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47 Cards in this Set

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Hypothyroidism

-Sx?
-Tx?
Sx:
*Hashimoto's (non-pitting myxedema in face, decr HR, decr DTR's)
*cool dry skin, cracked fingernails
*↑↑TSH, ↓free T4

Tx: L-thyroxine
MOA: exogenous T4 (also helps T3 levels b/c T4 converted to T3 intracellularly)

S/E:
-MI or A fib in pt's with CAD/heart dz b/c T4 incr B1 receptors in heart
Tx myxedematous coma
(myxedematous coma d/t hypothyroid pt's non-compliance)

Tx: L-thyroxine (give large IV load)
EXAM-propylthiouracil
(PropylThioUracil=PTU)

Tx:
*Hyperthyroidism
*use PTU instead of methimazole in pregnant women
(PTU binds plasma proteins and less likely to cross placenta)

"Tx Graves' Dz w/PTU + propanolol (not PTU + atenolol!)"

MOA:
1. prevents peripheral conversion of T4==>T3
2. inhibits thyroid peroxidase
==>no conversion of iodide==>iodine ("iodine organification")
3. blocks the coupling of MIT and DIT (PTU prevents "MIT nerd from "coupling" with a hot DITz"), which is req to synthesize T4/T3
==>prevent synthesis of T4 but not release
==>slows onset of T4 action

S/E:
-if woman on PTU begins taking OCP, she can become hypOthyroid b/c estrogen causes incr synthesis of TBG
==>decr free thyroxine
==>hypothy
==>incr total T4, decr free T4, incr TSH
non-pitting myxedema suggests?
Hashimoto's
pretibial myxedema suggests what?
hypERthyroidism
what hormones can lead to hypothy?
estrogen.

estrogen ↑ TBG==>↓free T4
==>hypothyroidism w/ ↑total T4, ↓free T4, ↑TSH

Situations where this occurs:
*woman on PTU (for hyperthy) but then begins taking OCP's (contain est)
*pregnant F (estrogen) taking thyroxine after being Tx with I-131 (radioactive iodine) for Graves
(hypothyroid d/t radioactive iodine)
*Pregnant F (estrogen) w/Hashimoto's who is taking thyroxine
Tx autonomic Sx of hyperthyroidism
DOC=propanolol

MOA: blocks peripheral conversion of T4==>T3
(the only BB that does this!)

PE:
*does not alter underlying xs T4
*controls autonomic Sx only
(tachycardia, palpitations, sweating, fatigue, wt loss, heat intolerance, tremor, & anxiety)
Tx thyroid storm
DOC=propanolol

"thyroid storm"
-fever
-exertional dyspnea, weakness
-vomiting
-can't sleep
*d/t hyperthyroid pt who gets stressed or stops taking Rx

MOA: blocks peripheral conversion of T4==>T3
(the only BB that does this!)

PE:
-does not correct underlying xs T4
*Tx autonomic Sx only:
-tachy, palpitations
-diaphoresis, heat intolerance
-wt loss
-anxiety
propanolol
Tx:
*hyperthy
*"thyroid storm"
-fever
-exertional dyspnea, weakness
-vomiting
-can't sleep
*d/t hyperthyroid pt who gets stressed or stops taking Rx

MOA: blocks peripheral conversion of T4==>T3
(the only BB that does this!)

PE:
-does not correct underlying xs T4
*Tx autonomic Sx only:
-tachy, palpitations
-diaphoresis, heat intolerance
-wt loss
-anxiety
iodide
Tx: hyperthyroidism

*NOT used in routine Tx of hyperthyrodisim
*NOT used as a single agent

MOA:
*immediately decr release of T3/T4 by preventing proteolysis of thyroglobulin
*prevent iodide trapping
==>prevent organification of iodide==>iodine
==>transient decr release of T3/T4
Tx complete/partial central DI
Desmopression (DDAVP)

Tx:
*complete/partial central DI
*partial nephrogenic DI

MOA: synthetic AVP (ADH)

PE: incr urine Osm
Tx partial nephrogenic DI
1. Desmopression (DDAVP)
2. Hydrochlorothiazide


1. Desmopression (DDAVP):
Tx:
*complete/partial central DI
*partial nephrogenic DI

MOA: synthetic AVP (ADH)

PE: incr urine Osm

2. Hydrochlorothiazide

Tx:
*complete nephrogenic DI
(renal tubule unresponsive to ADH)

*partial nephrogenic DI
(larger concentrations of ADH needed)
desmopressin
Tx:
*complete/partial central DI
*partial nephrogenic DI

MOA: synthetic AVP (ADH)

PE: incr urine Osm
Tx: complete nephrogenic DI
Hydrochlorothiazide

Tx:
*complete nephrogenic DI
(renal tubule unresponsive to ADH)

*partial nephrogenic DI
(larger concentrations of ADH needed)
FINAL EXAM:
Tx lithium-induced DI
DOC=amiloride

*amiloride blocks Na channels in principal cells of late DT/CD
==>prevents Li entry

[Note: Lithium enters principal cells of late DT/CD via apical Na channel
==>once inside the principal cell, it inhibiting adenyl cyclase coupled to V2-ADH receptors in CD (so can’t absorb WATERin CD)
==>nephrogenic DI]

causes nephrogenic DI by inhibiting adenyl cyclase coupled to V2-ADH receptors in CD (so can’t absorb Na in CD) (final exam): tx nephrogenic DI with amiloride (see end of section on DI)
Tx Addison's Dz
Hydrocortisone (replaces cortisol) + fludrocortisone (replaces ALDO)
hydrocortisone
Tx: Addison's Dz
PE: replaces missing cortisol
Rx for chronic steroid therapy?
-PREDnisone
-PREDnisolone
-methylPREDnisolone
-triamcinolone

PE: intermediate acting (12-36 hrs) good for chronic steroid Tx

*most effective + minimal suppression of HPA (hypo-pit-adrenal) when do "alternate day therapy" (high dose one day, low-dose next day, then high-dose)
Tx SIADH
demeclocycline

mneum: The murderer in a recent episode of the scientific thriller "CSI ADH" (SIADH) was a really mean demon riding on a cycle killing people!!! (deme-clocycline)

Tx: SIADH (small cell lung CA)

PE: inhibits antidiuretic action of ADH in CD
prednisone
chronic steroid therapy
prednisolone
chronic steroid therapy
methylprednisolone
chronic steroid therapy
triamcinolone
chronic steroid therapy
most potent, longest-acting corticosteroid?
BETamethasone or
DEXamethasone

PE:
greatest anti-inflamm effects and longest duration

mneum: "i BET you that 1000 DEX of cards will last a very long time!"
fludrocortisone
Tx: Addison's Dz

**Tx Addison's with hydrocortisone (replaces cortisol) + fludrocortisone (replaces ALDO
Tx CHILD with asthma
BUDesonide or FLUTicasone

(mneum: imagine the child's toy "my BUDdy and me" playing the FLUTe)

PE:
*inhaled glucocorticoid
*high first-pass metabolism
==>won't stunt a child's growth (b/c less systemic exposure)
budesonide
mneum: child's toy "my BUDdy and me" playing the FLUT

PE:
-inhaled corticotetoid
*high 1st pass metabolism so won't stunt child's growth (b/c less systemic exposure
fluticasone
Tx: child's asthma

mneum: child's toy "my BUDdy and me" playing the FLUT

PE:
-inhaled corticotetoid
*high 1st pass metabolism so won't stunt child's growth (b/c less systemic exposure
Tx dermatitis on scalp
clobetasol

mneum: If see person with dermatitis on scalp, CLOBber their head w/CLOBetasol

PE:
-topical
-suspended in EtOH, so goes right thru hair, evapoates etc (not cream which would be really hard to put on head thru hair)
inhibits steroid synthesis
aminogluthethimide

mneum: Drug talking: "I mean to glut (gorge) all steroids in your body!!!" (amino-gluthethimide, inhibits all steroids in body)

Tx:
*Breast cancer: suppress androgen/est synthesis
--use with dexamethasone for breast cancer
*Cushing's syndrome (adrenal CA)

MOA:
*blocks CYP450scc
==>no conversion of chol to pregnenolone (no adrenal steroids!)
*blocks CYP45011
*blocks aromatase

PE:
"Medical adrenalectomy" (inhibits all steroids in body)
lispro insulin
Tx: DM

PE:
*ultra-short acting insulin
(*glargine (Lantus) + lispro or aspart most closely mimics nl insulin levels in euglycemic pt)
*Adv of regular insulin:
-faster (thus, can take 10 min before meal)
-no incr in duration of action with incr dose

MOA:
-AA substitution of PROline and LYSine prevents lispro from forming hexamers
==>LISPRO (LIS=LYSine, PRO=PROline) MONOMERS quickly absorbed
insulin aspart
Tx: DM

PE:
*ultra-short acting insulin
(*glargine (Lantus) + lispro or aspart most closely mimics nl insulin levels in euglycemic pt)
*Adv of regular insulin:
-faster (thus, can take 10 min before meal)
-no incr in duration of action with incr dose

MOA:
-AA substitution of Proline for ASPARTic acid (thus "insulin ASPART")
ultra-short acting insulins?
*lispro insulin
*insulin aspart
what most closely mimics nl insulin levels in euglycemic pt?
glargine (Lantus) + lispro or aspart
glargine
(lantus)

PE:
-provides BASAL insulin for the day
-give ONCE DAILY b/c absorbed very slowly
==>flat profile on plasma insulin with NO peak concentration
repaglinide
mneum: "RAPID-glinide"

Tx: Type 2 DM

MOA: directly causes insulin release from B cells

PE:
*orally active hypoglycemic Rx
*very rapid & short duration of action
(so can take 10-30 min before meals, peaks in 1 hr)

S/E:
hypoglycemia if OD or used in euglycemic pt
orally-active antihyperglycemic drugs
1. metformin (Glucophage)
2. rosiGLITAZONE
3. pioGLITAZONE

*EXAM-These are #1 first-line drugs for DM 2! b/c they reverse insulin resistance/enhance sensitivity
EXAM: first-line drugs for DM 2?
1. metformin (Glucophage)
2. rosiGLITAZONE
3. pioGLITAZONE

*EXAM-These are #1 first-line drugs for DM 2! b/c they reverse insulin resistance/enhance sensitivity
USMLE: which drug causes Lactic acidosis
metformin (Glucophage)
Metformin
=Glucophage

Tx: 1st line Tx for DM 2

PE:
*orally-active antihyperglycemic
*incr insulin sensitivity in peripheral tissues & liver
==>incr insulin-stimualted glucose utilization via anaerobic pathway
==>LACTIC ACIDOSIS

S/E: LACTIC ACIDOSIS,
thus contraindicated in pts with any previous lactic acidosis of any etiology
USMLE: what drug is contraindicated in pts with any previous lactic acidosis of any etiology?
Metformin (glucophage)
rosiglitazone
PE:
*orally active antihyperglycemic drugs
*incr insulin sensitivity in peripheral tissues
*1st line Tx for DM 2

MOA:
*bind to PPAR-gamma
==>incr expression of genes for:
*GLUT-4 transporter
*insulin receptors
*lipoprotein lipase in periphery
what incr insulin sensitivity in peripheral tissues
1. metformin
2. rosiglitazone
3. pioglitazone

(1st line tx for DM 2)
pioglitazone
PE:
*orally active antihyperglycemic drugs
*incr insulin sensitivity in peripheral tissues
*1st line Tx for DM 2

MOA:
*bind to PPAR-gamma
==>incr expression of genes for:
*GLUT-4 transporter
*insulin receptors
*lipoprotein lipase in periphery
EXAM-sitagliptin
Tx:
*add to Tx of DM 2 who are already on metformin + glitazone
*taken PO--THUS EASIEST TO USE

MOA:
*"incretin" (=GI hormone, =GIP & GLP1) mimetic

*inhibits DPP-4 (Dipeptidyl Peptidase 4)
==>GIP & GLP-1 not degraded

[GIP=Glucose Dependent Insulinotropic Peptide
==>incr insulin secretion after oral glucose]
[GLP-1=Glucagon-like peptide 1
~amylin:
*incr insulin secretion before rise plasma glucose
*decr glucagon secretion
*decr gastric empyting, decr appetite]
EXAM-what DM2 drug is easy to take, take po?
sitagliptin
what can you add to Tx of DM 2 pts already taking metformin and glitazone?
sitagliptin