Physio Ii Endocrin

Front 1

What is contained in the lobule of the thyroid gland?

Back 1

What is contained in the lobule of the thyroid gland?

- thyroid follicles, parafollicular cells, dense networks of sinusoidal capillaries.

Front 2

ADD ADDITIONAL QUESTIONS for EXERCISES

Back 2

ADD ADDITIONAL QUESTIONS 4 EXERCISES

Front 3

What is the structure of normal thyroid follicles?

Back 3

Filled with gel-like substance (colloid) and lined by cuboidal follicular cells.

- colloid is the secretory product of the follicular cell (extracellular storage!).

Front 4

Two types of hormones (in terms of where originate):

Back 4

1. Tissue hormones - produced by individual endocrine cells; not in large glands
2. Glandular hormones - e.g. cytokines

Front 5

How do thyroid cells appear at rest?

Back 5

How do thyroid cells appear at rest?

epithelium appears low cuboidal very dense colloid.

- colloid is the secretory product of the follicular cell (extracellular storage!).

Front 6

Which organs/tissues produce the most hormones?

Back 6

1. CNS (brain)
2. GI

Front 7

How do thyroid cells appear when stimulated?

What is released?

Back 7

Epithelium becomes cuboidal or low columnar and colloid is dissolved. Secretes thyroid hormones thyroxin

Front 8

What are endocrines or hormones? functions?

Back 8

Produced in a gland and secreted directly into circulation w/o ducts

chemical messangers, regulators of homeostasis and metabolic pathways, etc.

Front 9

Parafollicular cells of the thyroid gland secrete what? function?

Back 9

occur as single cells in the basal lamina of the follicle. Cells secrete Calcitonin (lowers blood calcium levels by suppressing bone resorption)

FYI: bone resorption = bone broken down and Ca+ released

Front 10

autocrine hormones

Back 10

affect cell of production

Front 11

what is function of calcitonin?

where secreted from?

Back 11

Parafollicular cells of the THYROID secrete calcitonin which LOWERS blood calcium level by suppressing bone resorption

-so counteracts break down of bone by PTH
(remember PTH = incr blood calcium, incr. bone resorption/remodeling)

~when think of calcitonin, think of making bone

Front 12

Are endocrine hormones present in high concentrations?

Back 12

No, always in extremely low concentration (pg - ug/ ml), which why they are difficult to detect.

Front 13

major integrating link between the
nervous and the endocrine
systems.

Back 13

HYPOTHALAMUS

Front 14

Types of hormones in terms of chemical structure?

Back 14

1. peptide hormones (like insulin)
2. steroid hormones (e.g. vit.D)
3. amines (e.g. dopamine, epinephrine)
4. eicosanoids (e.g. prostaglandins)

Front 15

receives input from various other CNS regions such as ? (6)

Back 15

input from -> e.g. thalamus, limbic system, cortex, RAS, and sensory signals from viscera and the eye.

Front 16

which hormone type is most common?

Back 16

peptide hormones

Front 17

is involved in emotions, stress, fear, control of hunger, thirst, sexual behaviour

Back 17

HYPOTHALAMUS

Front 18

what hormones are hydrophilic?

Back 18

peptide hormones

Front 19

largely controls homeostasis, e.g. osmolality, body temperature,
and controls the autonomic nervous system.

Back 19

HYPOTHALAMUS

Front 20

which hormones are lipophilic?

Back 20

steroid hormones

Front 21

is a “master” endocrine gland.

Back 21

The Hypothalamus is a “master” endocrine gland. Its many neuroendocrines influence other CNS areas as well as various peripheral endocrine glands via the Pituitary Gland.

(in past learned pituitary gland is master but this prof says otherwise)

Front 22

What is term Dr. Zeigler uses for parts of hormone precursor which are cleaved off during protein/peptide synthesis? Are these cleaved off pieces ever active on their own?

Back 22

pre-pro sequences; can be active compounds also!

Front 23

The Hypothalamus is connected with the PITUITARY GLAND via the

Back 23

hypophyseal stalk.

Front 24

What are differences between nervous and endocrine system?

Back 24

endocrine system is slower to react, much slower, because it relies on chemical messengers

also endocrine system responds to INTERNAL stimuli; while nervous system responds to external ones.

Front 25

PITUITARY GLAND consists of what 2 parts?

Back 25

1. ANTERIOR pituitary
2. POSTERIOR pituitary

Front 26

How long (approx.) does it take protein hormone to be produced?

Back 26

~45-60 minutes

Front 27

How long does it take for protein hormone to be released?

How are hormones released so quickly, when protein synthesis takes so long?

Back 27

2-5 minutes

* b/c after prepro seq. cleaved off, hormone stored in secretory granule or vesicle where can secrete immediately upon stimulation via exocytosis

* also hydrophilic so dissolves easily in plasma

Front 28

neurohypophysis extension of the hypothalamus is which part of pit.gland?

What tissues/structures does it have?

Back 28

POSTERIOR pituitary

consists of nervous tissue stores and releases the 2 hypothalamic hormones produced in the Nucleus supraopticus and Nucleus paraventricularis:

Front 29

What type of hormones made in adrenal cortex:
A. peptide hormones?
B. steroid hormones?
C. amines?
D. eicosanoids?

Back 29

* hormones made in adrenal cortex are steroid h's e.g. mineralocorticoids (aldosterone) and glucocorticoids (cortisol).
* also a secondary site of androgen synthesis.

Front 30

Nucleus supraopticus and Nucleus paraventricularis release what 2 hypothalamic hormones ??

Back 30

the 2 hypothalamic hormones produced in the
Nucleus supraopticus and Nucleus paraventricularis:
ADH and Oxytocin

Front 31

True or false: Protein hormones generally have longer half-life then steroids.

Back 31

False, b/c proteases are found everywhere in tissues, esp. concentrated in blood flow of liver&kidney.

Front 32

formed from Rathke’s pouch = glandular epithelium
produces and secretes hormones under hypothalamic control

Back 32

ANTERIOR pituitary = adenohypophysis

Front 33

Steroid Hormones are derived
from ? In one sentence, describe how made.

Back 33

Steroid Hormones are derived
from Cholesterol

* stimulus activates enzymes -> starts a series of 3 conversions to produce steroid hormones

Front 34

also called vasopressin

Back 34

ADH

Front 35

How are steroid transported in plasma?
What % of bound?

Back 35

* not hydrophilic, are lipophilic, so need to attach to carrier (like albumin) in plasma

1-10% are in free form=active; rest is bound=inactive (acts as a hormone reserve in plasma)

Front 36

Glucocorticoid

Back 36

any hormone of adrenal cortex that affects carb,fat, and/or protein metabolism; chiefly cortisol and corticosterone

Front 37

Why is half life of steroids extended (last longer than peptide hormones)?

Back 37

* binding to albumin helps protect steroids from degradation and quick destruction in liver (longer half-lives -> hours to days)
* also makes "reservoir" in circulation

Front 38

ADH and Oxytocin synthesized where?

Back 38

hypothalmus

Front 39

How are most steroids metabolized?

Back 39

glucuronidation in liver

Front 40

ADH and Oxytocin stored and RELEASED from where?

Back 40

Most of it is stored in the posterior pituitary (neurohypophysis) to be released into the bloodstream

Front 41

How tissues get cholesterol?
Flows around body in what form?

Back 41

* from diet (although can be converted from Acetyl CoA)
* TriG and cholesterol all condensed into VLDL
* LPL off loads cholesterol in tissues making steroids

Front 42

Does hypothalmus also regulate ANTERIOR pituitary = adenohypophysis?

Back 42

Yes

Front 43

Receptor location for hydrophilic hormones?
Describe these receptors; are they complex?

Back 43

* Cell membrane (cannot diffuse through); so receptor on surface of membrane
* most of these receptors are very large and complex w/external binding portion and internal transducing portion

Front 44

Hormones produced in hypoth. go to AP?

Back 44

Releasing Hormones (RH) and/or Inhibiting Hormones (IH)

RHs / IHs reach the Anterior Pituitary gland
(via – hypophyseal portal system)

Front 45

Receptor location for lipophilic hormones:

Back 45

* Cytoplasm or Nucleus; receptor inside target cell b/c lipophilic hormones have no problem entering cell to bind to it

Front 46

RHs /IHs stimulate/inhibit the production and release of hormones from the ?

What are these type of hormones known as?

Back 46

from the anterior
pituitary gland into circulation = Tropic Hormones (mostly)

Tropic Hormones

Front 47

All hormones affect their target tissues by forming first a ________ , which alters the activity of their target cells.

Back 47

HORMONE - RECEPTOR complex

Front 48

These tropic hormones in turn stimulate ?

Back 48

These tropic hormones in turn stimulate a peripheral endocrine gland to produce /
release its own hormones.

Front 49

We know number of particular receptor can increase and decrease; which is more common: up regulation or down regulation?

Back 49

down regulation

Front 50

Where are some stimulating/releasing hormones that the hypoth. makes?

Hint: gd cn G Tt P

Back 50

Gnrh
Crh
GHrh
Trh
Prh

Front 51

What is example of up regulation of receptor number?

Back 51

Example: Aldosterone (steroid) initiates synthesis of enzyme ATPase in its target cells -> stimulates Na/K pumps

Front 52

GnRH = ?

GHRH = ?

Back 52

GnRH = Gonadotropin R.H.

GHRH = Growth Hormone Rel. Hormone

Front 53

True or false: Antagonist does opposite action of hormone.

Back 53

False, antagonist simply blocks binding of hormone to receptor.

Front 54

Gonadotropin Stimulates?
Which in term stumulates?

Back 54

Gonadotropin RH. stimulates A.P. to produce FSH and LH!!!

..gonads to make sex hormones

Front 55

Lipophilic hormones induce protein synthesis, w/newly formed proteins being mostly enzymes, which now stimulate or inhibit certain metabolic pathways = ?

Back 55

= METABOLIC EFFECT

Front 56

Another name for growth hormone

Back 56

Growth h. = Somatotropin
= Somatotropic Hormone = ST(H)

Front 57

In following example: which represents the secondary messanger?

Back 57

cAMP

Note: The first messenger (= hormone) remains outside of its target cell b/c cannot enter, but transmits its message via cAMP = second messenger

Front 58

Obviously GHRH stimulates AP to GH..but what peripheral gland does growth hormone stimulate?

Back 58

Liver (and direct effects) to make Somatomedins,
which works on multiple tissues

Front 59

phosphorylation is usually stimulatory or inhibitory event?

Back 59

stimulatory

Front 60

Corticotropin = Adreno-corticotropic hormone = ACTH
stimulates what organ? to make what?

Back 60

adrenal cortex to synthesize Glucocorticoids (aka cortisol)

Front 61

this an example of _______: effect of plasma glucose levels on
glucagon secretion

Back 61

NEGATIVE FEEDBACK LOOP

Front 62

Targets of ACTH?

Back 62

many targets

Front 63

What is stimulated (to start) if glycogen stores are full?

Back 63

lipogenesis, creation of fat

Front 64

What is TRH?

Back 64

TRH = Thyrotropin Releasing Hormone

Front 65

What cells are not affected by insulin? (examples)

Back 65

glucose independent cells

neurons, retina, lens, blood
cells, pancreatic B cells, kidney,
GI mucosa, placenta

Front 66

Where does Thyrotropin come from?

Back 66

ant. pituitary

Front 67

?% of body cells contain insulin
receptors

Back 67

80% of body cells contain insulin
receptors = insulin-sensitive tissues

Front 68

Where does TSH come from?

Back 68

Ant.Pit.Gland

Thyroid stimulating hormone and thyrotropin are same thing

Front 69

Where is insulin receptor located?
what type of mechanism?

Back 69

* its a protein, so on cell membrane
- called a tyrosine kinase
* 2nd messanger mechanism (these are usually G-coupled) but not sure
* insulin binds to external part alpha subunit, and stimulates beta subunits

Front 70

TSH stimulates thyroid to stimulate what?

Back 70

T3
T4

Front 71

After insulin – receptor binding (= in
insulin-sensitive tissues): what happens?

Back 71

Beta parts of receptor become the
activated tyrosine kinase (= second messenger)
-> leads phosphorylation of various enzymes

Front 72

Where are some INHIBITING hormones that the HYPOTHALMUS. makes?

Back 72

GHih (counteracts GHrh)
Pih (counteracts Prh)

Front 73

What is stimulated by insulin binding?

Back 73

* glucose uptake by GLUTs
* fat uptake and storage in fat tissue via lipoprotein lipase enzyme - extracts fat from VLDL or chylomicrons
* inhibits hormone specific lipase
* inhibits proteases / proteolytic enz. / protein brk.down
* stim. protein temporary storage and synthesis (organ function, growth, clotting factors & albumin in liver)

Front 74

Prostaglandins made in the ?

What is target organ?

Back 74

Ant.Pituitary gland

direct effects (e.g. mammary gland)

Front 75

What happens without w/o insulin, but with circulating chylomicrons?

Back 75

LDL not active, full of chylomicrons

Front 76

Which part (inner OR outer layer) makes the mineralcorticoids?

Which part (inner OR outer layer) makes the glucocorticoids?

Back 76

Zona glomerulosa (outer portion of AC) makes the mineralcorticoids!

Zona fasciculata (middle layer) makes the glucocorticoids!

Front 77

Glucagon opposes Insulin effects on _____ in the LIVER


Glucagon ____ blood glucose level

Back 77

Glucagon opposes Insulin effects on carbohydrate metabolism (which were storage, breakdown)

Glucagon INCREASES blood glucose level

Front 78

Low levels of calcium stimulates ?

Back 78

Low levels of calcium stimulates release of PTH from chief cells of parathyroid gland. In addition to its effects on kidney and intestine, PTH also increases activity of osteoclasts to release calcium from bone, by stim. bone resorption.

Front 79

How does glucagon increase blood glucose levels?
(what 3 processes?)

Back 79

Stimulation of hepatic glycogenolysis -> blood glucose levels can double within minutes

Stimulation of hepatic gluconeogenesis (via increased amino acid uptake)

Stimulation of lipolysis in fat tissue in very high concentrations

Front 80

What is primary mineralcorticoids?

Back 80

Aldosterone (makes up 90% of mineralcorticoids) secreted from outer layer (Z.G.) of A.C.

AMC

Front 81

What might stop glucagon from secreting?

What cells are involved?

Back 81

high blood glucose, like after high carb. meal

(pancreatic alpha cells are insulin-sensitive: high plasma glc -> high insulin ->
glc uptake into alpha cells -> glucagon secretion is inhibited!)

Front 82

What is primary Glucocorticoids made by adr. cortex?

Back 82

Cortisol (95% glucocorticoids secreted in mammals)

GC

Front 83

Main signal for glucagon release

Back 83

HYPOGLYCEMIA -> stimulates glucagon secretion

Front 84

What 2 components are required to make thyroid hormone?

Back 84

- amino acid tyrosine and iodine

Front 85

high plasma amino acid levels ___ glucagon secretion

Back 85

also stimulate glucagon secretion

but only when blood glc levels are low (A.A. are then channeled into gluconeogenesis)

Front 86

How does Iodide (I-) gets into thyroid cell ?

Where does it go? in what form?

Back 86

Iodide uptake into thyroid cell via active pump btw. thyrocyte and blood vessel
Enters colloid space in follicle, Iodide oxid. by perixidase into iodine

Front 87

= IDDM

Back 87

Type I DM
circulating insulin levels are low

Front 88

TGB? made where?

primary component of ____?

Back 88

thyoglobulin, made in follicular cells, is glycoprotein containing lots of tyrosine AA's

it is primary component of colloid

Front 89

What causes Type I DM?

Back 89

Causes: islet cell destruction b/o pancreatitis, senile degeneration, autoimmune disease -> hyperglycemia (b/c low insulin; cells can't take up glc.)

Front 90

difference between T1 and T2

where does all this happen?

Back 90

(iodine joins the TGB)

T1 contain only 1 iodine; T2 contains 2 iodines
(still in colloid)

Front 91

Definition of Diabetes Mellitus:

Back 91

absolute or relative lack of insulin leading to impaired
carbohydrate, lipid and protein metabolism

Front 92

what happens when form T3 or T4?

Which is find in higher conc.in plasma?

Back 92

T1&T2 are mere primary peptide chains - condense, fold over and form secondary structures, couple with eachother
(still in colloid)
T4 makes of 93% in thyroid hormone in plasma?

Front 93

Non-insulin dependent DM =

Back 93

Type II DM

Front 94

storage form of thyroid hormone

active form of thyroid hormone? what does it do?

Back 94

T4

T3 (active hormone; T4 is converted to T3 after enters target cell)

Front 95

Causes of Type II DM?

Insulin resistance?

Back 95

* something goes wrong with insulin receptors, not binding insulin right, or not enough of them
* insulin present but not responding to it; known as insulin resistance aka "relative" lack of insulin

Front 96

Thyroid hormones are controlled via the ____?

Back 96

Hypothalamic–Pituitary–Thyroid Axis

Front 97

%2 of ___ suffer from diabetes m.

Back 97

%2 of burmese cats

Front 98

Hypothalamic TRH release is
- stimulated by _?
- inhibited by _?

Back 98

Hypothalamic TRH release is
- stimulated by COLD
- inhibited by stress (sympathetic n.s.)

Front 99

Are beta cells of pancreas intact in type 2 diabetes?

Back 99

yes at first, insulin still being made in excess as way to compensate blas
eventually the beta cells become "exhausted" and type I diabetes develop

Front 100

TRH stimulates anterior pituitary to
synthesize and secrete __

Back 100

TSH

Front 101

Secondary type diabetes or type 3 diabetes

Back 101

high levels of other hormones like cortisol
high glucagon

Front 102

T3 or T4 is lipophilic?

transported by?

Back 102

yes

Binding of lipophylic T4 & T3 to plasma proteins
(~99%), e.g. thyroxin-binding protein (& albumin);
half-life of T4 in dogs: 12-14 hours
half-life of T4 in man: ~6 days

Front 103

Which type of diabetes has normal insulin levels?

Back 103

Type II DM

Front 104

TSH stimulates thyroid gland to
synthesize and secrete thyroid
hormones through: what mechanisms?

Back 104

- stimulation of iodide pump
- stimulation of iodination of tyrosine
- stimulation of TGB proteolysis
- stimulation of growth of thyroid cells
(can lead to gland enlargement)

Front 105

Which hormone responds to high osmoregularity in plasma? causes what?

Back 105

ADH, causes incr. in thirst

Front 106

Increased levels of ___ inhibit further release of
TSH -> by decreasing_____?

Back 106

Increased levels of circulating thyroid hormones inhibit further release of
TSH (by decreasing TRH receptor no.)

Front 107

two initial clincal signs of diabetes?

Back 107

1a. rapid weight loss
(b/c of excess lipolysis, proteolysis), 1b. polyphagia (b/c body thinks it's hypoglycemic)
2. glucosuria

Front 108

Thyroid hormone affect on basal metabolism?

Back 108

INCREASES metabolic rate:
nutrient utilization up
ATP formation up
oxygen consumption up
HEAT production up

Front 109

What is consequence of excess lipolysis?

Back 109

Excessive Lipolysis -> FATTY LIVER and KETOACIDOSIS -> diabetic COMA

FYI: Ketones produced when FA broken down in liver. Before this FA are enz. broken down via β-oxidation to form acetyl-CoA. However, if conditions not right for TCA cycle (intermediates not present), A/CoA become ketones instead.. In high lvl. lower pH of blood, leading to 'ketosis'

Front 110

True or False: High levels of thyr.hormone lower blood cholesterol.

Back 110

FALSE
incr. lipolysis
incr. beta oxidation
incr. bile secretion ->
lowers blood cholesterol
-> geared towards supplying
fat for energy

Front 111

Glycated Proteins/Acidosis/Proteolysis/Swelling further lead to?

Back 111

* vascular damage -> microangiopathies / neuropathies
(e.g. glomerula, TIBIAL nerve/cat, retina/humans)

Front 112

Signs of thyroid hormone deficiency on skin?

Back 112

HD: follicle atrophy ->
bilateral ALOPECIA
myxedema (edema under skin)
pigmentation

Front 113

What is consequence of weight loss and proteolysis?

Back 113

proteolysis -> WEIGHT LOSS, muscle weakness and reduction of organ functions

Front 114

name for non-neoplastic hyperplasia of thyroid gland

cause?

Back 114

goiter

iodine deficiency, or goitergenic substances like cabbage, etc.

Front 115

At what glc. plasma level will glucose start appearing in urine?

Back 115

if over 180mg/dL

Front 116

How would you explain animal which has all symptoms of hypothyroidism but has normal levels in plasma?

Back 116

T4 is converted to T3 intracellularly, so could be a problem with intracellular mechanism

Front 117

what 2 clinical signs of diabetes usually appear as a result of glycosuria?

Back 117

1. polyuria
2. polydipsia (incr. thirst)

Front 118

Other ways of hypothyroidism aside from testing T4 level?

Back 118

1. inject TSH and see if T4 levels go up
2. inject thyroid hormones themselves and see if they are used

Front 119

Does polyphagia (as hypothalamic satiety centre is insulin-dependent) continue?

Back 119

initially only as hypothalamic satiety centre is insulin-dependent; later anorexia and vomiting following tissue damages a/o acidosis

Front 120

True or False: These are symptoms of old cat with hyperthyroidism?
* hyperactivity, nervousness (10% of cats are apathetic)
* body temperature down and skin temp. decreased
* tachycardia; hypertension (retinal detachment)
* diarrhea; polyuria / polydipsia (thirst) (b/o medullary washout)
* skin changes (matted hair or alopecia)

Back 120

all true, except body temp. would NOT go down
* would see heat intolerance and INCREASED skin temp.

Remember: metabolism / functions are accelerated in all organs!

Front 121

What tissues get too much glucose with diabetes?

Do do these tissues with excess glucose?

Back 121

insulin independent tissues (neurons, liver, RBC, etc.)

do not have a lot of glucogen storing ability, also cannot convert to FAs
~form complexes w/proteins -> glycated proteins

Front 122

What causes activates trx of genes in virtually all tissues? And also stimulates following:
* synthesis of many enzymes, structural & transport proteins
* general increase of metabolic activities in many tissues

Back 122

Thyroid hormone

Front 123

Are glycated proteins functional?

Examples?

Back 123

No

glycated hemaglobin! (A chain more often that B chain), after ~6 wks. of hyperglycemia

Front 124

Causes of hypothyroidism in dogs?

Typical hormone levels?

Back 124

mostly defects of the thyroid gland (autoimmune, lymphocytic infiltration or iodiopathic atrophy)

In dogs 95% cases caused by destruction of follicular cells due to autoimmune inflammation. Typical findings are incr. conc. of TSH and low T4, may also be aB against TGB thyroperox. in blood

Front 125

What are glycated proteins in plasma called (e.g. glucosa + albumin)?
Time frame? (like when does this start to happen?)

Back 125

fructose amines

2 weeks

Front 126

True or False: These are signs of hypothyroidism?
- skin alterations are most common: (alopecia)
- myxedema = accumulation of hyaluronic acid in face and tail and folded skin
(sometimes in nerves)
- reproductive dysfunction
intolerance; heat seeking

Back 126

True
Most importantly in hypothyroidism -> reduction of metabolic rate: lethargy; weight gain; exercise
Remember: metabolism / functions slow down!

Front 127

What glycated protein test is most frequently done in vet medicine?

Back 127

fructose amine test, for detecting glc. & albumin complexes

Front 128

Why does Cholesterol increase in hypothyroidism?

Back 128

Cholesterol: Increase, because there is a lack of liver enzymes due to a decreased lipolysis. This means that the body is not digesting all of the fats in the diet so cholesterol levels would be elevated in blood. Fat filled feces would also be seen (according to Sjaastad p.217 constipation and passage in intestine reduced in hypoth.)

Front 129

In the tissues excess glucose is converted into ___ in the lens?
Eventual consequence of this?

Back 129

sorbitol

H2O acc. in lens, gets cloudy -> nerve damage and blindness

Front 130

Why does Cholesterol decrease in hyperthyroidism?

Back 130

Decreased cholest. due to a stimulation of lipolysis. Almost all fats in the body would be broken down

TH stim. production of bile juice. so micelle form. and fat abs. liver excretes of xs cholesterol w/bile as waste....so blood levels of chol. decline at high thyroid levels

Front 131

What are animals with diabetes prone to UTI?

Back 131

tract has lots of sugar in it

Front 132

Why wud urea (in plasma) increase in Hyperthyroid cat?

Back 132

high; more proteolysis -> more deamination of proteins, more conversion to urea

liver not functioning well?

Front 133

which type of diabetes most common in cats?

Back 133

DM type 2

Front 134

TSH level in hyperthyroid cat?

Back 134

low, b/c T4 inhibits APG?

Front 135

how would u treat DM type 1?

Back 135

give insulin

Front 136

Dog got contraceptive treatment
(progesterone) for the past 2 years. Owners calls b/c heard that bitch might develop serious side effects causing
her joints or bones to “grow funny”.
Which condition have these owners heard about?
. In this case, what causes this condition?

Back 136

Acromegaly
Progesterone-increased GH, can affect joints. Long standing progesterone levels cause GH to be released, if she is beyond sexual maturity, bone epiphysis are closed, so bones would growth in width, not length

Front 137

Why do u have to inject insulin?

Back 137

have to inject all peptide hormones otherwise get degraded by the acid in stomach, etc.

Front 138

List / explain the clinical signs that can be associated with Acromegaly
disorder?

Back 138

Acromegaly or hypertrophy of extremities, frontal bone and mandible (membranous bones), increased interdental space (loss of teeth), increase muscle growth. Arthrosis & arthritis due to increase in CARTILAGE growth throwing off statics of joint.
Fluid retention due to a build up of proteins circulating in blood; increases osmoregularity. Secondary diabetes could develop due to progesterone’s increase in insulin resistance. This leads to hypertrophy of heart.

Front 139

why are steroid able to taken as pills?

Back 139

lipophilic

Front 140

progesterone is normally released when?

Back 140

In pregnant bitch, progesterone released during pregnancy; stimulates hypothalamus to produce GH-RH (growth hormone releasing hormone). Growth hormone makes pregn.bitch slightly insulin res. (hyperglycemic) which ensures fetus gets adequate glucose, etc. Remember fetus counts as glucose dependent tissue!

Front 141

what maintenance diet wud you feed animal with diabetes?

Back 141

high in quality protein, low soluble carbs, low FA (b/c often obesity is cause, and leads to fatty liver), high in fiber

Front 142

Why are young, growing animals usually thin?

Back 142

GH is lipolytic hormone

growing animal need protein for muscle/bone development; not fat

Front 143

Which type of diabetes is potentially reversible?

Back 143

diabetes type 2

Front 144

Tropic effect of GH?

Back 144

Tropic/indirect effects (inducing release of another hormone from target tissue) on liver to produce "somatomedin" aka Insulin-like Growth factors

These are IGF effects are typical protein ANABOLIC effects, mitotic rates, A.A. uptake,

Front 145

how would you treat T2 diabetes to begin recovery process and why?

Back 145

would give insulin along with exercise so BW reduced; this gives exhausted beta cells in pancreas (have churning out extra insulin) a chance to recover and make insulin again on own

Front 146

Direct effect of GH?

Back 146

* stimulates hormone sensitive lipase, to force body to use fat as energy source
* in contrast spares glucose (excess can lead to insulin resistance - DM type 2!) for unknown reason, and spare protein

Front 147

What must be functional in animal to recover?
(unanswered questions)

Back 147

* Beta cells can't be completely shot
* Need at least some insulin receptors on insulin dep. tissue
>But aren't receptors the source of problem with T2??

Front 148

Where are Somatotropins made?

Back 148

Growth hormone (=Somatotropin) is an anterior pituitary (protein) hormone, produced by acidophils

Front 149

What is course of action if animal recovers from T2 diabetes? (What would you watch for?)

Back 149

* animals blood glucose levels must monitered closely
* if beta cells making insulin again, must reduce or stop insulin supplements
* otherwise can become hypoglycemic

Front 150

Where are somatomedins made?

Back 150

liver produces
somatomedins (or insulin-like
growth factors = IGF)
upon stim. from GH (somatotropin)

Front 151

Could you cure/reverse type 1 diabetes?

Back 151

Theoretically could do pancreas transplant, but normally only done in human medicine
(remember in type 1 is absolute of insulin, so beta cells not functional at all)

Front 152

True or False:
Somatotropin is hyperplastic & hypertrophic

Back 152

True
Somatotropin is growth hormone

Front 153

How treat diabetes type 3?
(unanswered question)

Back 153

Secondary DM or Type III ( TRANSIENT DM)
* high levels of other hormones like cortisol, or glucagon
* caused by DM Type II; insulin resistance

Does it fix itself?
What is connection between cortisol and insulin/hyperglycemia?

Front 154

GROWTH HORMONE DEFICIENCY in young dog?

Back 154

Dwarfism: inherited deficiency of GH and/or somatomedins

delay in physical maturity, keep puppy coat

Front 155

If glucagon levels really HIGH, which metabolic pathway favored?

Back 155

lipolysis (2.3.1)

Front 156

GROWTH HORMONE DEFICIENCY if occurs later in life ?

Back 156

Early Aging

caused by: damage to pituitary cells
(tumor,hemorrhage, radiation)
OR if have liver disease -> no IGF also early aging

Front 157

Where is glucagon made?

Back 157

secreted in pancreatic
α cells AND stomach <- gut glucagon

Front 158

Panhypopituitarism

Back 158

tumor,hemorrhage, radiation usually don't only affect cells producing GH

none of hormones produced in ant. pituitary gland are made

Front 159

Half life of glucagon?

Back 159

5 minutes (it's a peptide - shorter half life than steroid, b/c proteases are everywhere)

Front 160

IS there any overlap in the function of mineralcorticoids and Gluco-
corticoids?

Back 160

Yes, Cross activity exists between some members of the mineralocorticoid and
glucocorticoid group

Front 161

How are pancreatic alpha cells and beta cells different aside from the hormones they make?

Back 161

* Beta cells are insulin independant (they just make it)
* alpha cells are insulin dependent

Front 162

True or False:
Each cortical zone is controlled by a separate mechanism !
(Zona glomerulosa, Zona fasciculata)

Back 162

True, but some cross reactivity

Front 163

What happens when insulin binds alpha cells?
(unanswered question)

Back 163

glucagon secretion stops being released
(remember peptide hormones stored, so inhibiting synthesis..i dont think)

Front 164

Corticotropin aka ?

Back 164

Corticotropin or ACTH

Front 165

Name two most common health problems affects in ferrets:

Back 165

1. Adrenal disease - excess sex steroids

2. Insulinoma - tumor in beta cells of pancreas

Front 166

Stress stimulates hypothalamus to release

Back 166

Corticotropin Releasing Hormone

Front 167

True or False: Regarding adrenal disease in ferrets, characterized by rise in cortisol & aldersterone.

Back 167

False!

Ferrets w/adrenal disease have excess sex steroids (estrogens > androgens); but cortisol & aldosterone are normal

Front 168

CRH stimulates release of ___ from ___?


ACTH stimulates release of ____

Back 168

CRH stimulates release of CORTICOTROPIN = ACTH from anterior pituitary

Cortisol (and androgens)

Front 169

Symptoms of Adrenal disease in ferrets?

Back 169

Ferret with Adrenal Disease:
estrogens > androgens:

symptoms include alopecia, enlarged vulva, prostate hypertrophy, sexual aggression, bone marrow depression (anemia)

Front 170

Main stimuli which lead to release of cortisol?

Back 170

stress (epinephrine)
metabolic stress (hypoglycemia)
pain, fever, inflammatory mediators - histamine, pyrogens

Front 171

True or False: Insulinoma in ferrets causes rapid increase in blood glucose

Back 171

False!!!

Insulinoma in ferrets causes rapid DROP in blood glucose

because more insulin secreted

Front 172

How does cortisol help bring up blood glucose?
(remember hypoglyc. is one of stimuli for cortisol release)

Back 172

These are anabolic effects of glucocorticoids!
>need to provide fuel (glucose) to muscles/brain with energy
1. mostly gluconeogenesis (from amino acids)

2. strangely glycogenesis also because gluconeogenesis generates so much glucose in liver; some goes to storage*
(*Prerequisite for glucagon’s glycogenolytic effects)

Front 173

Where do anabolic effects of glucocorticoids take effect?

Back 173

gluconeogenesis in LIVER

Front 174

Besides stress-related release, ACTH & Cortisol secretion also follow a circadian rhythm:
In dog cortisol highest in AM or PM?

In cat cortisol highest in ?

Back 174

AM - highest activity level


PM - higher cortisol for cat

Front 175

Cortisol exerts negative feedback on ___ release

Back 175

Cortisol exerts negative feedback on CRH (hypoth.) and ACTH (apg) release

FYI: CRH is CORTICOTROPIN (ACTH) releasing hormone

Front 176

Why might artificial or synthetic corticoids be used clinically?

Back 176

fewer side effects (cross reactivity) than natural steroids

Front 177

Glucocorticoids/CORTISOL promote Gluconeogenesis
(from amino acids); but where do AA's come from?

Back 177

* liver supplies some
* but mostly via proteolysis from peripheral tissues/muscle
(not CNS & cardiac muscle)

Front 178

Name other catabolic affects of Glucocorticoids/CORTISOL:

Where does this occur?

Back 178

Extra-hepatic tissue
=========================1. Decreased Glucose uptake
(in muscle and fat tissue = insulin resistant effect); muscle must rely on fat
2. Increased Proteolysis
3. Lipolysis
Redistribution of fat (abdomen)

Front 179

Animal under high-standing Glucocorticoids (for long time), what happens to liver?

Back 179

liver enlarges, becomes full of glycogen and fat

Front 180

What happens to GH production in older animals?

Why significant?

Back 180

decreased GH production

prof. says mitotic tissues are not maintained -> tissue aging...whatever just go along with it

Front 181

glucocorticoids’ effects on GI?

Back 181

HCl and appetite up; but mucus down
GC's are also anti-inflammatory unfortunately so PGE2 and all prostaglandins down, leads to ulcers

Front 182

glucocorticoids’ effects on blood glucose?

Back 182

* hyperglycemia;
* insulin resistance -> steroid diabetes aka secondary diabetes

fyi: called b/c caused by GC's which are steroids

Front 183

glucocorticoids’ effects on CNS/ apg?

Back 183

drop in synthesis of all these: ACTH,ADH,TSH,GH,
FSH/LH
(leads to "Panhypopituitarism")

Front 184

2 types of neutriphils?

Back 184

circulating pool
marginal pool

Front 185

glucocorticoids’ effects on LEUCOGRAM?

Back 185

Lymphos & Eos numbers drop
Neutriphil (from marginal pool) increases in number in circulation

platelet number increases
RBC number increases

Front 186

Is the overall amount of neutriphils increasing in number?

Back 186

No, neutrilphils from marginal pool avoid selectin-dependent capture due inhibition of binding by cortisol; consequently more neutriphils enter from marginal pool

Front 187

Glucocorticoids prevent release of inflammatory mediators, e.g. from ?

Back 187

from lysosomes, macrophages,
monocytes

Front 188

physiological controller of inflammatory processes

Back 188

Glucocorticoids

Front 189

Glucocorticoids reduce / prevent inflammations and resolve existing inflammations, probably by ?

Back 189

deactivating inflammatory mediators

Front 190

pre-pro-hormone of ACTH is called ?

Back 190

Pro-Opio-MelanoCortin = POMC

Front 191

When GC's enter cell, induce protein synthesis of ____, group of intracellular proteins which bind to trx. factors like nuclear factor kappa B to inhibit synthesis of interleukin

Back 191

lipocortin, protein which inhibit enzymes (like phospholipase A2 and COX1/2) in cytoplasm which convert arachdonic acid to prostanglandins

Front 192

NF kappa B is inhibited by ___?

Back 192

cortisol receptor complex

Front 193

True or False
Collagen synthesis increased by Glucocorticoids

Back 193

False; Collagen synthesis (part of wound healing) is inhibited by GC's

Front 194

Which type of immune response is affected or inhibited to a greater extent: by glucocorticoids: cell mediated or humeral?

Back 194

cell mediated immune response (T cells)

Front 195

The cleaving of POMC gives rise to several active polypeptides:

Back 195

1. α-MSH ( Melanocyte Stimulating Hormone)
2. β-ENDORPHIN (another stress factor to reduce incoming pain)
3. CLIP = Corticotropin-Like Intermediate Peptide
4. ACTH - controls release of Cortisol
- is also crucial to maintain the viability of the entire adrenal cortex !!

Front 196

α-MSH does what?

overproduction of MSH?

Back 196

darkening of skin/mucosa

dark blotches on mucosa!

Front 197

CLIP function?

Back 197

Not much - probably little physiological function; but pathological effects in horses similar to ACTH (aka Corticotropin)

Front 198

ACTH another piece cleaved off from POMC is important why?

Back 198

In addition to controls release of Cortisol,
ACTH required to maintain viability of entire adrenal cortex!!!!
Disorders of ACTH production can affect all POMC compounds !!
Also req. for production of mineralcorticoids?

Front 199

What might cause drop in ACTH production for long period of time?

What must been considered when treating with GC's?

Back 199

if animal treated for long period of time with GC's, tissues which make ACTH can shut down completely - entire adrenal cortex is in jeopardy

Front 200

Hyperadrenocorticism aka?

Back 200

Cushing’s Syndrome
excess of glucocorticoids

Front 201

Causes Cushing’s Syndrome aka Hyperadrenocorticism ?

Back 201

1. Adenomas of adrenal glands -> excess cortisol (rare)
2. Adenomas of ant.pituitary
3. Iatrogenic = prolonged glucocorticoid therapy
4. HORSE: Pituitary Pars intermedia tumors produces P.O.M.C (and excess amounts of active metabolites)

Front 202

Which Adenomas of Cushing's is more common?

What is pathway here?
What is it in excess here?

Back 202

Adenomas of ant.pituitary gland more common

Adenomas of ant.pituitary -> excess ACTH -> cortisol (common)

Front 203

Cushing’s Syndrome caused by prolonged GC treatment?

Back 203

Latrogenic Cushing's

Front 204

Adenomas of adrenal glands: what is pathway here?

Back 204

Adenomas of adrenal glands -> excess cortisol (rare)

Front 205

____ is thought to increases the ACTH efficiency 6x

Back 205

CLIP

Front 206

90% are ___?

Back 206

90% are pituitary-dependent = PDH;

Front 207

What animals is Cushings common in?

Back 207

common in middle-aged to old dogs (boxer, poodle, terrier,dachshund), also in ponies (not horses), very rare in cats

Front 208

PATHOPHYSIOLOGY of hyperadrenocorticism?

Back 208

PROTEOLYSIS, LIPOLYSIS, (like in diabetes), redistribution of fat, Hepatomegaly (enlarged liver), DM3 in cats&horse (see section for symptoms!), PU/PD, ADH receptor gone, so can't reabs. H2O

Front 209

HIRSUTISM

unusual because?

Back 209

slow hair shedding
in horses

b/c in dog lose hair, color of fur gone

Front 210

These are all symptoms of final stages of what?
IMMUNODEPRESSION
POLYPHAGIA
PITUITARY GLAND DEPRESSION (TSH,FSH,LH,
GH) -> Panhypopituitarism
BEHAVIORAL CHANGES (docility in horses
caused by endorphins)
GASTRIC ULCERS
HYPERPIGMENTATION (sometimes, if ACTH )
LAMINITIS / Horses

Back 210

Cushings - can get everything

e.g. DM3, hypothyroidism, reproductive failure (lack of LH, FSH), early aging (GH)

Front 211

TREATMENT of PDH

Back 211

(Surgical removal of tumors; difficult so usually only in people)

> Preferred method via suppression of adrenocortex with mitotane (poison) therapy (=DDD insecticide)
selectively suppress/destroy from of adrenal cortex
* enz. inhibitors also available (safer)
~showed pics of dog whose fur grew back

Front 212

"Moon Face" =

Back 212

Cushings Disease

Front 213

How might Cushings lead to LAMINITIS / Horses ?

Back 213

In Theory:
hypoglycemia ->Endothelins release -> vasoconstriction -> damage/hypoxia in digital joints -> LAMINITIS / Horses

Front 214

Main stimulus for ALDOSTERONE synthesis?

Back 214

HYPOVOLEMIA & Low Blood Pressure -> Renin (released in kidney) -> converted to Angiotensin -> ALDOSTERONE

Front 215

Other stimuli of leading to aldosterone secretion?

Back 215

* Is also stimulated by HYPERKALEMIA
* moderately stimulated by hyponatremia (low Na+)

Front 216

WHICH tissues respond to aldersterone?

Back 216

large intestine, salivary glands, sweat glands

Front 217

If lack aldersterone?


Too much alderstorone?

Back 217

loss of Na+ and water, PU/PD


blood volume increases, preload incr., BP up

Front 218

Most powerful method of reducing excess BP?

Back 218

diuresis

Front 219

Main cause of (Hyperaldosteronism)

Back 219

* Causes?
1. any condition which cause polyuria
2. infarction of kidney (kidney thinks it's hypervolemic but isn't)
3. Main cause -> cyst formation in kidney (polycystic renal disease = PRD) grow over time, pressure up (a.) with renal dysfunction (b.) w/o RD

Front 220

renin is vasodilator?

Back 220

no vasoconstrictor and become angiotensin blas

Front 221

HYPOADRENOCORTICISM =

which hormones low?

Back 221

ADDISON’S DISEASE

= deficiency in adrenal cortex hormones -> Glucocorticoids (first) and
Mineralocorticoids (later) are reduced

Front 222

Why concerned about hypertension?

Back 222

endothelial lining, brain damage, etc

Front 223

What happens to K+, Na+, Ca+?

Back 223

* also lost , so many + charges get metabolic alkalosis
* hypokalemic outside leads to farther diffusion of K+ out
* leads to hyperpolarization of membranes, stops transmission (mild alkalosis stimulates Na/K pumps) -> weakness

Front 224

What animals is HYPOADRENOCORTICISM = ADDISON’S DISEASE more common in?
- specifically type involving immune mediated destruction of cortex

Back 224

(youngish fem. dogs)
- immune mediated destruction of cortex

Front 225

Other causes of HYPOADRENOCORTICISM = ADDISON’S DISEASE?

Back 225

2. OVERTREATMENT for Cushings - mitotane induced adreno- cortical necrosis (mitotane therapy)

3. - long standing cortisol therapy -> depression of ACTH -> cortex atrophy

> GLUCOCORTICOID Deficiency -> hypoglycemia, can't control inflammatory processes
> MINERALOCORTICOID Deficiency:

Front 226

most powerful hormone controlling
plasma calcium and phosphate levels via:

Back 226

PTH is the most powerful hormone controlling
plasma calcium and phosphate levels via:

Front 227

What does aldersterone do?

Back 227

Aldosterone stimulates: Na/K pump
- Sodium absorption
- Potassium & hydrogen looser
- Aldosterone stimulates renal
H+ excretion (via Na+ / H+ exchanger)

Front 228

MINERALOCORTICOID Deficiency:
leads to?

Back 228

(NO ALDERSTERONE)

Na+ & WATER loss, K & hydrogen retention -> Na/K plasma ratio less than 20 (normal 30-40) (so too much K+!!!!!)

Front 229

Messed up Na/K+ ratio is a sign of? (low K+)

Back 229

HYPOADRENOCORTICISM = ADDISON’S DISEASE

Front 230

What stimulates release of PTH?

Back 230

1.Hypocalcemia:
2. Hyperphosphatemia:

Front 231

Net effect of PTH

Back 231

Plasma Calcium increases
Plasma Phosphate DECREASES

Front 232

PTH stimulates?

Back 232

1. Stimulates bone mobilization (resorption) = increases plasma Ca and P
2. Stimulates renal calcium absorption = increases plasma Ca
3. Inhibits renal phosphate absorption = decreases plasma P
4. Stimulates activation of Vit. D = increases plasma Ca via GI absorption

Front 233

D-Hormone =

Back 233

Calcitriol

Front 234

Activation to D hormone occurs
in ?
Requires?

Back 234

liver and kidney
PTH

Front 235

Calcitriol actions?

Back 235

Actions:
1. increases intestinal and renal calcium and phosphate absorption
2. increases mobilization of bone (in high concentrations)

Front 236

Calcitonin stim. by?

Back 236

- Stimulated by hypercalcemia

- Decreases activity and proliferation of osteoclasts

Front 237

Calcitonin favors __formation?

Back 237

 Favors bone formation

 Decreases calcium and phosphate levels

Front 238

Calcitonin seems more important in what age group?

Back 238

Calcitonin seems more important in young animals than adults and the
removal of thyroid gland / C cells has little effect on Ca balance

Front 239

Calcitonin secreting C-cells located where?

Back 239

between thyroid follicle cells

Front 240

Compensatory Hyperparathyroidism

Back 240

1. Lack of dietary Vit D or lack of UV exposure -> reduced Ca absorption -> crooked legs
2. Dietary Ca/P imbalances
3. Renal Diseases with insufficient P excretion

Front 241

In all 3 cases:

Back 241

body releases
PTH  mobilizes Ca from bone tissue 
plasma Ca returns to low/normal  if
long-term, leads to softening of bone
= DEMINERALIZATION
= Compensatory Hyperparathyroidism

Front 242

Bran Disease or Big Head in Horses

Back 242

Dietary hyperparathyroidism
- on pasture grasses high in oxalates,
which binds Ca
- on high bran diet = excess P

Front 243

6 months old beagle / Rubberjaw caused by?

Back 243

Renal Hyperparathyroidism

Front 244

milk fever

Back 244

Parturient Paresis
Acute hypocalcemia within 72 hrs p.p.
due to rapid loss of Ca via milk

Front 245

Why doesnt PTH release help?

Back 245

 PTH is released, but osteoclasts are reduced
in numbers or inactive due to dry period; takes time for them to reactivate
->  Bone cannot respond fast enough -> acute hypocalcemia

Front 246

Signs of milk fever?

Back 246

increased conductivity of Na channels -> excitability, tremors, seizures, tachycardia

- laccid paresis
(may be caused / exacerbated by concomitant Mg increase)

Front 247

Prevention?

Back 247

feed diet low in Ca+ just before animal gives birth, to force reactivation of osteoclasts!

Front 248

where does the liver get the precursors for Gluconeogensis?

Back 248

aa (precursors ) from muscle break down (or stored aa pool)

Front 249

main effects of cortisol

Back 249

provide Glucose for blood via gluconeogen. and excess Glycogen gets stored - ironic but TRUE!

Front 250

what is the precursor of ACTH?

Back 250

POMC - Pro-Opio-MelanoCortin

Front 251

cleaving of POMC gives rise to several active polypeptides

Back 251

Pro-Opio-MelanoCortin -
alpha-MSH
beta endorphin
CLIP
ACTH

Front 252

what hormone is necessary to keep the adrenal cortex alive?

Back 252

ACTH**

Front 253

if an animal has been given long term exogenous cortisol (for years), can the adrenal cortex release Glucocorticoids?

Back 253

no

Front 254

excess of Glucorticoids eventually leads to what dz?

Back 254

Cushings dz