Endo - 1-29 - Endocrine Htn

Front 1

Associate the following with weight loss

Back 1

Hyperthyroidism
Adrenal insuff
uncontrolled diabetes

Front 2

Associate the following with fatigue

Back 2

Hyper/hypo thyroidism
hypercalcemia
adrenal insuff

Front 3

Best time to test a HTN pt for secondary causes

Back 3

before you start meds - so usually the time of dx

Front 4

Complications of endocrine disorders which can cause HTN

Back 4

atherosclerosis
retinopathy
nephropathy

(more often the other way around where endocrine issues cause HTN which causes complications)

Front 5

BP =

Back 5

(HR * EDV * contractility) * resistance.

(first term is cardiac output)

Front 6

Catecholamines increase...

Back 6

resistance, contractility, HR and CO

leads to vasoconstrictive HTN

Front 7

mineralocorticoids increase...

Back 7

EDV and CO

leads to volume dependent HTN

Front 8

Thyroid homones increase...

Back 8

HR and heart contractility

Front 9

Serum calcium increases...

Back 9

peripheral resistance

Front 10

Primary hyperparathyroidism

Back 10

Hypercalcemia causes vasoconstriction.

REnal impairment occurs from nephrocalcinosis (small calcium deposits in the kidneys)

Hypercalcemia also causes increased plasma renin activity

Front 11

MEN2 syndrome

Back 11

pheochromocytoma and hyperparathyroidism

and that makes sense why medullary thyroid carcinoma (secretes too much calcitonin - a product of C cells of the parathryoid - is associated with MEN2)

Front 12

Acromegaly

Back 12

low renin, GH (severity correlates with GH levels), inc symp tone.

diastolic affected more.

Usually if acromegaly is untreated, pts die of CV disease due to the HTN

Front 13

Pt with many silent MIs

Back 13

they might by hypothyroid and CPK is elevated from that.

remenber, large tongue also with hypothyroidism.

Front 14

Hyperthyroidism

Back 14

increased CO, inc sensitivity to catecholamines, more renin because these pts sweat so much and they can also get dehydrated

usually affects systolic.

Front 15

hypothyroidism

Back 15

diastolic HTN

low renin

these pts may also be hypotensive or normotensive

Front 16

Obesity and HTN

Back 16

Often falsely high reading if small cuff is used.

Probably mainly due to increased insulin resistance (inc insulin levels leads to more Na+ reabsorption)

Front 17

"writing a paper on what causes metabolic syndrome, PCOS, HTN, and obesity - you could use insulin resis as one of the main things that causes all these."

Back 17

adsfasd

Front 18

Type II or I has more HTN?

Back 18

II - especially at time of dx.

Front 19

Etiology of HTN in DM

Back 19

Obesity (II)
insulin resistance --> endothelial changes (II)
hyperglycemia decreases NO
inc sodium renal reabs due to hyperglycemia and insulin resistance)
nephropathy

and HTN makes micro and macrovascular disease more likely to occur too.

Front 20

Cushing's syndrome

Back 20

stretch marks under arms because you are thinning the skin so you see more vascularity.

Excess cortisol goes to liver to inc renin to cause aI-->aII to cause vasoconstriction and aldosterone release.

Cortisol in excess also has a mineralocorticoid effect on its receptor (normally broken down too fast) - so you get sodium and water retention

Front 21

Why is HTN less common with exogenous Cushing's syndrome?

Back 21

this is steroids (medically or non)

because exogenous hrmones don't bind the mineralocorticoid receptor.

Front 22

How long to associated HTN with cushings?

Back 22

years

Front 23

oral contraceptives

Back 23

might activate RAA systemic since estrogen increases renin substrate (angiotensinogen)

so the recommendation is to avoid OCPs if older than 35 and you are a smoker.

Front 24

Congenital adrenal hyperplasia

Back 24

defective synth of cortisol leads to more ACTH which tries to make more cortisol but it cant - so you get shunting to make androgens and mineralocorticoids.

Tx - glucocorticoids

Front 25

21-hydroxylase deficiency

Back 25

a congenital adrenal hyperplasia

There is a mineralocorticoid block where you can't make them - so there is just more androgen and estrogen production

NO HTN

Front 26

11-hydroxylase deficiency

Back 26

Cortisol blockage decreases pit inhibition. So ACTH makes more DOC.

In this case, not more aldosterone but the product before the defective enzyme (11-deoxycortisol) can work on the mineralocorticoid receptor to cause HTN.

Front 27

Pheochromocytoma

Back 27

Of the medulla of the adrenal gland (orig in chromaffin cells) or extra-adrenal chromaffin tissue that didn't involute after birth.

Secretes epi and norepi.

PURELY VASOCONSTRICTIVE FORM OF HTN

Renin and aldos goes down. Pts get dehydrated (so there will be some orthostatic drops in BP)

Most pts have persistent HTN, but some have intermittent and some have palpitations, sweating and no HTN or HA (due to HTN)

Front 28

Familial pheos

Back 28

from mutations in VHL, RET, NF1, SDHB, SDHD

Front 29

Location of pheos

Back 29

90% - adrenal medulla
Mostly unilat, but genetically predisposed ones are more likely to be bilat.

10% - Extra-adrenal chromaffin tissue.

Front 30

Tips to dx pheo

Back 30

suspect, document, locate and treat

Front 31

Dx of pheo

Back 31

24-hr excretion of urinary catecholamines and/or metabolites (metanephrines, vanillylmandelic acid AKA VMA)

Plasma free metanephrines which measures metanephrine or normetanephrine

Localize with imaging.

Front 32

Tx of pheo

Back 32

Pre-op phenoxybenzamine (oral alpha blocker) or phentolamine (IV alpha blocker).

Then beta blocker for arrythmias - after alpha because beta normally causes some vasodilation so you don't wanna have lots of unopposed alpha constriction.

SUrgery

Front 33

Pts with genetic predisp to pheo...

Back 33

Need to be tested every year. More likely to get it in the future.

Front 34

Peri-op management of pheo

Back 34

Alpha blockage to control BP during surg

Beta block for arrhthmias

CVolume expansion after tumor is removed because there will be intravasc dehydration once you get rid of the vasoconstriction

Front 35

If pt has low potassium..

Back 35

worry about primary hyperaldosteronism and don't start pt on thiazides (they excrete K)

Front 36

Primary hyperaldosteronism

Back 36

Secretion of aldosterone by benign adrenocortical adenoma or bilat adrenocortical hyperplasia which leads to soidum retention, vol overload and K wasting and HTN

Front 37

Clinical char of primary hyperaldosteronism

Back 37

Water (which normal supp renin and aldosterone) doesn't suppress aldosterone.

Do a bilateral adrenal vein sampling to see if diff aldos levels are coming out of both sides.

Front 38

How to tell if adenoma or hyperplasia is causing hyperaldosteronism

Back 38

Hyperplasia responds less well to spironolactone bc there may be a circulating substance that leads to bilat hyperplasia and causes vasoconstriction and thus HTN

adenomas suppress renin profoundly and standing doesn't stimulate rise in renin
hyperplasia partially suppresses renin and standing stimulates the RAA axis to cause a slight rise in aldosterone.

Adenomas make more 18-hydrocycorticosterone.

Measurement of aldosterone from each adrenal vein can detect unilat increase of aldosterone which strongly suggests an adenoma.

(so adrenal vein sampling is standard before operation)

Front 39

Why were subtle cases of hyperaldosteronism missed in the past?

Back 39

they used to screen by looking at hypokalemia. but not all HTN pts are hypokalemic.

so now they look for the plasma aldosterone-renin ratio (ARR)

Front 40

11 beta hydroxysteroid dehydrogenase deficiency - apparent mineralocorticoid excess

Back 40

Very very rare cause of endocrine HTN

this converts cortisol to cortisone normally.

will have suppressed aldosterone levels.

tx with dexamethasone (suppresses ACTH) or spironolactone.

licorice contains glycyrrhizic acid which inhibits this enzyme as well.

cortisol binds aldosterone receptor, cortisone does not.

will have HTN, hypokaliema, suppressed renin and supp aldosterone.

Front 41

Glucocorticoid-remediable aldosteronism

Back 41

Very very rare causes of endocrine HTN

(fusion of ACTH activator gene and aldosterone synthase gene). - autosomal dom - hypokal and HTN - Tx is dexamethasone

Front 42

Renin secreting tumors of the JG cells

Back 42

Very very rare causes of endocrine HTN

(will have HTN and hypokalemia)

Front 43

what to order with a newly HTN pt to r/o endocrine causes.

Back 43

Serum aldosterone/renin ratio
Serum potassium level
Serum calcium level
TSH
Serum creatinine
Plasma free metanephrine if there is any clinical suspicion of pheochromocytoma
Other specific endocrine testing if history and/or physical suggest specific endocrine disorder (acromegaly, cushing's syndrome, diabetes)

Front 44

last 10 slides...

Back 44

prractice question

Front 45

Which one of the following mechanisms appears to be the most important factor leading to hypertension in a patient with Cushing’s Disease?

Back 45

mineralocorticoid effects