MOD 6 Flashcards
High iodine uptake/ hyperthyroidism diseases
Graves Multinodular Goiter Toxic solitary nodule TRH secr tumor HCG secr tumor
Low iodine uptake/hypOthyroidism diseases
Hashimotos Subacute thyroiditis Silent thyroiditis Iodine induced (eg from amiodarone) Exogenous L thyroxine admin Struma Ovarii (ectopic thryoid tissue)
Graves patients may have ab’s to what?
TSH
Hashimotos pts/ autoimmune thyroiditis pts have ab’s to?
TPO ab’s
TSI level in graves?
HIGH!
Sx of Graves?
PROPTOSIS (protrusion/Exphthalamos bulging) INCREASED BOWEL MOVEMENTS TREMORS THYROID BRUIT (only in graves!) PERIORBITAL PAIN Anxiety/Irratibility Weakness/fatigue Heat intolerance Can also have infiltrative dermopathy
Free T4 and TSH levels in graves? RAI? (radioactive iodine uptake)
T4 will be high, LOWERING tsh!
RAI uptake high
Toxic solitary nodule sx
Nodular goiter
High free T4, low TSH , incr RAI in part of thyroid
NO proptosis/bruit/abs
Thyroiditis (hypothyroidism) sx
Cervical lymphadenopathy
High T4 low TSH, then switches, positive TPO ab’s, RAI low
NO trempor bruit etc
fatigue and weight gain
Thyroiditis (hypo) graph of T4 and TSH?
thyroid inflamed releasing T4 into circ, so PEAKS, reducing TSH via neg feedback
Eventually thyroid atrophies w fibrosis and produces less T4 (so lowers back down to match TSH), but then TSH rises
PATIENTS CAN RECOVER BACK TO EUTHYROID!
Types of thyroiditis:
Hashimotos
Subacute lymphcytic
Granulomatous (de Quervian)
Hashi- autoimm progressive destr of thryoid parenchyma, histo shows lympho infiltrates
Subacute lymphocytic- autoimm also, occurs AFTER PREGNANCY (postpartum), PAINLESS, lymphocytic inflam of thyroid
Granulo/Quervian- SELF LIMITED secondary to viral infxn, gran inflamm and pain
Sx of interferon induced thyroiditis?
sx: facial puffiness, slow heavy voice, weight gain, cold intolerance, normal gland on exam, feeble heart sounds, slow relaxation reflexes (graves has strong), dry skin and large tongue, TPO ab’s, EKG with low volt complexes and echo with pericardial effusion
What can thyroiditis look similar too?
MENOPAUSE!
However, menopause also inv breast tenderness and hot flashes
(Test for both!)
Addison’s disease
sx
CHRONIC ADRENAL INSUFFICIENCY
-sx: hypotension/shock (not enough cortisol) pigmentation (since reduce cortisol feeds back to incr ACTH which is similar to MSH)
Primary adrenal insuff
all adrenal hormones have issues (cortisol, aldosterone, sex hormones), issue with the ADRENAL GLAND ITSELF in kidney
Low morning cortisol but high ACTH
low aldo but high renin
Secondary adrenal insuff
Problem with the PITUITARY, so ACTH will be LOW from pit, thus low cortisol, but ALDO will be normal bc adrenals are fine
Cosyntropin Stimulation Test
Cosyn= ACTH analog
if given, intact adrenal gland should respond by making cortisol and if it doesn theres primary adrenal insuff (we measure cortisol boudn to cortisol binding globulin)
-but there could be false + if it APPEARS like cortisol is low but it isnt, say due to cirrhosius or nephrotic, or false negative where it looks normal or hgih but hisnt (due to high cortisol binding prot from preg or OCPs)
What do normal adrenal son CT look like? Abnormal/ TB?
elongated comma, if abnormal look v large (if they have stippled calcs its TB)
Tx of adrenal insuff
Primary– hydrocortisone in morning and eve oral (if major give 10x normal) and FLUDROCORTISONE (mineralocorticoid replacement) and DHEA replacements
-for secondary just give hydrocort bc only cortisol isnt working (Adrenal sare fine)
what coudl sxe of cortisol replacement be?
weight gain, insomnia, edema
Congenital Adrenal Hyperplasia (CAH)
Deficiency in 21-OH enzyme inv mineralocorticoid and glucocorticoid pathway
-results in def of aldo and cortisol and overprod of DHEA/andrugens thus test/estr
General path of adrenal steroid synth and where does CAH occur?
cholest to preg
then preg either goes to form DHEA via 17-OH (then to androst which becomes test or estr) (17OH overproduced in CAH)
OR
forks into two other paths which eventually each make aldo and cortisol from 21-OH (CAH is def in 21-OH)
CAH genetics and sx at birth and later on
AR
due to aldo def, salt-wasting
due to dhea excess, females have genital amb and males have early puberty/growth (harder to detect)
-17OH rise with CAH
CAH dx
rise in 17-OH, liquid chrom with mass spec, genotyping for AR
Tx for CAH
hydrocortisone (just like adrenal insuff, since this/Addisons involve cortisol insuff too)
and mineralocorticoid replacement FLUDROCORTISONE and salts (salt wasting common cause of death) (if growth slows then slow down tx)
Possibly feminizing surg etc
Complicatiosn or sxe of CAH tx
Overuse of cortisol can cause cushing like sx
CAH pts can have adrenal masses (it IS hyperplasia after all)
and Leftover adrenal tissue in testicle in some boys (testicular adrenal rests)
Hyperaldosteronism
Too much aldo in zona glom causes Na retention and loading, which can incr blood vol and bp (HTN) causing CV dmg (fibrosis remodeling LV issues MI risk etc)
- can also cause renal dmg (incr glom pressure, incr albumin exr in urine, incr in GFR then decr)
- can also cause hypokalemia and met alkalosis
By what mech does hyperaldo cause hypokal and met acidosis
at DCT, in prinical cell it causes exchange for Na in and K out (Na enters CELL from lumen thru ENac then exits cell into blood thru NaK) in principal cell, and H exits into lumen via channel in a-intercalated cell
What else does aldo do in body
increases SNS tone
Vascon
Incr endothelin (VASOCON)
so can cause HTN
What can hyperaldosteronism be CAUSED by?
Adrenal adenoma and assoc Conn syndrome, bilat adrenal hyperplasia, or Liddles (etc)
-primary dir affects organ but secondary is upreg of upstream signals eg RAAS
Who would we screen/what signs for hyperaldo?
Dx methods?
screen pts with persistent stage 2/3 HTN, or OSA
- correct for hypokal
- captopril challenge test, saline infusion test, adrenal CT scans, adrenal vein sampling
Captopril challenge test
CAPTOPRIL suppresses aldo, so give to pt and if aldo high then they have disease (still producing too much aldo somehow)
(Saline infusion test also confirms)
Tx for hyperaldo
surg to remove tumor, if adenoma/carc
-bileteral adrenal hyperplasia –> give meralocorticoid recept antag (spironolactone, or eplerenone–less potent but fewer gynecomastic sxe)
Pheochromocytoma vs Paraganglioma
Pheochrom produce catechols from adrenal chromaffin cells (E and NE)
Paragang come from extra-adrenal chromaffin cells (like from thorax/ab/pelvis) and only produce epi
What do pheochrom and paragangliomas do?
produce catecholamines (pheo is BOTH e and NE) -sx: paroxysma HTN, headache/palp/sweating triad
Dx of pheochrom and paragang
incr catechol in urine (obv) and metanephrines (epi conv to metanephrine if it sits around)
- false + can be from incr cafeeine/nicotine/uppers bc they can incr epi
- I-123 MIBO scan (I-123 MIBG transported into sns tissues via NE transporter called NET1), confirmatory
pheochrom and paragang rule of 10s
10% are bilateral, familial, malig, outside adr medulla
Associated syndromes with pheochrom and paragang
MEN2A and MEN2B
VHL
Neurofibromatosis type 1
MEN2A MEN2B VHL NF 1 sx
MEN2A cutaneous lichen amyloidosis (rash)
MEN2B mucocutaneous neuromas on mucous membranes
VHL (retinal angiomas)
NFT1 (cafe au late spots, neurofibromas, axillary freckling, Lisch nodules aka spots on iris)
What med must you give if removing a pheochrom or paragang surgically?
irrev a-1 antag (phenoxybenzzamine) first in case epi leeches out of tumor
Metformin SXE and cXI
LACTIC ACIDOSIS (thus liver dmg/alc/chf reducing blood flow to liver) cxi in ppl with high creatinine
TZD sxe and cxi
HEART FAILURE and BONE FRACTURES
(NO hypoglycemia!)
cxi liver and heart disease
Insulin secretagogues for DM2?
Sulfs and glinides!
Glinides timing?
Act fast! Take before each meal (block ATP K+ channels in pancreatic beta cells)
Glinides sxe?
HyPOglycemia and weight gain
What type of drug is metformin and what is its MOA?
Biguanide! decreases liver glucose production
TZD suffix and MOA? dm type?
“zone”
do PPAR-y stuff (in skm, adipose and liver), reduces insulin resistance
T1 DM
Glucosidase inhibitors
Examples? Use? MOA?
acarbose and miglitol
significant postprandial hyperglycemia
carb analogs that act in gut to inhibit gluco
-but may not reach glycemic goal
Glucosidase inhib sxe?
Flatulence and GI issues from unabsorbed carbs by colon bacteria
What do bile acid sequestrants do?
lower LDL cholest
DA agonist examples and what type of DM>
bromocriptine for T2DM–helps ppl get out of circardian clock and not hibernate
DPP-IV inhibitors (GLIPTINS) example and moa
eg incretins
Amplifies glucose-dependent insulin release, no weight change
SGLT2 inhibitors
suffix
MOA
“flozin”
prevents reabs of glucose
SGLT2 inhib flozin SxE
GU stuff etc
What should you treat ketoacidosis with?
short acting insulin IV
what tests do you use to assess glycemic control?
hga1bc and fructosamine
injectable noninsulin hypoglycemics examples/ suffix?
glucagon-like-peptide (GLP-1) receptor agonists (TIDE)
lowers POSTPRANDIAL glucose
short acting noninsulin hypoglycemics? suffix?
exen (LIZARD), lira, lix (-tide), logn acting are albi, dula and exen ER (GLP1 analogs!)
(lowers FASTING glucose)
sxe of noninsulin hypoglycemics?
acute pancreatitis and
C-cell/THYROID hyperplasia
pramlinitide is what type of analog? use?
amylin analog
slow gastric emptying in t2 AND t1DM (glp-1 analogs like exenetide cannot be used in t1DM)
Sulfonurea preffix?
GLI/GLY
INSULINS
PRANDIAL:
Rapid acting: lispro, aspart, glulisine, inhaled
Short-acting: regular crystalline zinc
BASAL:
Intermediate acting: NPH (or Isophane)
Long acting: glargine, detemir
Ultra-long acting: degludec
Which drug causes weight loss?
GLP-1
same with SGLT
adv of metformin?
doesnt cause weight gain, doesnt cause hypogly
insulin and sulfonyureas do?
drugs with hypogly risks?
Insulin, sulfonylureas, glinides (BUt LESS than SU’s!)
