Physiology Ii - Endocrinology Part 2

Front 1

Normal thyroid follicles are filled with what gel like substance?

Back 1

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

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

Front 2

When thyroid cells stimulated, what hormone is released?

Back 2

Secretes thyroid hormones THYROXIN

FYI: When stimulated, epithelium becomes cuboidal or low columnar and colloid is dissolved.

Front 3

Parafollicular cells of the thyroid gland secrete what? function?

Back 3

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 4

what is function of calcitonin?

where secreted from?

Back 4

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 5

major integrating link between the
nervous and the endocrine
systems.

Back 5

HYPOTHALAMUS

Front 6

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

Back 6

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

Front 7

What does aldersterone do?
What ion absorption does it promote? At expense of what?

Back 7

Aldosterone acts mainly on distal tubules and collecting ducts of nephron; stimulates:
- Aldosterone is a SODIUM SAVER! = promotes sodium absorption and K+ loss (Na/K pump)
- Hydrogen loss (via renal Na+ / H+ exchanger)

Front 8

Part of CNS involved in emotions, stress, fear, control of hunger, thirst, sexual behaviour?

Back 8

HYPOTHALAMUS

Front 9

Part of CNS that largely controls homeostasis, e.g. osmolality, body temperature, and controls the autonomic nervous system?

Back 9

HYPOTHALAMUS

Front 10

is a “master” endocrine gland.

Back 10

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 11

The Hypothalamus is connected with the PITUITARY GLAND via the

Back 11

hypophyseal stalk.

Front 12

PITUITARY GLAND consists of what 2 parts?

Back 12

1. ANTERIOR pituitary
2. POSTERIOR pituitary

Front 13

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

What tissues/structures does it have?

Back 13

POSTERIOR pituitary

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

Front 14

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

Back 14

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

Front 15

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

Back 15

ANTERIOR pituitary = adenohypophysis

Front 16

also called vasopressin

Back 16

ADH

Front 17

Glucocorticoids = ?

What do they control? Example(s) ?

Back 17

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

Front 18

ADH and Oxytocin synthesized where?

Back 18

hypothalmus

Front 19

ADH and Oxytocin stored and RELEASED from where?

Back 19

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

Front 20

Does hypothalmus also regulate ANTERIOR pituitary = adenohypophysis?

Back 20

Yes

Front 21

Releasing Hormones (RH) and/or Inhibiting Hormones (IH) come from where? Target organ?

Back 21

hormones produced in hypoth. go to ANTERIOR PITUITARY

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

Front 22

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

What are these type of hormones known as?
(hint: movie '___ thunder' with stiller, j.black, and t.cruise)

Back 22

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

Tropic Hormones

Front 23

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

Back 23

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

Front 24

Where are 5 stimulating/releasing hormones that the hypoth. makes?

Hint: gd cn G Tt P

Back 24

Gnrh
Crh
GHrh
Trh
Prh

Front 25

GnRH = ?

GHRH = ?

Back 25

GnRH = Gonadotropin R.H.

GHRH = Growth Hormone Rel. Hormone

Front 26

Gonadotropin Stimulates?
Which in term stumulates?

Back 26

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

..gonads to make sex hormones

Front 27

Another name for growth hormone

Back 27

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

Front 28

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

Back 28

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

Front 29

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

Back 29

adrenal cortex to synthesize Glucocorticoids (aka cortisol)

Front 30

Targets of ACTH?

Back 30

many targets

Front 31

What is TRH?

Back 31

TRH = Thyrotropin Releasing Hormone

Front 32

Where does Thyrotropin come from?

Back 32

ant. pituitary

Front 33

Where does TSH come from?

Back 33

Ant.Pit.Gland

Thyroid stimulating hormone and thyrotropin are same thing

Front 34

TSH stimulates thyroid to stimulate what?

Back 34

T3
T4

Front 35

Where are some INHIBITING hormones that the HYPOTHALMUS. makes?

Back 35

GHih (counteracts GHrh)
Pih (counteracts Prh)

Front 36

Prostaglandins made in the ?

What is target organ?

Back 36

Ant.Pituitary gland

direct effects (e.g. mammary gland)

Front 37

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

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

Back 37

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

Zona fasciculata (middle layer) makes the glucocorticoids!

Front 38

Low levels of calcium stimulates ?

Back 38

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 39

What is primary mineralcorticoids?

Back 39

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

AMC

Front 40

What is primary Glucocorticoids made by adr. cortex?

Back 40

Cortisol (95% glucocorticoids secreted in mammals)

GC

Front 41

What 2 components are required to make thyroid hormone?

Back 41

- amino acid tyrosine and iodine

Front 42

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

Where does it go? in what form?

Back 42

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 43

TGB? made where?

primary component of ____?

Back 43

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

it is primary component of colloid

Front 44

difference between T1 and T2

where does all this happen?

Back 44

(iodine joins the TGB)

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

Front 45

what happens when form T3 or T4?

Which is find in higher conc.in plasma?

Back 45

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 46

storage form of thyroid hormone

active form of thyroid hormone? what does it do?

Back 46

T4

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

Front 47

Thyroid hormones are controlled via the ____?

Back 47

Hypothalamic–Pituitary–Thyroid Axis

Front 48

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

Back 48

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

Front 49

TRH stimulates anterior pituitary to
synthesize and secrete __

Back 49

TSH

Front 50

T3 or T4 is lipophilic?

transported by?

Back 50

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 51

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

Back 51

- 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 52

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

Back 52

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

Front 53

Thyroid hormone affect on basal metabolism?

Back 53

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

Front 54

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

Back 54

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

Front 55

Signs of thyroid hormone deficiency on skin?

Back 55

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

Front 56

name for non-neoplastic hyperplasia of thyroid gland

cause?

Back 56

goiter

iodine deficiency, or goitergenic substances like cabbage, etc.

Front 57

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

Back 57

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

Front 58

Other ways of hypothyroidism aside from testing T4 level?

Back 58

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

Front 59

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 59

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 60

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 60

Thyroid hormone

Front 61

Causes of hypothyroidism in dogs?

Typical hormone levels?

Back 61

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 62

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 62

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

Front 63

Why does Cholesterol increase in hypothyroidism?

Back 63

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 64

Why does Cholesterol decrease in hyperthyroidism?

Back 64

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 65

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

Back 65

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

liver not functioning well?

Front 66

TSH level in hyperthyroid cat?

Back 66

low, b/c T4 inhibits APG?

Front 67

Dog got contraceptive treatment
(progesterone) for the past 2 years. Owners calls b/c heard that ***** 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 67

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 68

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

Back 68

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 69

progesterone is normally released when?

Back 69

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

Front 70

Why are young, growing animals usually thin?

Back 70

GH is lipolytic hormone

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

Front 71

Tropic effect of GH?

Back 71

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 72

Direct effect of GH?

Back 72

* 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 73

Where are Somatotropins made?

Back 73

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

Front 74

Where are somatomedins made?

Back 74

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

Front 75

True or False:
Somatotropin is hyperplastic & hypertrophic

Back 75

True
Somatotropin is growth hormone

Front 76

GROWTH HORMONE DEFICIENCY in young dog?

Back 76

Dwarfism: inherited deficiency of GH and/or somatomedins

delay in physical maturity, keep puppy coat

Front 77

GROWTH HORMONE DEFICIENCY if occurs later in life ?

Back 77

Early Aging

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

Front 78

Panhypopituitarism

Back 78

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

none of hormones produced in ant. pituitary gland are made

Front 79

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

Back 79

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

Front 80

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

Back 80

True, but some cross reactivity

Front 81

Corticotropin aka ?

Back 81

Corticotropin or ACTH

Front 82

Stress stimulates hypothalamus to release

Back 82

Corticotropin Releasing Hormone

Front 83

CRH stimulates release of ___ from ___?


ACTH stimulates release of ____

Back 83

CRH stimulates release of CORTICOTROPIN = ACTH from anterior pituitary

Cortisol (and androgens)

Front 84

Main stimuli which lead to release of cortisol?

Back 84

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

Front 85

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

Back 85

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 86

Where do anabolic effects of glucocorticoids take effect?

Back 86

gluconeogenesis in LIVER

Front 87

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 87

AM - highest activity level


PM - higher cortisol for cat

Front 88

Cortisol exerts negative feedback on ___ release

Back 88

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

FYI: CRH is CORTICOTROPIN (ACTH) releasing hormone

Front 89

Why might artificial or synthetic corticoids be used clinically?

Back 89

fewer side effects (cross reactivity) than natural steroids

Front 90

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

Back 90

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

Front 91

Name other catabolic affects of Glucocorticoids/CORTISOL:

Where does this occur?

Back 91

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 92

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

Back 92

liver enlarges, becomes full of glycogen and fat

Front 93

What happens to GH production in older animals?

Why significant?

Back 93

decreased GH production

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

Front 94

glucocorticoids’ effects on GI?

Back 94

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

Front 95

glucocorticoids’ effects on blood glucose?

Back 95

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

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

Front 96

glucocorticoids’ effects on CNS/ apg?

Back 96

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

Front 97

2 types of neutriphils?

Back 97

circulating pool
marginal pool

Front 98

glucocorticoids’ effects on LEUCOGRAM?

Back 98

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

platelet number increases
RBC number increases

Front 99

Is the overall amount of neutriphils increasing in number?

Back 99

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

Front 100

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

Back 100

from lysosomes, macrophages,
monocytes

Front 101

physiological controller of inflammatory processes

Back 101

Glucocorticoids

Front 102

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

Back 102

deactivating inflammatory mediators

Front 103

pre-pro-hormone of ACTH is called ?

Back 103

Pro-Opio-MelanoCortin = POMC

Front 104

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 104

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

Front 105

NF kappa B is inhibited by ___?

Back 105

cortisol receptor complex

Front 106

True or False
Collagen synthesis increased by Glucocorticoids

Back 106

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

Front 107

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

Back 107

cell mediated immune response (T cells)

Front 108

The cleaving of POMC gives rise to several active polypeptides:

Back 108

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 109

α-MSH does what?

overproduction of MSH?

Back 109

darkening of skin/mucosa

dark blotches on mucosa!

Front 110

CLIP function?

Back 110

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

Front 111

ACTH another piece cleaved off from POMC is important why?

Back 111

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 112

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

What must been considered when treating with GC's?

Back 112

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 113

Hyperadrenocorticism aka?
Excess of what?

Back 113

Cushing’s Syndrome
excess of glucocorticoids

Front 114

Causes Cushing’s Syndrome aka Hyperadrenocorticism ?

Back 114

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 115

Which Adenomas of Cushing's is more common?

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

Back 115

Adenomas of ant.pituitary gland more common

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

Front 116

Cushing’s Syndrome caused by prolonged GC treatment?

Back 116

Latrogenic Cushing's

Front 117

Adenomas of adrenal glands: what is pathway here?

Back 117

Adenomas of adrenal glands -> excess cortisol (rare)

Front 118

____ is thought to increases the ACTH efficiency 6x

Back 118

CLIP

Front 119

90% are ___?

Back 119

90% are pituitary-dependent = PDH;

Front 120

What animals is Cushings common in?

Back 120

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

Front 121

PATHOPHYSIOLOGY of hyperadrenocorticism?

Back 121

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 122

HIRSUTISM

unusual because?

Back 122

slow hair shedding
in horses

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

Front 123

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 123

Cushings - can get everything

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

Front 124

TREATMENT of PDH

Back 124

(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 125

"Moon Face" =

Back 125

Cushings Disease

Front 126

How might Cushings lead to LAMINITIS / Horses ?

Back 126

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

Front 127

Main stimulus for ALDOSTERONE synthesis?

Back 127

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

Front 128

Other stimuli of leading to aldosterone secretion? (hyper___)

Back 128

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

Front 129

WHICH tissues respond to aldersterone? (name 3; 2 are glands))

Back 129

large intestine, salivary glands, sweat glands

Front 130

If lack aldersterone, lose ___ and ____. Clinical sign owner might recognize? (basically seen with every endocrine dz)

Too much alderstorone, affects blood volume how? BP? Preload?

Back 130

loss of Na+ and water, PU/PD


blood volume increases, preload incr., BP up

Front 131

Most powerful method of reducing excess BP?

Back 131

diuresis

Front 132

Main cause of (Hyperaldosteronism)

Back 132

* 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 133

renin is vasodilator?

Back 133

no vasoconstrictor and become angiotensin blas

Front 134

PRIMARY HYPOADRENOCORTICISM =

which hormones low?

Back 134

ADDISON’S DISEASE

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

Front 135

Why concerned about hypertension?

Back 135

endothelial lining, brain damage, etc

Front 136

What happens to K+, Na+, H+ levels in blood in dog with Addison's? Why?

Back 136

With Addison’s (Primary Hypoadrenocorticism) -> decreased mineralocorticoid e.g. Aldosterone -> get hyponatremia (no more “sodium saver”) and hyperkalemia and acidosis (more H+!)
Note: Glucocorticoids also decreased..obviously

Front 137

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

Back 137

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

Front 138

Other causes of HYPOADRENOCORTICISM = ADDISON’S DISEASE?

Back 138

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 139

most powerful hormone controlling
plasma calcium and phosphate levels via:

Back 139

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

Front 140

MINERALOCORTICOID Deficiency:
leads to what electrolyte changes in plasma?

Back 140

(NO ALDERSTERONE)

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

Front 141

What stimulates release of PTH? (2 things)

Back 141

1.Hypocalcemia:
2. Hyperphosphatemia:

Front 142

Net effect of PTH = plasma ___ increases, plasma ____ decreases

Back 142

Plasma Calcium increases
Plasma Phosphate DECREASES

Front 143

PTH stimulates?

Back 143

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 144

D-Hormone =

Back 144

Calcitriol

Front 145

Activation to D hormone occurs
in what 2 places?
Requires?

Back 145

liver and kidney
requires PTH

Front 146

Calcitriol actions?

Back 146

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

Front 147

Calcitonin stim. by?

Back 147

- Stimulated by hypercalcemia

- Decreases activity and proliferation of osteoclasts

Front 148

Calcitonin favors __formation?

Back 148

 Favors bone formation

 Decreases calcium and phosphate levels

Front 149

Calcitonin seems more important in what age group?

Back 149

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

Front 150

Calcitonin secreting C-cells located where?

Back 150

between thyroid follicle cells

Front 151

Compensatory Hyperparathyroidism can be caused by ? (name 3)

Back 151

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 152

In all 3 cases of Compensatory Hyperparathyroidism, body releases ____ and mobilizes ____ from bone tissue.

If longterm, leads to ____ of bone.

Back 152

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

Front 153

Bran Disease or Big Head in Horses cause by ?

Back 153

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

Front 154

6 months old beagle / Rubberjaw caused by?

Back 154

Renal Hyperparathyroidism

Front 155

Milk fever = ?
Due to ?

Back 155

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

Front 156

Why doesnt PTH release help?

Back 156

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 157

Signs of milk fever?

Back 157

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

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

Front 158

Prevention of milk fever?

Back 158

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

Front 159

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

Back 159

HYPOADRENOCORTICISM = ADDISON’S DISEASE

Front 160

*skip -> What is contained in the lobule of the thyroid gland?

Back 160

What is contained in the lobule of the thyroid gland?

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