3-Mnu - Week 1

Front 1

What is the structure of Vassopressin and how does this compare to oxytocin?
What is ADH used to treat primarily? What are 3 other uses of vprsns?

Back 1

It's a cyclic peptide and only differs from oxy by 2 amino acids.
Used to treat Diabete Insipidus
Vasopressins can also be used for:
- local hemostasis
- expelling flatus
- treatment of V-fib and V-tach

Front 2

What is the name, action, T1/2, and side effects of V2 receptor agonists.

Back 2

1. V2-receptors: Desmopressin
- Action: bind G-protein, cause a cascade and ( inc cAMP) and PKA-mediated P-lation of aquaporis that causes their retention in the plasma membrane = water retention
- T1/2 = 6-20hrs
- Side Effects: hypo Na, waterintoxication

Front 3

What is the name, action, T1/2, and side effects of V1 receptor agonists.

Back 3

"Arg Vasopressin" (Pitressin)
- G-protein cascade, increases PLC = an increase in IP3 (= inc Ca+) and DAG (=inc PKC), and this causes smooth muscle contraction.
- T1/2 = 3-4hrs
- HTN, ischemia (especially coronary)

Front 4

What 2 drugs are used to treat a clear-cut deficiency in thyroid hormone?
Which is the drug of choice? Why?

Back 4

Levothyroxine sodium (T4) and Liothyronin (T3).
L-thyroxine is the drug of choice b/c it is more tightly bound in the plasma and thus less easily degraded. This gives it a longer half life and allows it to deliver more steady [plasma] over time.
** Different brands are NOT bioequivalent, therefore must use caution when switching a pt!

Front 5

How do Thionamides work? Will they treat the disease process in Grave's?

Back 5

They block the iodination and condensation of thyroglubin thereby prevention it from being phagocytozed by the follicular cells.
They won't work on Grave's disease b/c they will have no effect on the TSH Ab's that are causing that disease.

Front 6

Why do the thionamides have a delayed onset of action?

Back 6

B/c it take a long time to deplete endogenous stores of T3. B/c it only affects the synthesis of new T3, it's affects won't be noticed for a while.

Front 7

How do Iodide salts and radioactive iodide treat hyperthyroidism?

Back 7

Iodide salts: blocks the hydrolysis of I-TG thereby preventing the release on the Th into the blood.
Radioactiv iodide: kills thyroid tissue by emitting lethal B-particles.

Front 8

What are 3 adjuvant therapies for the treatment of hyperthyroid?

Back 8

1. Porpanolol: relieve adrenergic symptoms (tachycardia, tremor, anxiety, etc).
2. Ca channel blockers: relieves tachycardia
3. Dexamethasone: inhibits peripheral conversion of T4 to T3

Front 9

What are 5 complications of growth hormone excess?

Back 9

1. Excess growth of tissues in face, hands and feet
2. sleep apnea
3. increased risk of colon polyps
4. Metabolic syndrome (HTN, high blood sugar, abnormal lipids)
5. Osteoarthritis

Front 10

What sorts of lab tests and results would confirm excess GH?

What 2 criteria need to be met to diagnose pituitary hypofunction?

Back 10

1. High plasma GF, IGF-1
2. Oral glucose challenge - expect GH levels to go down to < 1. If not then you have a problem

1. pituitary hormone levels are low in the plasma
2. If it does not respond appropriately (ie to target level) in stimulation test. Think triple bolus (Insulin, TRH, GnRH)

Front 11

What 2 drugs could be used to treat excess GH?

Back 11

1. Somatostatin
2. GH receptor blockers
** Can also do a transphenoidal surgery to remove the pituitary

Front 12

What comes from the hypothalamus to stim and inhibit Prolactin? What does PRL feedback to inhibit?

How could a mass effect cause prolactinoma?

Back 12

+ PRL release: PRH
- release: dopamine

Prolactin will feedback to inhibit GnRH (GnRH stimulates LH & FSH) and Testosterone

Could get a tumor so big that the stalk gets compressed and you lose hypothalmic control over the pituitary

Front 13

What are the 5 potential causes for high prolactin?
How is high prolactin treated?

Back 13

1. Physiologic (prego/bfeeding)
2. Pituitary prolactinoma
3. Loss of dopaminergic inhibition d/t stalk compression, hypothalmic lesion or drugs
4. Hypothyroidism (?proque?) incr TRH = inc prolactin?
5. Renal and liver failure

Tx: give dopamine agonists (will usually shrink the tumor by ~50%)

Front 14

Define:
Autocrine
Paracrine
Neuro/endocrine

Back 14

Autocrine = affects the same cell
Paracrine = affects neighboring cells through ECF and not synapses
Neuro/endocrine = affects distant cells through the circulation

Front 15

All steroid hormones come from a cholesterol precursor that is cleaved down. What(3) classes/groups of hormones are produced as Carbons are removed?

Back 15

27 C's: Cholesterol -->
21 C's: Pregnane derivatives (Progesterone & corticosteroids (mineral + gluco) ) -->
19 C's: Androstane (Androgens) -->
18 C's: Estrane (estrogens

Hint 15

P
A
E

Front 16

Explain how the hypothalmic neurons communicate with the anterior and with the posterior pituitary?

Back 16

Anterior: The neurons release trophic hormones into the capillaries of the median eminence. These hormones are then carried down to the cells of the ant pituitary where they stimulate the production of ant pit hormones.
Posterior: hypothalmic neurons synapse directly onto the capillary bed of the post-pit and release the ADH and oxytocin.

Front 17

Where is GH released from? What controls it's release? What effects (4) does it have?

Back 17

GH is released from the anterior pituitary.
The ratio of somatostatin and GHRH in the hypothalamus will determine the release of GH.
GH will:
1. Act on the liver and other tissues to cause the release of IGF-1, that along with GH, will:
2. stimulate cartilage growth
3. increase blood glucose
4. stimulate bone and tissue growth

Front 18

What is interesting about the location of GH (on Xsome 17)
There are 2 types of hGH, what are they and which one has a known function?
How does GH travel in the plasma?
T1/2?

Back 18

It is found amidst a cluster of genes that code for proteins with GH-like functions (e.g. hCG)
- hGH-N (known function), and hGH (10% of the GH in circulation - precise function unknown)
- 50% is bound to a protein that closely resembles the GH receptor
-GH is rapidly metabolized: T1/2 = 6-20min

Front 19

What type of receptor does GH have? What is the main pathway that is activated when GH binds??

Back 19

GH has a cytokine receptor.
When GH binds to JAK2 which activates Stat which acts as a TF to regulate gene expression

Front 20

Both IGF 1 and 2 are peptide hormones that have a plasma-binding protein. For each hormone list the following characteristics:
- Other names
- Source
- Regulating molecule
- physiological role

Back 20

- Other names
1 = Somatomedin
2 = Multiplication-Stimulating activity (MSA)

- Source
1 = Liver & other tissue
2 = diverse tissues

- Regulating molecule
1 = GH (only after birth), and nutriotional status
2 = unknonwn

- physiological role
1 = skeletal and cartilage growth
2 = growth during fetal development

Front 21

What is meant by "promiscuous receptors" and what does this refer to?
There are 6 IGF binding proteins located in the plasma and in the tissues. Which one binds 95% of the IGF in the plasma?

Back 21

The fact that IGF 1 & 2 can bind to each others receptor and the insulin receptor! The receptors bind quite promiscuously. SLoots!

IGFBP 3 binds 95% of the IGF in the plasma.

Front 22

How is the temporal release of GHRH and Somatostatin different?

What is the effect of IGF on GH and somatostatin?

Back 22

GHRH is release in an episodic pulsatile fashion, while the release of somatostatin is tonic (more regular)

IGF will inhibit the release of GH and stimulate the release of somatostatin

Front 23

What 2 effects do GH and IGF have in common?
What 2 things do they cause (in opposites)?
What does GH regulate that IGF does not?

Back 23

They both stimulate the epiphyseal plate and protein synthesis.
IGF is antilipolytic, GH stimulates lipolysis. IGF will have insulin-like activity, whereas GH will decrease insulin sensitivity in the muscles.
GH causes Na+ retention
** they both work in several different tissues and this is why they have opposite effects.

Front 24

What do IGF and GH do at the epiphyseal plate?

Back 24

GH binds a receptor on the prechondrocyte and it causes an intracellular cascade that results in the production of IGF mRNA
IGF then promotes differentiation and clonal expansion of the chondrocytes.

Front 25

What are 5 symptoms of acromegaly?

Back 25

1. Osteoarthritic vertebral changes
2. bitemporal hemianopia
3. prognathism and acromegalic facies
4. hirsutism (d/t the overstimulation of the ACTH system --> causes adrenal hypertrophy --> excess androgens increase size of accessory reproductive organs)
5. gynecomastia & lactation (d/t increases in prolactin)

Front 26

Why/how does excessive GH cause diabetes?

Back 26

It increases glucose metabolism by decreasing it's uptake into cells, and increasing hepatic release. This, combined with a decrease in insulin sensitivity, causes the blood sugar to rise out of control

Front 27

What 5 things will cause an increase in GH secretion?
What are the effects of the following on GH secretion:
- sleep
- L-dopa and dopamine?

Back 27

1. decrease in energy substrate (exercise, hypoglycemia, fasting)
2. increase in circulating amino acids
3. Glucagon (a potent GH stimulator; can be used as a test)
4. Stressful stimuli

In the first stages of sleep, the levels of GH go up, and in REM the levels go down (thus is person REM deprived their GH levels will go up)
L-Dopa acts on the hypothalamus to increase GHRH and decrease Somatostatin; whereas dopamin works on the pituitary to decrease GH secretion

Front 28

What 5 hormones/molecules will decrease GH secretion?

Back 28

1. Glucose
2. Cortisol (glucocorticoids will inhibit growth at the cellular level)
3. Free fatty acids
4. Provira (Medroxyprogesterone)
5. Growth Hormone (via negative feedback)

Front 29

The thyroid gland releases what 3 things? Which are the most active?
How does the thyroid make T3 and T4?

Back 29

T3 (ring with 1 iodine, then ring with 2)
T4 (both rings have 2)
Reverse T3 (ring with 2 iodine then ring with one)
T3 > active than T4, and RT3 is inactive!
The gland mostly releases T4 which is deiodinated in the tissues.
Thyroid peroxidases make Monoiodotyrosine and/or diiodotyrosines:
M-i + D-i = T3
D-i + D-i = T4

Front 30

Almost all thyroid hormone is bound in the plasma to what 3 things? Which is bound more, T3 or T4?

Back 30

1. Thyroid binding globulin(T4 67%>T3 46%)
2. Transthyretin (T4 20% > T3 1%)
3. Albumin (T4 13% < T3 53%)
So most T4 is bound to TBP, and most T3 is bound to albumin. Overall there is more free T3 than free T4.

Front 31

What 3 things will upregulate thyroid binding globulin? What 3 will down regulate it?
Where are the deiodinases types 1-3 found?

Back 31

up-regulate TBG:
1. Estrogen & pregnancy
2. Methadone/heroin
3. tranquilizers

Down- regulate:
1. glucocorticoids
2. androgens
3. chemotherapy

D1 -- plasma
D2 -- tissues
D3 -- placenta & brain

Front 32

How many thyroid receptors are there?
How does Thyroid hormone have an effect on cells (how does it get in and what does it do?)
How does the body get rid of thyroid hormone?

Back 32

There are 2 thyroid receptor (TR) genes ( a & B) and these can be alternatively spliced into 4 different receptors: a1, a2, B1, B2* found in brain!) .
T3 diffuses through the cellular membrane and binds to a receptor in the cytoplasm. It then moves into the nucleus where it acts as a transcription factor. It can bind one receptor = monomer, or two receptors (to form homo or heterodimers).
TH is de-iodinated and conjugated in the liver, the iodine is recycled and the tyrosine is excreted.

Front 33

What (specifically) does TH do to increase cardiovascular functioning (2 things)?
What effect does TH have in the CNS (2)?
Why is TH important in general growth and reproduction?

Back 33

In the cardiovascular system, TH will:
- inc B-adrenergic receptors
- promote the production of a-MHC (as opposed to B-MHC), and this increases contraction speed

- Promotes the development of the cerebral cortex and the cochlea

- required for milk production and
- normal menstrual cycles and fertility

Front 34

What will inhibit TRH?
What 4 things will inhibit TSH?
DTSG

Back 34

Stress will inhibit TRH
Inhibitors of TSH:
- Dopamine
- T3 (converted from T4 in the pituitary by D2)
- Somatostatin
- Glucocorticoids

Front 35

What is the half like of TSH?

How much iodine do you need a day?

How does low iodine cause a goiter to develop?

Back 35

T 1/2 = 60 min for TSH

50 ug / day

Low iodine = low levels of T3 and T4; this stimulates the release of TSH from the pituitary. High levels of TSH cause the thyroid gland to hypertrophy and form a goiter.
** there is a loss of negative feedback b/c can't make enough T3 and T4 = system goes forward unchecked.

Front 36

What could you give a pt to see if there is a problem with their thyroid or with their pituitary?

Back 36

Give TSH and see if levels of T3 and T4 come up.
OR:
Give TRH and see if levels of TSH come up, if not then there's a problem with their pituitary.

Front 37

What are 5 potential causes of congenital hypothyroidism?

Back 37

1. Maternal iodine deficiency
2. fetal thyroid dysgenesis
3. errors of thyroid synthesis
4. maternal anti-thyroid antibodies that cross the placenta
5. fetal hypopituitary hypothyroidism

Front 38

What are some of the adverse affects of anemia in infants (4) ?

Back 38

1. increased fearfulness/wariness (decrease willingness to leave a caregivers side)
2. Irritability and unhappiness
3. Lower IQ scores
4. Motor: decreased willingness to explore environment (r/t fatigue)

Front 39

If TSH and T3 / T4 are moving in the opposite direction then where is the problem?

Back 39

It is with the thyroid gland!! (ie a primary defect). If they are moving in the same direction it is a problem with the ant. pituitary and is a secondary defect (rare).

Front 40

What are the 4 common causes of primary thyrotoxicosis?

In a broad sense what are the 3 possible causes?

Back 40

1. Grave's Disease - autoimmune, antibodies are produced that behave just like TSH
2. Toxic adenoma - benign, makes TH independently of TSH
3. Multinodular goitre - several benign nodules that make TH
4. Thyroiditis - self-limiting release of hormone from a damaged gland. Can be sub-acute or painless

Causes: increased production (grave's), increased secretion (from a leak) or increased ingestion

Front 41

What test is used to distinguish the cause of thyrotoxicosis?

Back 41

Radioactive Iodine uptake (RAI):
If it is high then the gland is overactive
If it is low then the gland in leaking or there is an exogenous source

Front 42

What are the 4 most common causes of hypOthyroidism?

This is usually treated with 1.5ug/kg/day, what test do you use for therapeutic drug monitoring of this?

Back 42

1. Congenital absence of the gland or enzyme defects
2. Hashimotos autoimmune destruction
3. Subacute thyroiditis (following hyper phase)
4. Iatrogenic: thiouracils, iodine, amiodarone, lithium, RAI, Sx

** can also get peripheral resistance

Use TSH to monitor dose of L-thyroxine

Front 43

What are the differential Dx for a solitary thyroid mass? (3)

What is the approach to a thyroid nodule? (3 steps

Back 43

1. cyst
2. Adenoma
3. Carcinoma (in order of decr frequency: papillary, follicular, medullary, anaplastic)
1. Assess cancer risk (radiation, FHx, rapid growth, etc)
2. Check TSH: if normal --> step 3, if low do a radioisotope scan (tx for hyperthyroidism if nodule hot, and do step 3 if cold)
3. USS & Fine-need biopsy
- if suspicious cytology then Sx, otherwise follow the patient

Front 44

When would you do a radioisotope scan?
What is the difference between a hot and a cold nodule?

Back 44

Only if a person has a thyroid nodule and low TSH.

Hot: the nodule is producing TH and this is supressing the TSH. The low levels of TSH have caused the rest of the gland to atrophy (cold background)
Cold = (most nodules) they look blank and are not secreting, the TSH levels will be normal (hot background). They have a 5% risk of malignancy overall

Front 45

Describe the movement of Ca+ between these compartments:
- GI <---> ECF
- ECF <---> Kidneys
- ECF <---> Bones
How much Ca+ is eaten and excreted? What is the net movement?

Back 45

- GI <---> ECF:
Net absorption of 2.5;

- ECF <---> Kidneys
247.5 mmol reabsorbed (of 250mmol)

- ECF <---> Bones
rapid exchange of 500 mmol

Eat 25mmol, urine - 2.5mmol, feces -22.5mmol thus NO net movement!

Front 46

What stimulates (7) and Inhibits (1) osteoblasts?
What stimulates (4) and Inhibits (5) osteoclasts?

Back 46

Osteoblasts:
1. PTH; Calcitonin, 2. IL - 1, 3. T3/4, 4. HGH, IGF-1, 5. Prostaglandins, 6. TNF, 7. Estrogens
Inhibited by Glucocorticoids

Osteoclasts:
- Stimulated: 1. PTH & Vit D, 2. Calcitonin, 3. IL-6/11
-Inhibited: Calcitonin, Estrogens, TGF - B, IFNa, PGE2

Front 47

When do estrogen levels peak in men and women? When is menopause? What happens?

Back 47

Estrogen peaks in the late 20's mid 30's. There is a period of rapid loss during menopause (age 50-60)

Front 48

How is the absorption of Ca different from the absorption of Pi?
What happens if there is low [Ca] in the plasma?

Back 48

Ca+ absorption is adaptive, meaning more is absorbed when intakes are low. Absorption of Pi however is linearly related to intake.

When [Ca] is low in the plasma, neurons become more excitable and this can cause hypocalemic tetany. (will be worsened by acidosis b/c more Ca+ will become bound)

Front 49

What are the 3 PTH receptors?

What stimulates the secretion of PTH and what are the 3 effects of PTH?

Back 49

PTH receptors:
1. hPTH/PTHrP: binds both PTH and PTHrP
2. hPTH2-R: will not bind PTHrP, located in brain placenta, pancrease
3. CPTH: binds to the carboxyl end of PTH

Low [Ca] causes the release of PTH, which will:
- increase bond resorption (oclasts)
- increase kidney Ca absorption and Pi excretion
- stimulate the production of calcitrol which leads to increased Ca+ absorption

Front 50

Vitamin D3 comes from the skin and diet. Where are the next 2 stops on the metabolism train? What happens in each stop? What are the 3 main actions of the final prooduct?

Back 50

1. To the liver, converted into 25-OH-Vit D3
2. To the kidneys where 1a-OHlase converts it to 1,25-OH-Vit D3 (aka calcitrol).
Calcitrol stimulates Oclasts > Oblasts and bone is resobed, also promotes Ca+ absorption thru calbindins, and facilitates kidney reabsorption

Front 51

What are where is (in the metabolism pway) is vitamin D regulated?
(4)

Back 51

1. PTH (in response to low [Ca+] will stimulate 1a-OHlase to make 1, 25 OH-Vit D3 and raise plasma [Ca+]
2. The 1,25-OH-Vit D3 will increase plasma [Ca] and this will feedback and inhibit PTH
3. 1,25-OH-Vit D3 will feedback and inhibit both PTH and 1a-OHlase
4. Prolactin will stimulate 1a-OH-lase

Front 52

What 2 hormones stimulate Ca+2 absorption from the intestines?
What hormones move Ca+ into and out of the bones?
What hormones promote renal absorption of Ca+? How about excretion?

Back 52

Intestinal absorption: Calcitrol (vit D) and PTH

Bone: from bone: calcitrol, PTH, cortisol
into bone: calcitonin

Kidney: re-absorption - PTH, calcitrol
excretion: calcitonin

Front 53

What stimulates the release of Calcitonin and where does it come from?
What does Calcatonin do?

Back 53

High levels of serum Ca+ stimulate the release of calcitonin from the parafollicular or C-cells
A precise physiological role is not know (no syndromes of excess/deficiency), however it stimulates kidney excretion and inhibits Oclasts. THis has a possible protective role on maternal bones during pregnancy (where Ca+ is needed by fetus)

Front 54

How do the following hormones contribute to Ca+ regulation?
1. Corticosteroids
2. GH
3. IGF-1
4. TH
5. Estrogen
6. Insulin

Back 54

1. Corticosteroids - will lower plasma Ca by inhibiting oClasts. Only problem in in long-term this causes -+---> PTH = bone loss
2. GH: +absorption > +excretion; net effect in more plasma [Ca]
3. IGF-1: stimulates protein synthesis of bones
4. TH: may cause increase of Ca in plasma and urine
5. Estrogen: inhibits oClasts
6. Insulin: increase bone formation (bone loss in diabetes!)

Front 55

Bone Density Scans:
- What is a T score? Z score?
- What are the T scores for:
Osteopenia
Osterporosis
Severe Osteoporosis

Back 55

T-Score - a comparison to the mean BMD of young adults. Z-score is a comparison of the mean BMD to age matched adults.
T-scores for:
Osteopenia - +2.5 --> +1.0 inclusive
Osterporosis: _< -2.5
Severe Osteoporosis: _< -2.5 & a fragility fracture

Front 56

In Canada, when should you do a BMD test (2 instances):

Back 56

1. For all men & women > 65yrs
2. Postmenopausal women < 65 and men > 50 who have:
1 major risk fact (compression or fragility #, family hx, systemic steroid therapy >3mo, malabsorption, hyperPTH, etc)
OR: 2 minor risk factors: (RA, wt<57kg, chronic a-convulsts, HyperTH, smoker, excess EtOH/caffeine, low dietary Ca, heparin, etc)

Front 57

What is the best way to asses Vitamin D stores?
Bone loss occurs from impaired oBlasts and increased bone turnover. What 3 things cause impaired oBlasts? What 2 things cause increased bone turnover?

Back 57

Check plasma 25-OH-VitD3
Impaired oBlasts:
- decreased physical activity, estrogen and GH.
Increased bone turnover: decreased estrogen, low Vit D --> less Ca+ absorbed from gut --> increase PTH

Front 58

How do bisphosphonates work?
What is their bioavailability like?
Adverse effects? (4)

Back 58

They get incorporated into bones and then disable oClasts who come along and eat them.
Very poorly absorbed - must be take after an overnight fast and 2hrs before eating. 50% excretion from kidneys.
- upper GI irritation
- fever/flu (IV only & usually with 1st infusion)
- Bone & joint pain
- osteonecrosis of the jaw (= exposed bone that doesn't heal after 6wks, sx makes it worse, occurs mainly in pt's with prolonged IV therapy - rare in oral dosing)

Front 59

What are SERMs and what are they used for (how do they work)?
Raloxifene is as effective as tamoxifen. What are 2 side effects of raloxifene?

Back 59

Selective Estrogen Receptor Modulatros, they bind to Est receptors in some tissues - have agonist effects in the bones and CNS, but antagonist effects in the breast and uterus.
** Raloxifene is the only one approved in Canada
SE: increased hot flashes and leg cramps, but NO increased endometrial hyperplasia/cancer

Front 60

Calcitonin is sometimes used for osteoporosis. What does it do? What is the therapeutic benefit? Side effects?
What drug has ironically been shown to improve bone structure and density? How must it be given?

Back 60

Calcitonin binds to receptors on oClasts, decreasing their #'s and activity. It also acts as an analgesic and can reduce vertebral # pain. (give nasally or SC). SE = N/V, flusing rash.
PTH, if given intermittently, will increase the # and activity of oBlasts = improved strength and density. Mild SE.

Front 61

Hypercalacemia - when will symptoms develop? What are they?

What are the 2 most common causes of hypercalcemia?

Back 61

No absolute value at which symptoms occur - if high Ca develops suddenly will get symptoms.
Moans - lethargy, confusion, decr alertness
Groans - anorexia, constipation, N/V
Stones - risk of kidney stones
Bones - risk of #
Causes: primary hyperparathyroidism and malignancy (PTHrP-producing, ectorpic 1,25-OH-Vit D, lytic bone mets)

Front 62

What are the 3 mechanisms that protect the body from increased plasma [Ca]? What is the net effect of these?
How do you treat primary Hpth?

Back 62

Less PTH is secreted:
1. Kidneys - increased PO4 absorption and Ca+ excretion
2. Vit D - less 1,25-OH-D produced = less Ca/Pi absorbed from intestine and released from the bones
3. Low PTH will cause less Ca+/PO4 to be lost from the bone
Net effect = loss of Ca+ but no change in Pi!
Tx: Sx is curative and in the meantime avoid dehydration as that will dramatically increase [Ca+]

Front 63

What 5 things do you do to manage acute hyperCa?

** Hyper-Ca is a grave prognostic sign for malignancies. Around 50% of people who present with this will die w/in 30days

Back 63

1. Hydrate
2. inhibit bon resorption - bisphosphonates & calcitonin
3. Calciuresis - loop diuretics
4. Glucocorticoids - inhibits osteoclasts
5. Dialysis - if renal failure develops

Front 64

What happens if you have an extra-renal source of 1,25-OH-D? (as seen in some granulomas?)

Back 64

If you're 1,25-OH-D is high (d/t over-expression of 1a-hyroxylase) then you will have increased release of Ca from the bones and increased Ca absorption from the gut. This will increase the plasma [Ca] (which will have neg feedback onto PTH, but these effects are overshadowed).

Front 65

What are 3 causes of hypOcalcemia? What are the neuromuscular, CNS and cardio symptoms?

Back 65

Causes: HypoPTH (post-Sx, autoimmune, idiopathic, PTH resistance), HypoVit D (rickets, dietary, osteomal), Organ disfunction (malabsorption/renal loss)
Symptoms:
Neuromuscular: tetany, Chvostek's sign (hyper CN VII), Trousseau's (bp cuff)
CNS - irritability, seizures, personality change
Cardio - prolonged QT

Front 66

What is the difference between primary and secondary hyperPTH?
What usually causes hypoCa?

Back 66

Primary is a problem with the parathyroid tissue (high [Ca], high PTH), whereas secondary (low [Ca] , high PTH) is a physiologic response to low [Ca], ie an elevation of PTH.
Secondary hypoCa is usually d/t:
- problems with absorption
- urinary Ca+ losses
- disorders of vit D

Front 67

What is osteomalacia? What are 3 potential causes?
What is is called when it happens to children?
What are the clinical features of these diseases?
Treatment?

Back 67

Impaired mineralization of the bony matrix. Caused by: lack of vitD, impaired synthesis of VitD or lack of Ca/Pi at the mineralisation site.
Rickets is osteomalacia of childhood - occurs d/t disorders of Vit D, Pi deficiency, CRF or primary disorders of bone metabolism.
Unlike Osteomalacia, it will cause bony deformities and short statures, myopathy, bone pain. Both have increased # risk.
Tx: supplementation of Ca and Vit D.

Front 68

What is tertiary hyperparathyroidism?
What 2 things will it cause?
Treatment?

Back 68

Autonomous parathyroid glands that secrete PTH regardless of serum [Ca] - resembles primary HPT
Caused by:
- increased # of PT cells
- abnormalities in the Ca-sensing mechanisms
Tx: partial parathyroidectomy, with calcitrol and Ca given post-op.

Front 69

How do corticosteroids induce osteoporosis?
- bones
- hormones (2)
- GI/GU

Back 69

1. reduce oBlastic bone formation by increasing apoptosis and decreasing their life-span and functioning
2. will lower est/test/androgens and will cause an increase in PTH (d/t changes below)
3. cause an decrease in Ca absorption and an increase in renal excretion
** 2 & 3 will cause an increase in oClasting bone resorption.