visible

throughout the pancreas. This is a case of
mild acute pancreatitis.
Enzymatic release from the exocrine

pancreas leads to autodestruction. Trypsin
activation triggers a cascade of additional
proenzyme activation, including proelastase
and prophospholipase, which disintegrate
adipocytes and pancreatic parenchyma.
Chronic pancreatitis
There are scattered chronic inflammatory

cells in a collagenous stroma with
absence of acini, but a few remaining
islets of
Langerhans.
Chronic alcohol abuse is a common cause

of this condition. Depending on the
amount of remaining functional
parenchyma, pancreatic insufficiency with
malabsorption and steatorrhea may occur,
and diabetes mellitus may eventually
occur from loss of islets of Langerhans.
Pancreatic carcinoma
A poorly defined, firm grayish mass

obliterates the normal pancreatic
architecture.
Pancreatic cancer is the fourth most

frequent cause of cancer death in the
United States. Few cases are
diagnosed early, so the typical
prognosis is poor, with a 5-year
survival rate of less than 5%.
Pancreatic carcinoma
This pancreatic malignancy is

moderately differentiated, showing
some irregular gland formation
with gland luminal mucin
accumulation. These neoplasms often
have significant desmoplasia.
They infiltrate locally and are difficult to

resect because they are invariably
diagnosed at a late stage. Perineural
invasion is common and accounts for
the constant pain typical of cancer.
Parathyroid adenoma
a round brown to yellowish mass with

homogeneous appearance interrupted
by foci of fresh hemorrhage or cystic
changes.
Parathyroid adenomas occur in women

and men in a ratio of 3 : 1. They can
develop at almost any age, but most
occur in patients in the fourth decade.
Parathyroid adenoma
Section show encapsulated highly cellular

tumor composed mainly of chief cells with
adjacent rim of normal parathyroid at the
upper right.
Adenoma accounts for nearly 85% to 95% of

all cases of primary hyperparathyroidism. In
addition to elevated serum ionized calcium
with hypophosphatemia, a PTH assay reveals
a high-normal to elevated level of PTH.
Parathyroid carcinoma
Section of parathyroid tumor invading

the blood vessel. The nests of
neoplastic cells are not very
pleomorphic.
The high serum PTH levels with

parathyroid carcinomas, adenomas,
and hyperplasia can increase bone
osteoclast activity and bone remodeling
to produce osteitis fibrosa cystica and
brown tumor of bone

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FIGURE 20-1 Copyright © McGraw-Hill Companies

Figure 20–1 Locations of the major

Copyright © McGraw-Hill Companies

The gland occupies a fossa of the sphenoid

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The infundibular stalk (IS) and pars nervosa

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Role of growth hormone

Factors affection on growth

Type of growth hormone blood test

 Is a peptide hormone that stimulates growth, cell

reproduction, and cell regeneration in humans. Also

known as somatotropin, because it synthesized and

secreted by the somatotrophs of the anterior pituitary

growth high Amino

affecting of  Increase free fatty acid

hormone:  Excess cortisol

 stop taking certain prescription medications a few days before the

test, if they might interfere with the test results

 It’s uncommon for people to have GH levels outside the typical

 Growth hormone may not offer enough information to help in

 A GH suppression test helps in

 A GH stimulation test helps in

ass .lec :suhad taha mohammed

The Fed State ( Absorptive State);

The Fasting State;

• Evaluate glucose tolerance in subjects with equivocal

3- Unexplained episodes of hyperglycemia

4- history of recurrent infections

5- in women, history of delivery of large infants, stillbirth, neonatal death,

6- transitory glycosuria or hyperglycemia during pregnancy, surgery, trauma,

1- Normal diet & carbohydrate intake (150 g/dl) for 3 days.

2- Overnight fast ( 10-16 hours ).

3-Resting for 30 min (seated) prior to test .

4- No smoking during test .

5- No drugs known to interfere with test , e.g. steroids

 Glucose load : adult 75g of glucose dissolved in 250 ml of water,

 Must be performed in morning and to remain seated during test .

 Glucose load given in flavored water and consumed within 5 min.

 Blood samples : basal ( pre-glucose) , 60min, 90min,120min.

Normal Blood Glucose :

Basal : < 5.6 mmol/L ( 100 mg/dl)

Intermediate sample : < 11.1 mmol/l ( 200 mg/dl)

2 hr sample : < 7.8 mmol/l ( 140 mg/dl)

HbA1c : 5-5.5 % ( B.G=100-125mg/dl)

 persistent fasting hyperglycemia > 140 mg/dl

Persistent fasting normal glucose

Patients with overt diabetes mellitus

Glucometer Enzymatic estimation

1- fast 1- fast ( not like glucometer)

Laboratory Diagnosis of Bacterial Infection

In a punch biopsy, a tubular punch (diameter usually 4 mm) is

Skin scrapings help diagnose fungal infections.

Then a drop of 10 to 20% potassium hydroxide (KOH) is added,